Aim Following cerebral isehemia, microglia respond to the injury acting as the first defense of central nervous system. Activated microglia play a dual role in the ischemie injury depending on the phenotype of micro-...Aim Following cerebral isehemia, microglia respond to the injury acting as the first defense of central nervous system. Activated microglia play a dual role in the ischemie injury depending on the phenotype of micro- gila, including deleterious M1 phenotype and neuroprotective M2 phenotype. However, microglia show transient M2 phenotype followed by a transition to M1 phenotype aggravating the ischemic injury. Many signal pathways par- ticipate in the modulation of microglial polarization , presenting potential therapeutic targets for selectively inducing the polarization of M2 microglia. In this review, we discuss M2 microglia phenotype mediated neuroprotective role and the signaling cascades controlling microglial phenotype after ischemic stroke.展开更多
Background and Aim Vascular smooth muscle cell （SMC） phenotype change is a hallmark of vascu-lar remodeling, which can be regulated via MicroRNAs （miRNAs）-dependent mechanism. We recently identified Asymmetric dim...Background and Aim Vascular smooth muscle cell （SMC） phenotype change is a hallmark of vascu-lar remodeling, which can be regulated via MicroRNAs （miRNAs）-dependent mechanism. We recently identified Asymmetric dimethylarginine （ADMA） positively correlates to vascular remodeling-based diseases. Here, we hy-pothesized that ADMA induces SMC phenotypic change via a miRNA-dependent mechanism. Methods and Results Microarray analysis enabled the identification of 7 deregulated microRNAs in ADMA-treated human aortic artery smooth muscle cells （hASMCs）. miR-182 was validated by real-time-PCR. Isobaric tags for relative and absolute quantitation （iTRAQ） based analysis of the hASMC proteome revealed that transfection of an miR-182 inhibitor sig- nificantly increased myeloid-associated differentiation marker （MYADM）, which was verified using Western blot and reporter activity quantization with the MYADM 3＇-UTR dual-luciferase reporter system, miR-182 knockdown further repressed Sprouty2 and enhanced MYADM, leading to ERICZMAP kinase-dependent and MYADM-depend- ent hASMC phenotypic change including proliferation, migration and differentiation marker gene expression change. In vivo, adeno-miR-182 markedly suppressed carotid neointimal formation by using balloon-injured rat carotid artery model, specifically via decreased MYADM expression. Atherosclerotic lesions from patients with high ADMA plas- ma levels exhibited decreased miR-182 expression levels and elevated MYADM expression levels. In patients with coronary heart disease （n- 164）, the miR-182 expression level in plasma was negatively correlated with the plas- ma ADMA levels. Conclusions miR-182 is a novel SMC phenotypic modulator by targeting MYADM and can be a potential therapeutic target combating vascular remodeling-associated diseases. Reduced plasma miR-182 levels might be a new predictor of high vascular remodeling risk especially in patient with coronary heart disease.展开更多
Objective: Overexpression of the membraneepidermal growth factor receptor (EGFR) in humantumor cells predicts for poor prognosis. Hence, weexperimentally investigated the effects of humanEGFR to the malignant phenotyp...Objective: Overexpression of the membraneepidermal growth factor receptor (EGFR) in humantumor cells predicts for poor prognosis. Hence, weexperimentally investigated the effects of humanEGFR to the malignant phenotype in humen breastcancer cell line MDA-MB-231 and humannasopharyngeal carcinoma cell line CNE-2. Methods:展开更多
Objectives:To isolate tumor metastaticsuppressing genes or relating human DNA sequencesand to study the molecular biological regulatingmechanism of tumor metastasis. Methods: HumanDNA fragments were amplified by Inter...Objectives:To isolate tumor metastaticsuppressing genes or relating human DNA sequencesand to study the molecular biological regulatingmechanism of tumor metastasis. Methods: HumanDNA fragments were amplified by Inter Alu PCRtechnique from normal human genomic DNAtransfected mouse tumor cell clones of which themetastatic phenotype had been suppressed. Thehuman origin of the amplified DNA was furtherconfirmed by PCR in situ hybridization. One展开更多
Background and Objective Desminopathy is a largely heterogeneous group of conditions involving inherited or sporadic myofibrillar myopathy.In terms of its mode of inheritance,the autosomal dominant form is predominant...Background and Objective Desminopathy is a largely heterogeneous group of conditions involving inherited or sporadic myofibrillar myopathy.In terms of its mode of inheritance,the autosomal dominant form is predominant.Desmin gene(DES)mutations play a critical role among the pathogenic inherited factors associated with desminopathy.Desminopathy involves various phenotypes,mainly including different cardiomyopathies,skeletal myopathy and arrhythmia.The purposes of this study are characterization of a novel phenotype and identification of a DES splicing mutation in a Chinese family with desminnopathy.展开更多
OBJECTIVE Transgenic mouse model has been widely used in pathogenesis study and preclinical drug evaluation in Alzheimer disease(AD).However,key differences are found between current animal models and clinical AD pati...OBJECTIVE Transgenic mouse model has been widely used in pathogenesis study and preclinical drug evaluation in Alzheimer disease(AD).However,key differences are found between current animal models and clinical AD patients regarding phenotypes.Lack of complete models that recapitulate broad spectrum of human AD neuropathology restricts efficacy of research projects and leads to frequent failure in AD drug development at clinical trial stages.This study aims to develop better mouse models of AD through modifying key phenotype insufficiency.METHODS By crossing different single and double transgenic mice with different mutations of APP/PS1 or tau and under prion,Thy1 or PDGF-β promoter,as well as selected knockout mice,I produced a dozen of bigenic models for neuropathology screening.Further neurochemical,behavioral and pharmacological validations were conducted in the optimized mouse model.RESULTS Neuropathology phenotyping found remarkable differences in tau pathology and neurodegeneration among individual APP/PS1/tau transgenic models.I had identified a triple mouse model named FADT that showed(1) huge mature tau pathology in hippocampus and cortex;(2) abundant tau truncation,as seen in human AD brain;(3)progressive neurodegeneration;(4)selective brain atrophy in hippocampus and entorhinal cortex;(5) reproducible and late onset spatial memory defects,etc.Importantly,remarkable tau pathology in this FADT model is mainly driven by beta-amyloid pathology,which differs from high expression of tau in rTg4510 model.CONCLUSION I had developed a new triple transgenic mouse model that recapitulates broad spectrum of human AD neuropathology features.This study will not only establish a solid model basis for AD pathophysiology investigation and drug development,but also reveal important clues on the interaction of beta-amyloid and tau pathologies in the brain.展开更多
Introduction Atherosclerosis is a potentially life-threatening disease of large arteries that is strongly associated with systemic risk factors such as hypercholesterolemia,hypertension,smoking,and diabetes. However,a...Introduction Atherosclerosis is a potentially life-threatening disease of large arteries that is strongly associated with systemic risk factors such as hypercholesterolemia,hypertension,smoking,and diabetes. However,atherosclerosis develops as a展开更多
In addition to the negative consequences of climate change,sucking pest complexes severely limited cotton yields in the recent past.Although the damage caused by bollworms was much reduced by utilizing Bt cotton,the e...In addition to the negative consequences of climate change,sucking pest complexes severely limited cotton yields in the recent past.Although the damage caused by bollworms was much reduced by utilizing Bt cotton,the emergence of sucking pests(such as aphids,thrips,and whiteflies)poses a serious threat to cotton production,as they reduce lint yield by 40%–60%finally.Additionally,these pests also caused yield losses by spreading viral diseases.Promoting innovative and thorough control methods is necessary to counter the threat posed by these sucking pests.Such initiatives necessitate a multifaceted strategy that combines next-generation breeding technology and pest management techniques to produce novel cotton cultivars that are resistant to sucking pests.The discovery of novel genes and regulatory factors linked to cotton’s resistance to sucking pests will be possible by the combination of next-generation breeding technologies and omics approaches and employing those tools on special resistant donors.Continuous research aimed at understanding the genetic basis of insect resistance and improving integrated pest management(IPM)techniques is crucial to the sustainability and resilience of cotton cropping systems.To this end,a sustainable and viable strategy to protect cotton fields from sucking pests is outlined.展开更多
[Objective]Accurate prediction of tomato growth height is crucial for optimizing production environments in smart farming.However,current prediction methods predominantly rely on empirical,mechanistic,or learning-base...[Objective]Accurate prediction of tomato growth height is crucial for optimizing production environments in smart farming.However,current prediction methods predominantly rely on empirical,mechanistic,or learning-based models that utilize either images data or environmental data.These methods fail to fully leverage multi-modal data to capture the diverse aspects of plant growth comprehensively.[Methods]To address this limitation,a two-stage phenotypic feature extraction(PFE)model based on deep learning algorithm of recurrent neural network(RNN)and long short-term memory(LSTM)was developed.The model integrated environment and plant information to provide a holistic understanding of the growth process,emploied phenotypic and temporal feature extractors to comprehensively capture both types of features,enabled a deeper understanding of the interaction between tomato plants and their environment,ultimately leading to highly accurate predictions of growth height.[Results and Discussions]The experimental results showed the model's ef‐fectiveness:When predicting the next two days based on the past five days,the PFE-based RNN and LSTM models achieved mean absolute percentage error(MAPE)of 0.81%and 0.40%,respectively,which were significantly lower than the 8.00%MAPE of the large language model(LLM)and 6.72%MAPE of the Transformer-based model.In longer-term predictions,the 10-day prediction for 4 days ahead and the 30-day prediction for 12 days ahead,the PFE-RNN model continued to outperform the other two baseline models,with MAPE of 2.66%and 14.05%,respectively.[Conclusions]The proposed method,which leverages phenotypic-temporal collaboration,shows great potential for intelligent,data-driven management of tomato cultivation,making it a promising approach for enhancing the efficiency and precision of smart tomato planting management.展开更多
A fiberless seed mutant(fl)was identified in acommercial cotton(Gossypium hirsutum L.)variety Xu-Zhou 142(FL).This phenotype isassociated with lack of fiber cell initiation in theouter integument of the ovule,as wasch...A fiberless seed mutant(fl)was identified in acommercial cotton(Gossypium hirsutum L.)variety Xu-Zhou 142(FL).This phenotype isassociated with lack of fiber cell initiation in theouter integument of the ovule,as wascharacterized by analysis of genes related to展开更多
Background&Objective Tumor-associated macrophages(TAM)are induced by many cytokines,such as IL-4,IL-10,IL-13,and are considered to be of the M2 phenotype,which provides an immunosuppressive microenvironment for tu...Background&Objective Tumor-associated macrophages(TAM)are induced by many cytokines,such as IL-4,IL-10,IL-13,and are considered to be of the M2 phenotype,which provides an immunosuppressive microenvironment for tumor growth.However,biomechanistssuggest that cells in the tumor microenvironment are affected not only by chemical signals but also mechanical factors,of which the stiffness of tissues is a major determinant.Compared with normal tissues,including the peri-tumor tissues,tumor tissues are more rigid.Heretofore,the influence,on the differentiation and function of macrophages,of the differences in such physical aspect between展开更多
Introduction Regenerative medicine holds great promise for the treatment of diseases that are unbeatable at present,such as various gene and neurological disorders,cardiovascular diseases,as well as hematological mali...Introduction Regenerative medicine holds great promise for the treatment of diseases that are unbeatable at present,such as various gene and neurological disorders,cardiovascular diseases,as well as hematological malignancies.Realization of this potential remains limited by current challenges associated with the control of cell phenotype and function in cell culture.In this respect,the fate of cells is dictated by the in vivo microenvironment where these cells interact with both the extracellular matrix(ECM)and with neighboring cells.The ECM serves as a structural support for cells and provides,in concert with spatio-temporally arranged biochemical cues such as soluble factors,topographical and mechanical cues that direct cell adhesion,spreading,migra-展开更多
Aim It is well known that menopause could worsen age-related ventricular concentric remodeling and increased incidence of arrhythmias following estrogen （E2） deficiency. However, the underlying mechanisms of such ph...Aim It is well known that menopause could worsen age-related ventricular concentric remodeling and increased incidence of arrhythmias following estrogen （E2） deficiency. However, the underlying mechanisms of such phenomena are not fully understood. Mitochondria, as the ＇cellular power station＇ of hearts, play an impor- tant role in maintaining normal cardiac function and structure. Therefore, the present study aims to investigate whether mitochondrial compromise and gap junction impairment induced by miR-23a is responsible for E2 deficien- cy associated structural and electrical remodeling. Results： We found mitochondrial structural damages and respira- tory function impairment in myocardium of both postmenopausal and OVX mice and E2 supplement reversed mito- chondrial dysfunction in OVX mice, suggesting that E2 deficiency could induce mitochondrial compromise in the lar remodeling, which can be regulated via MicroRNAs （miRNAs）-dependent mechanism. We recently identified Asymmetric dimethylarginine （ADMA） positively correlates to vascular remodeling-based diseases. Here, we hy- pothesized that ADMA induces SMC phenotypic change via a miRNA-dependent mechanism. Methods and Results Microarray analysis enabled the identification of 7 deregulated microRNAs in ADMA-treated human aortic artery smooth muscle cells （hASMCs）. miR-182 was validated by real-time-PCR. Isobaric tags for relative and absolute quantitation （iTRAQ） based analysis of the hASMC proteome revealed that transfection of an miR-182 inhibitor sig- nificantly increased myeloid-associated differentiation marker （MYADM）, which was verified using Western blot and reporter activity quantization with the MYADM 3＇-UTR dual-luciferase reporter system, miR-182 knockdown further repressed Sprouty2 and enhanced MYADM, leading to ERIC/MAP kinase-dependent and MYADM-depend- ent hASMC phenotypic change including proliferation, migration and differentiation marker gene expression change. In vivo, adeno-miR-182 markedly suppressed carotid neointimal formation by using balloon-injured rat carotid artery model, specifically via decreased MYADM expression. Atherosclerotic lesions from patients with high ADMA plas- ma levels exhibited decreased miR-182 expression levels and elevated MYADM expression levels. In patients with coronary heart disease （n- 164）, the miR-182 expression level in plasma was negatively correlated with the plas- ma ADMA levels. Conclusions miR-182 is a novel SMC phenotypic modulator by targeting MYADM and can be a potential therapeutic target combating vascular remodeling-associated diseases. Reduced plasma miR-182 levels might be a new predictor of high vascular remodeling risk especially in patient with coronary heart disease.展开更多
Cancer gene therapy over the past several yearshas involved the introduction of genes intohematopoietic cells for: (1) protecting the normalcells from the side effects of chemotherapy; (2)introduction of genes into th...Cancer gene therapy over the past several yearshas involved the introduction of genes intohematopoietic cells for: (1) protecting the normalcells from the side effects of chemotherapy; (2)introduction of genes into the neoplastic cells for展开更多
We conducted this study to determine if marker-assisted mass recurrent selection for fiberstrength and resistance to Helicoverpa armigerawithin an upland cotton complex populationcould he more efficient than conventio...We conducted this study to determine if marker-assisted mass recurrent selection for fiberstrength and resistance to Helicoverpa armigerawithin an upland cotton complex populationcould he more efficient than conventionalphenotype selection.Two cycles of marker-assisted selection,phenotypic selection,andmarker and phenotype concurrent selection,展开更多
Objective To establish three-dimensional phenotyping system for congenital heart disease in mouse and to lay a foundation for the study of phenotype identification and mechanism of congenital heart disease.Methods Twe...Objective To establish three-dimensional phenotyping system for congenital heart disease in mouse and to lay a foundation for the study of phenotype identification and mechanism of congenital heart disease.Methods Twelve SPF C57BL/6 J wild type pregnant mice(8-10 week-old)were randomly divided into control group(n=6)and experimental group(n=6).展开更多
To define the function of Zbtb20 in vivo,we generated knockout mice by homologous recombination.Zbtb20 null mice displayed a stark phenotype characterized by postnatal growth retardation,
The NSF Cotton Genome Centers EST projecthas released】36000 cotton fiber EST sequencesfrom Gossypium arboreum,an A-genome diploidspecies.Of the approximately 10000 genesexpressed in rapidly elongating cotton fibers,5...The NSF Cotton Genome Centers EST projecthas released】36000 cotton fiber EST sequencesfrom Gossypium arboreum,an A-genome diploidspecies.Of the approximately 10000 genesexpressed in rapidly elongating cotton fibers,50% or more encode unknown gene functions.The next challenge facing cotton researchers isdetermining the function of the fiber genes,andwhat role each plays in determiningagronomically important fiber traits.展开更多
文摘Aim Following cerebral isehemia, microglia respond to the injury acting as the first defense of central nervous system. Activated microglia play a dual role in the ischemie injury depending on the phenotype of micro- gila, including deleterious M1 phenotype and neuroprotective M2 phenotype. However, microglia show transient M2 phenotype followed by a transition to M1 phenotype aggravating the ischemic injury. Many signal pathways par- ticipate in the modulation of microglial polarization , presenting potential therapeutic targets for selectively inducing the polarization of M2 microglia. In this review, we discuss M2 microglia phenotype mediated neuroprotective role and the signaling cascades controlling microglial phenotype after ischemic stroke.
文摘Background and Aim Vascular smooth muscle cell （SMC） phenotype change is a hallmark of vascu-lar remodeling, which can be regulated via MicroRNAs （miRNAs）-dependent mechanism. We recently identified Asymmetric dimethylarginine （ADMA） positively correlates to vascular remodeling-based diseases. Here, we hy-pothesized that ADMA induces SMC phenotypic change via a miRNA-dependent mechanism. Methods and Results Microarray analysis enabled the identification of 7 deregulated microRNAs in ADMA-treated human aortic artery smooth muscle cells （hASMCs）. miR-182 was validated by real-time-PCR. Isobaric tags for relative and absolute quantitation （iTRAQ） based analysis of the hASMC proteome revealed that transfection of an miR-182 inhibitor sig- nificantly increased myeloid-associated differentiation marker （MYADM）, which was verified using Western blot and reporter activity quantization with the MYADM 3＇-UTR dual-luciferase reporter system, miR-182 knockdown further repressed Sprouty2 and enhanced MYADM, leading to ERICZMAP kinase-dependent and MYADM-depend- ent hASMC phenotypic change including proliferation, migration and differentiation marker gene expression change. In vivo, adeno-miR-182 markedly suppressed carotid neointimal formation by using balloon-injured rat carotid artery model, specifically via decreased MYADM expression. Atherosclerotic lesions from patients with high ADMA plas- ma levels exhibited decreased miR-182 expression levels and elevated MYADM expression levels. In patients with coronary heart disease （n- 164）, the miR-182 expression level in plasma was negatively correlated with the plas- ma ADMA levels. Conclusions miR-182 is a novel SMC phenotypic modulator by targeting MYADM and can be a potential therapeutic target combating vascular remodeling-associated diseases. Reduced plasma miR-182 levels might be a new predictor of high vascular remodeling risk especially in patient with coronary heart disease.
文摘Objective: Overexpression of the membraneepidermal growth factor receptor (EGFR) in humantumor cells predicts for poor prognosis. Hence, weexperimentally investigated the effects of humanEGFR to the malignant phenotype in humen breastcancer cell line MDA-MB-231 and humannasopharyngeal carcinoma cell line CNE-2. Methods:
文摘Objectives:To isolate tumor metastaticsuppressing genes or relating human DNA sequencesand to study the molecular biological regulatingmechanism of tumor metastasis. Methods: HumanDNA fragments were amplified by Inter Alu PCRtechnique from normal human genomic DNAtransfected mouse tumor cell clones of which themetastatic phenotype had been suppressed. Thehuman origin of the amplified DNA was furtherconfirmed by PCR in situ hybridization. One
文摘Background and Objective Desminopathy is a largely heterogeneous group of conditions involving inherited or sporadic myofibrillar myopathy.In terms of its mode of inheritance,the autosomal dominant form is predominant.Desmin gene(DES)mutations play a critical role among the pathogenic inherited factors associated with desminopathy.Desminopathy involves various phenotypes,mainly including different cardiomyopathies,skeletal myopathy and arrhythmia.The purposes of this study are characterization of a novel phenotype and identification of a DES splicing mutation in a Chinese family with desminnopathy.
基金Science and Technology Development Fund of Shanghai Pudong New District (PKJ2017-Y37)Shanghai Natural Science Foundation(18ZR1417900).
文摘OBJECTIVE Transgenic mouse model has been widely used in pathogenesis study and preclinical drug evaluation in Alzheimer disease(AD).However,key differences are found between current animal models and clinical AD patients regarding phenotypes.Lack of complete models that recapitulate broad spectrum of human AD neuropathology restricts efficacy of research projects and leads to frequent failure in AD drug development at clinical trial stages.This study aims to develop better mouse models of AD through modifying key phenotype insufficiency.METHODS By crossing different single and double transgenic mice with different mutations of APP/PS1 or tau and under prion,Thy1 or PDGF-β promoter,as well as selected knockout mice,I produced a dozen of bigenic models for neuropathology screening.Further neurochemical,behavioral and pharmacological validations were conducted in the optimized mouse model.RESULTS Neuropathology phenotyping found remarkable differences in tau pathology and neurodegeneration among individual APP/PS1/tau transgenic models.I had identified a triple mouse model named FADT that showed(1) huge mature tau pathology in hippocampus and cortex;(2) abundant tau truncation,as seen in human AD brain;(3)progressive neurodegeneration;(4)selective brain atrophy in hippocampus and entorhinal cortex;(5) reproducible and late onset spatial memory defects,etc.Importantly,remarkable tau pathology in this FADT model is mainly driven by beta-amyloid pathology,which differs from high expression of tau in rTg4510 model.CONCLUSION I had developed a new triple transgenic mouse model that recapitulates broad spectrum of human AD neuropathology features.This study will not only establish a solid model basis for AD pathophysiology investigation and drug development,but also reveal important clues on the interaction of beta-amyloid and tau pathologies in the brain.
基金support from National Heart Lung and Blood Institute Grants P50-HL56985 and R01-HL61794
文摘Introduction Atherosclerosis is a potentially life-threatening disease of large arteries that is strongly associated with systemic risk factors such as hypercholesterolemia,hypertension,smoking,and diabetes. However,atherosclerosis develops as a
基金M/s.RASI Seeds Pvt.Ltd.,Attur,Tamil Nadu,India for their generous financial assistance in setting up a MAS study in cotton for genetic improvement of sucking pest resistance.
文摘In addition to the negative consequences of climate change,sucking pest complexes severely limited cotton yields in the recent past.Although the damage caused by bollworms was much reduced by utilizing Bt cotton,the emergence of sucking pests(such as aphids,thrips,and whiteflies)poses a serious threat to cotton production,as they reduce lint yield by 40%–60%finally.Additionally,these pests also caused yield losses by spreading viral diseases.Promoting innovative and thorough control methods is necessary to counter the threat posed by these sucking pests.Such initiatives necessitate a multifaceted strategy that combines next-generation breeding technology and pest management techniques to produce novel cotton cultivars that are resistant to sucking pests.The discovery of novel genes and regulatory factors linked to cotton’s resistance to sucking pests will be possible by the combination of next-generation breeding technologies and omics approaches and employing those tools on special resistant donors.Continuous research aimed at understanding the genetic basis of insect resistance and improving integrated pest management(IPM)techniques is crucial to the sustainability and resilience of cotton cropping systems.To this end,a sustainable and viable strategy to protect cotton fields from sucking pests is outlined.
文摘[Objective]Accurate prediction of tomato growth height is crucial for optimizing production environments in smart farming.However,current prediction methods predominantly rely on empirical,mechanistic,or learning-based models that utilize either images data or environmental data.These methods fail to fully leverage multi-modal data to capture the diverse aspects of plant growth comprehensively.[Methods]To address this limitation,a two-stage phenotypic feature extraction(PFE)model based on deep learning algorithm of recurrent neural network(RNN)and long short-term memory(LSTM)was developed.The model integrated environment and plant information to provide a holistic understanding of the growth process,emploied phenotypic and temporal feature extractors to comprehensively capture both types of features,enabled a deeper understanding of the interaction between tomato plants and their environment,ultimately leading to highly accurate predictions of growth height.[Results and Discussions]The experimental results showed the model's ef‐fectiveness:When predicting the next two days based on the past five days,the PFE-based RNN and LSTM models achieved mean absolute percentage error(MAPE)of 0.81%and 0.40%,respectively,which were significantly lower than the 8.00%MAPE of the large language model(LLM)and 6.72%MAPE of the Transformer-based model.In longer-term predictions,the 10-day prediction for 4 days ahead and the 30-day prediction for 12 days ahead,the PFE-RNN model continued to outperform the other two baseline models,with MAPE of 2.66%and 14.05%,respectively.[Conclusions]The proposed method,which leverages phenotypic-temporal collaboration,shows great potential for intelligent,data-driven management of tomato cultivation,making it a promising approach for enhancing the efficiency and precision of smart tomato planting management.
文摘A fiberless seed mutant(fl)was identified in acommercial cotton(Gossypium hirsutum L.)variety Xu-Zhou 142(FL).This phenotype isassociated with lack of fiber cell initiation in theouter integument of the ovule,as wascharacterized by analysis of genes related to
文摘Background&Objective Tumor-associated macrophages(TAM)are induced by many cytokines,such as IL-4,IL-10,IL-13,and are considered to be of the M2 phenotype,which provides an immunosuppressive microenvironment for tumor growth.However,biomechanistssuggest that cells in the tumor microenvironment are affected not only by chemical signals but also mechanical factors,of which the stiffness of tissues is a major determinant.Compared with normal tissues,including the peri-tumor tissues,tumor tissues are more rigid.Heretofore,the influence,on the differentiation and function of macrophages,of the differences in such physical aspect between
基金supported by the National Institute of Health(NIH HL83008)
文摘Introduction Regenerative medicine holds great promise for the treatment of diseases that are unbeatable at present,such as various gene and neurological disorders,cardiovascular diseases,as well as hematological malignancies.Realization of this potential remains limited by current challenges associated with the control of cell phenotype and function in cell culture.In this respect,the fate of cells is dictated by the in vivo microenvironment where these cells interact with both the extracellular matrix(ECM)and with neighboring cells.The ECM serves as a structural support for cells and provides,in concert with spatio-temporally arranged biochemical cues such as soluble factors,topographical and mechanical cues that direct cell adhesion,spreading,migra-
文摘Aim It is well known that menopause could worsen age-related ventricular concentric remodeling and increased incidence of arrhythmias following estrogen （E2） deficiency. However, the underlying mechanisms of such phenomena are not fully understood. Mitochondria, as the ＇cellular power station＇ of hearts, play an impor- tant role in maintaining normal cardiac function and structure. Therefore, the present study aims to investigate whether mitochondrial compromise and gap junction impairment induced by miR-23a is responsible for E2 deficien- cy associated structural and electrical remodeling. Results： We found mitochondrial structural damages and respira- tory function impairment in myocardium of both postmenopausal and OVX mice and E2 supplement reversed mito- chondrial dysfunction in OVX mice, suggesting that E2 deficiency could induce mitochondrial compromise in the lar remodeling, which can be regulated via MicroRNAs （miRNAs）-dependent mechanism. We recently identified Asymmetric dimethylarginine （ADMA） positively correlates to vascular remodeling-based diseases. Here, we hy- pothesized that ADMA induces SMC phenotypic change via a miRNA-dependent mechanism. Methods and Results Microarray analysis enabled the identification of 7 deregulated microRNAs in ADMA-treated human aortic artery smooth muscle cells （hASMCs）. miR-182 was validated by real-time-PCR. Isobaric tags for relative and absolute quantitation （iTRAQ） based analysis of the hASMC proteome revealed that transfection of an miR-182 inhibitor sig- nificantly increased myeloid-associated differentiation marker （MYADM）, which was verified using Western blot and reporter activity quantization with the MYADM 3＇-UTR dual-luciferase reporter system, miR-182 knockdown further repressed Sprouty2 and enhanced MYADM, leading to ERIC/MAP kinase-dependent and MYADM-depend- ent hASMC phenotypic change including proliferation, migration and differentiation marker gene expression change. In vivo, adeno-miR-182 markedly suppressed carotid neointimal formation by using balloon-injured rat carotid artery model, specifically via decreased MYADM expression. Atherosclerotic lesions from patients with high ADMA plas- ma levels exhibited decreased miR-182 expression levels and elevated MYADM expression levels. In patients with coronary heart disease （n- 164）, the miR-182 expression level in plasma was negatively correlated with the plas- ma ADMA levels. Conclusions miR-182 is a novel SMC phenotypic modulator by targeting MYADM and can be a potential therapeutic target combating vascular remodeling-associated diseases. Reduced plasma miR-182 levels might be a new predictor of high vascular remodeling risk especially in patient with coronary heart disease.
文摘Cancer gene therapy over the past several yearshas involved the introduction of genes intohematopoietic cells for: (1) protecting the normalcells from the side effects of chemotherapy; (2)introduction of genes into the neoplastic cells for
文摘We conducted this study to determine if marker-assisted mass recurrent selection for fiberstrength and resistance to Helicoverpa armigerawithin an upland cotton complex populationcould he more efficient than conventionalphenotype selection.Two cycles of marker-assisted selection,phenotypic selection,andmarker and phenotype concurrent selection,
文摘Objective To establish three-dimensional phenotyping system for congenital heart disease in mouse and to lay a foundation for the study of phenotype identification and mechanism of congenital heart disease.Methods Twelve SPF C57BL/6 J wild type pregnant mice(8-10 week-old)were randomly divided into control group(n=6)and experimental group(n=6).
文摘To define the function of Zbtb20 in vivo,we generated knockout mice by homologous recombination.Zbtb20 null mice displayed a stark phenotype characterized by postnatal growth retardation,
文摘The NSF Cotton Genome Centers EST projecthas released】36000 cotton fiber EST sequencesfrom Gossypium arboreum,an A-genome diploidspecies.Of the approximately 10000 genesexpressed in rapidly elongating cotton fibers,50% or more encode unknown gene functions.The next challenge facing cotton researchers isdetermining the function of the fiber genes,andwhat role each plays in determiningagronomically important fiber traits.
