The klotho gene has been identified as an aging suppressor that encodes a protein involved in cardiovascular disease （CVD）. The inac- tivation of the klotho gene causes serious systemic disorders resembling human ag...The klotho gene has been identified as an aging suppressor that encodes a protein involved in cardiovascular disease （CVD）. The inac- tivation of the klotho gene causes serious systemic disorders resembling human aging, such as atherosderosis, diffuse vascular calcification and shortened life span. Klotho has been demonstrated to ameliorate vascular endothelial dysfunction and delay vascular calcification. Fur- thermore, klotho gene polymorphisms in the human are associated with various cardiovascular events. Recent experiments show that klotho may reduce transient receptor potential canonical6 （TRPC6） channels, resulting in protecting the heart from hypertrophy and systolic dys- function. Fibroblast growth factor23 （FGF23） is a bone-derived hormone that plays an important role in the regulation of phosphate and vi- tamin D metabolism. FGF23 accelerates urinary phosphate excretion and suppresses 1,25-dihydroxy vitaminD3 （1,25（OH）2D3）synthesis in the presence ofFGF receptorl （FGFR1） and its co-receptor ldotho, principally in the kidney. The hormonal affects of circulating klotho pro- tein and FGF23 on vascular and heart have contributed to an understanding of their roles in the pathophysiology of arterial stiffness and left ventricular hypertrophy. Klotho and FGF23 appear to play a critical role in the pathogenesis of vascular disease, and may represent a novel potential therapeutic strategy for clinical intervention.展开更多
Objective. This study was to investigate the effects of transforming growth factor-β(TGFβ) and fi- broblast growth factor (FGF) in the subcapsular opacification formation of the lens. Methods. Lens epithelial explan...Objective. This study was to investigate the effects of transforming growth factor-β(TGFβ) and fi- broblast growth factor (FGF) in the subcapsular opacification formation of the lens. Methods. Lens epithelial explants from 10-day-old rats were cultured with TGFβ1 or TGFβ2 in the presence of FGF for 5 days, then were examined by light and electron microscopy, and by immunolocal- ization of smooth muscle(α-sm) actin and type I collagen. Results. In TGFβ/FGF-treated explants,extensive proliferation occured, with formation of spindle and star-shaped cells. These cells showed ultrastructure and biochemical features of fibroblast or myofibroblast. Prominent Golgi apparatus and rough endoplaic reticulum were observed in some cells. Intracellular micro- filaments with cytoplasmic dense babies and membrane associated dense bodies, features of smooth muscle cells, were also observed. Some cells showed reactivity to -sin actin antibody. TGFβ/FGF-treated ex- plants were strongly stained with type I collagen antibody. Condusion. In the presence of FGF, TGFβ1 and TGFβ2 induced lens epithelial cell (LEC ) proliferation and transformation into fibroblast or myofibroblast-like cells, with producing of abundant collagen matrix in the explants. The changes are similar to the metaplasia that occurrs in subcapsular opacification of the lens. The findings suggest that TGFβ and FGF plays a role in the pathogenesis of subcapsular opacification of the lens.展开更多
文摘The klotho gene has been identified as an aging suppressor that encodes a protein involved in cardiovascular disease （CVD）. The inac- tivation of the klotho gene causes serious systemic disorders resembling human aging, such as atherosderosis, diffuse vascular calcification and shortened life span. Klotho has been demonstrated to ameliorate vascular endothelial dysfunction and delay vascular calcification. Fur- thermore, klotho gene polymorphisms in the human are associated with various cardiovascular events. Recent experiments show that klotho may reduce transient receptor potential canonical6 （TRPC6） channels, resulting in protecting the heart from hypertrophy and systolic dys- function. Fibroblast growth factor23 （FGF23） is a bone-derived hormone that plays an important role in the regulation of phosphate and vi- tamin D metabolism. FGF23 accelerates urinary phosphate excretion and suppresses 1,25-dihydroxy vitaminD3 （1,25（OH）2D3）synthesis in the presence ofFGF receptorl （FGFR1） and its co-receptor ldotho, principally in the kidney. The hormonal affects of circulating klotho pro- tein and FGF23 on vascular and heart have contributed to an understanding of their roles in the pathophysiology of arterial stiffness and left ventricular hypertrophy. Klotho and FGF23 appear to play a critical role in the pathogenesis of vascular disease, and may represent a novel potential therapeutic strategy for clinical intervention.
文摘Objective. This study was to investigate the effects of transforming growth factor-β(TGFβ) and fi- broblast growth factor (FGF) in the subcapsular opacification formation of the lens. Methods. Lens epithelial explants from 10-day-old rats were cultured with TGFβ1 or TGFβ2 in the presence of FGF for 5 days, then were examined by light and electron microscopy, and by immunolocal- ization of smooth muscle(α-sm) actin and type I collagen. Results. In TGFβ/FGF-treated explants,extensive proliferation occured, with formation of spindle and star-shaped cells. These cells showed ultrastructure and biochemical features of fibroblast or myofibroblast. Prominent Golgi apparatus and rough endoplaic reticulum were observed in some cells. Intracellular micro- filaments with cytoplasmic dense babies and membrane associated dense bodies, features of smooth muscle cells, were also observed. Some cells showed reactivity to -sin actin antibody. TGFβ/FGF-treated ex- plants were strongly stained with type I collagen antibody. Condusion. In the presence of FGF, TGFβ1 and TGFβ2 induced lens epithelial cell (LEC ) proliferation and transformation into fibroblast or myofibroblast-like cells, with producing of abundant collagen matrix in the explants. The changes are similar to the metaplasia that occurrs in subcapsular opacification of the lens. The findings suggest that TGFβ and FGF plays a role in the pathogenesis of subcapsular opacification of the lens.
