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- W2355140949 abstract "Excessive cardiac interstitial fibrosis impairs normal cardiac function. We have shown that the α11β1 (α11) integrin mediates fibrotic responses to glycated collagen in rat myocardium by a pathway involving transforming growth factor-β. Little is known of the role of the α11 integrin in the developing mammalian heart. Therefore, we examined the impact of deletion of the α11 integrin in wild-type mice and in mice treated with streptozotocin (STZ) to elucidate the role of the α11 integrin in normal cardiac homeostasis and in the pathogenesis of diabetes-related fibrosis. As anticipated, cardiac fibrosis was reduced in α11 integrin knockout mice (α11 −/− ; C57BL/6 background) treated with STZ compared with STZ-treated wild-type mice ( P < 0.05). Unexpectedly, diastolic function was impaired in both vehicle and STZ-treated α11 −/− mice, as shown by the decreased minimum rate of pressure change and prolonged time constant of relaxation in association with increased end-diastolic pressure (all P < 0.05 compared with wild-type mice). Accordingly, we examined the phenotype of untreated α11 −/− mice, which demonstrated a reduced cardiomyocyte cross-sectional cell area and myofibril thickness (all P < 0.05 compared with wild-type mice) and impaired myofibril arrangement. Immunostaining for desmin and connexin 43 showed abnormal intermediate filament organization at intercalated disks and impaired gap-junction development. Overall, deletion of the α11 integrin attenuates cardiac fibrosis in the mammalian mouse heart and reduces ECM formation as a result of diabetes. Furthermore, α11 integrin deletion impairs cardiac function and alters cardiomyocyte morphology. These findings shed further light on the poorly understood interaction between the fibroblast–cardiomyocyte and the ECM." @default.
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- W2355140949 date "2016-07-01" @default.
- W2355140949 modified "2023-10-18" @default.
- W2355140949 title "The α11 integrin mediates fibroblast–extracellular matrix–cardiomyocyte interactions in health and disease" @default.
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- W2355140949 doi "https://doi.org/10.1152/ajpheart.00918.2015" @default.
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