Role of transforming growth factor β1 in microvascular endothelial cell apoptosis associated with thrombotic thrombocytopenic purpura and hemolytic‐uremic syndrome

Pathogenesis of Shiga toxin-induced hemolytic uremic syndrome

“…We have found very high levels of bFGF in the circulation of children with D+ HUS [123]. Alternatively, a recent study has shown that the ability of microvascular endothelial cell types to produce TGF-β1 in response to an apoptotic stimulus may determine the susceptibility of these cells to undergo apoptosis [124]. TGF-β1 could be released by activated platelets and injured renal tubular epithelial cells [125,126].…”

Transforming growth factor-beta1 upregulation triggers pulmonary artery smooth muscle cell proliferation and apoptosis imbalance in rats with hypoxic pulmonary hypertension via the PTEN/AKT pathways

“…TGFβ1, a multifunctional cytokine, regulates cell proliferation, growth, differentiation and cell movement through receptors and various intracellular signaling pathways (Kajdaniuk et al , 2013). There is a growing body of evidence that suggests that abnormalities of TGFβ1 signalling pathway are linked to the pathogenesis of PAH (Gilbane et al , 2015, Lu et al , 2015, Ostriker et al , 2014, and that TGFβ1 protectes against apoptosis of pulmonary artery endothelial cell (PAEC) (Lu, 2008, Mauro et al , 2001.…”

Molecular Mechanisms in Thrombotic Thrombocytopenic Purpura

“…Various mechanisms have been proposed to explain the development of thrombosis in TTP, including impaired fibrinolysis, 26 platelet aggregating proteins, 27 calpains on platelet microparticles, 28 endothelial cytotoxic or activating antibodies, 29,30 or plasma factors causing endothelial apoptosis. 31 Other studies described increased levels of endothelial cell activation markers. However, these changes appear to be a consequence of the disease.…”