Recent experimental work implicates transforming growth factor-beta (TGF-beta) as an aetiologic mediator of diabetic nephropathy and the ubiquitous glucose transporter GLUT1 as an important permissive factor for the tissue injury caused by hyperglycaemia.

May 1, 1999 · The results of the Northern blot analysis indicate that TGF-β1 is able to stimulate the expression of mRNA for GLUT1 in a time- and dose-dependent manner in mesangial cells. Furthermore, the expression of GLUT1 protein was also induced by TGF-β1.

This study examined the effects of TGF-β1-mediated pathways on GLUT1 expression in vivo and in vitro, explored the relationship between GLUT1 and TGF-β1 and further investigated the potential underlying mechanisms.

The results link Glut1 repression and reduced glucose uptake to the anti-proliferative response of TGF-β1 and indicate that re-expression of Glut1 and increased glucose uptake during chronic TGF-β1 exposure allow breast cancer cells to develop a …

Because the linkage between glucose metabolism and ECM protein production was found in mesangial cells overexpressed with the brain-type glucose transporter (GLUT1), we hypothesized that TGF-beta 1 could affect glucose metabolism.

The data indicate that glucose transportation via GLUT1 is implicated in the PRR-dependent upregulation of TGF-β while CTGF is mediated mainly via a mechanism depending on ROS formation in renal medullary collecting duct cells.

Dec 1, 2020 · Knockdown of Glut1 resulted in growth inhibition and less induction of vimentin during TGF-β1-induced EMT. Intriguingly, Glut1 levels, glucose uptake and cell proliferation were restored during prolonged EMT.

Dec 1, 1999 · Treatment of rat mesangial cells with TGF-β up-regulates GLUT1 mRNA and protein levels and significantly increases glucose uptake. Addition of neutralizing anti-TGF- β antibody prevents the stimulatory effects of high glucose on GLUT1 expression.

Aug 1, 2016 · Here, we address these important issues and show that: 1) up-regulation of GLUT1 by TGF-β in fibroblasts is a general phenomenon; 2) GLUT1 induction and activity are critical for profibrotic TGF-β signaling; 3) enhanced GLUT1 expression is observed in the lungs of patients with idiopathic pulmonary fibrosis (IPF) and in the bleomycin mouse ...

Dec 1, 2020 · The results link Glut1 repression and reduced glucose uptake to the anti-proliferative response of TGF-β1 and indicate that re-expression of Glut1 and increased glucose uptake during chronic TGF-β1 exposure allow breast cancer cells to develop a more stable EMT and proliferate, in parallel.