AI Article Synopsis
- The study focuses on the TGF-β1/Smad3 signaling pathway and its role in reducing brain damage in rats experiencing cerebral ischemia and oxygen-glucose deprivation.
- TGF-β1 treatment led to smaller areas of brain infarction and lower levels of apoptosis in affected cells compared to untreated controls, while inhibiting TGF-β1 resulted in larger infarcts.
- Overall, the findings suggest that TGF-β1 and Smad3 could have protective effects against ischemic stroke by promoting cell survival and minimizing brain injury.
Article Abstract
We investigated the transforming growth factor-b1 (TGF-β1)/Smad3 signaling pathway in rats with cerebral ischemia and oxygen-glucose-deprived (OGD) microglia. Cerebral ischemia is a clinical condition that occurs when insufficient blood flows to the brain to maintain metabolic activity. TGF-β1 is a well-known functional peptide that regulates cell differentiation, migration, proliferation, and apoptosis. In the current study, we determined the infarct size and TGF-β1/Smad3 protein expression in stroke-induced rats. Apoptosis and TGF-β1/Smad3 mRNA and protein expression were determined in transfected OGD human microglial cells. TGF-β1 treatment resulted in smaller infarct regions than in control cells, whereas TGF-β1 inhibitor treatment resulted in larger infarcts. The TGF-β1-treated groups showed substantial TGF-β1 and Smad3 expression by immunofluorescence compared to the controls. Apoptosis was significantly reduced in TGF-β1- and Smad3-transfected cells, and an increased rate of apoptosis was observed in Smad3 or TGF-β1 siRNA-transfected cells. TGF-β1 and Smad3 mRNA and protein expression increased following TGF-β1 and Smad3 transfection. Taken together, our experimental results show that Smad3 and TGF-β1 play a protective role against ischemic stroke, as demonstrated by the reduced infarct size. Smad3 and TGF-β1 expression was increased in cells transfected with TGF-β1, whereas Smad3 and TGF-β1 expression was increased in TGF-β1 inhibitor-transfected cells.
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| http://dx.doi.org/10.1016/j.ijbiomac.2018.04.113 | DOI Listing |
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