ArticleNeurotoxicity research2010
The role of integrin alpha(v)beta (8) in neonatal hypoxic-ischemic brain injury.
Article in Neurotoxicity research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The Role of YB1 in Renal Cell Carcinoma Cell Adhesion.International journal of medical sciences · 2018Article
- Cardiac endothelial cell-derived exosomes induce specific regulatory B cells.Scientific reports · 2014Article
- Danhong injection: A modulator for Golgi structural stability after cerebral ischemia-reperfusion injury.Neural regeneration research · 2013Article
- Integrin β8 signaling in neonatal hypoxic-ischemic brain injury.Neurotoxicity research · 2012Article
- 14-3-3gamma and neuroglobin are new intrinsic protective factors for cerebral ischemia.Molecular neurobiology · 2010Review
- From death to recovery following hypoxia ischemia: if TGFbeta is a central regulator, is integrin beta8 the switch?Neurotoxicity research · 2010Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Integrin alpha(v)beta(8) plays an important role in cerebral vascular development. It has been proven that alpha(v)beta(8) is a key factor for transforming growth factor-beta1 (TGF-beta1) activation in epithelial cells. However, it is not clear whether alpha(v)beta(8) can activate TGF-beta1 and play a role in protection during neonatal hypoxic-ischemic brain injury. In this study, we investigated the relationship between alpha(v)beta(8) and TGF-beta1 activation, and thus the effects of TGF-beta1 activation in the protection of neurons after hypoxia-ischemia (HI). Astrocytes and neurons from rat brains were cultured and then subjected to oxygen-glucose deprivation to generate HI model in vitro. beta(8) expression was determined using immunocytochemistry, western blot, and reverse-transcriptase polymerase chain reaction. TGF-beta1 activation was determined by TGF-beta bioassay in a tested cell (astrocyte) and a reporter cell co-culture system. The pro-apoptotic protein, cleaved caspase-3, and the anti-apoptotic protein, Bcl-2 and Bcl-xL, were detected using western blot. Cellular apoptosis was detected with TUNEL. We found that beta(8) expression was stronger in astrocytes than that in neurons under normoxia. HI resulted in a rapid and persistent increase of beta(8) expression in astrocytes, but only in a slight and transient increase in neurons. Astrocytes beta(8) could induce TGF-beta1 leading to upregulation of Bcl-2 and Bcl-xL, and thus attenuated neuronal apoptosis. The present findings suggest that beta(8) protecting the brain against neonatal HI injury through TGF-beta1 signaling pathway, which may have implications for the treatment of HI brain injury.
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Registered trials
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