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|Title:||Effects of hypoxia on expression of transforming growth factor-β1 and its receptors I and II in the amoeboid microglial cells and murine BV-2 cells|
TGF-β receptor I
TGF-β receptor II
transforming growth factor-β1
|Source:||Li, J.-J., Wu, C.-Y., Kaur, C., Sivakumar, V., Ling, E.-A., Lu, J. (2008). Effects of hypoxia on expression of transforming growth factor-β1 and its receptors I and II in the amoeboid microglial cells and murine BV-2 cells. Neuroscience 156 (3) : 662-672. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neuroscience.2008.07.061|
|Abstract:||Transforming growth factor-β1 (TGF-β1) is widely recognized as a prototype of multifunctional growth factors and master switches in the regulation of key events of development, disease and repair. It is localized in neurons, astrocytes and brain macrophages in altered conditions but its localization in the amoeboid microglial cells (AMC), a nascent brain macrophage in the developing brain has remained unexplored. Here we report expression of TGF-β1 and its receptors namely, transforming growth factor-β receptor I (TβRI) and transforming growth factor-β receptor II (TβRII) in AMC and BV-2 cells induced by hypoxia. Firstly, increase in TGF-β1 mRNA expression and TGF-β1 release was observed in the corpus callosum in postnatal rats subjected to a single hypoxic exposure. RT-PCR and Western blot analysis revealed a concomitant upregulation of TβRI and TβRII mRNA and protein. Secondly, immunofluorescence labeling showed that the preponderant AMC in the corpus callosum were immunoreactive for TGF-β1 and its receptors. In rats subjected to hypoxia, immunoexpression of TGF-β1 and both receptors was markedly enhanced. In longer surviving rats, the AMC transformed into ramified microglia but retained in them the immunoreactivity. In BV-2 cells exposed to hypoxia, TGF-β1 mRNA expression and release of TGF-β1 into the medium were significantly increased. It is noteworthy that expression of TβRI and TβRII mRNA and protein in hypoxic BV-2 cells was reduced indicating a differential response of AMC and BV-2 cells to hypoxia. Notwithstanding, it is unequivocal that AMC in the developing brain express and release TGF-β1 into the ambient environment. We suggest that this may be a mechanism to help autoregulate microglial activation in adverse conditions via its receptors. © 2008 IBRO.|
|Appears in Collections:||Staff Publications|
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