Kaur,Charanjit
Email Address
antkaurc@nus.edu.sg
Organizational Units
ANATOMY
dept
YONG LOO LIN SCH OF MEDICINE
faculty
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Publication Search Results
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Publication Expression of Kv1.2 in microglia and its putative roles in modulating production of proinflammatory cytokines and reactive oxygen species(2008) Li, F.; Wu, C.-Y.; Sun, J.; Li, S.; Kaur, C.; Sivakumar, V.; Ling, E.-A.; Lu, J.; ANATOMYPublication Vascular changes in the developing rat retina in response to hypoxia(Academic Press, 2015) Rathnasamy G.; Sivakumar V.; Foulds W.S.; Ling E.A.; Kaur C.; ANATOMYPublication Fos expression in the suprachiasmatic nucleus in rats following high altitude exposure(2005) Kaur, C.; Singh, J.; ANATOMYPublication Transient expression of transferrin receptors and localisation of iron in amoeboid microglia in postnatal rats(1995) Kaur, C.; Ling, E.A.; ANATOMYPublication Immunohistochemical and tracer studies of macrophages/microglia in the pineal gland of postnatal rats(1997) Kaur, C.; Ling, E.A.; Wu, C.H.; ANATOMYPublication Endothelins-1/3 and endothelin-A/B receptors expressing glial cells with special reference to activated microglia in experimentally induced cerebral ischemia in the adult rats(2010) Li, J.J.; Wu, L.H.; Yuan, Y.; Yang, L.; Guo, Z.Y.; Wu, C.Y.; Cao, Q.; Kaur, C.; Sivakumar, V.; Ling, E.A.; ANATOMYWe reported previously that amoeboid microglial cells (AMC) in the developing brain exhibited endothelins (ETs) expression which diminished with advancing age and was undetected in microglia in the more mature brain. This study sought to explore if microglia in the adult would be induced to express ETs in altered conditions. By immunofluorescence microscopy, ETs and endothelin (ET)-B receptor were undetected in microglial cells in sham-operated and normal control rats. However, in adult rats subjected to middle cerebral artery occlusion (MCAO), lectin labeled activated microglia which occurred in large numbers in the marginal zones in the ischemic cortex at 3 days and 1 week intensely expressed ETs specifically endothelin (ET)-1 and ET-B receptor; ET-3 and ET-A receptor were absent in these cells. By RT-PCR and ELISA, ET-1 and -3 mRNA and protein expression level was progressively increased in the ischemic cerebral cortex after MCAO compared with the controls. ET-A and ET-B receptor mRNA and protein levels were concomitantly up-regulated. It is suggested that increased release of ET-1 following MCAO by massive activated microglia can exert an immediate constriction of local blood vessels bearing ET-A receptor. ET-1 may also interact with activated microglia endowed with ET-B receptor via an autocrine manner that may be linked to chemokines/cytokines production. ET-1, ET-3 and ET-B receptor were also localized in reactive astrocytes along with some oligodendrocytes. We conclude that activated microglia together with other glial cells in the marginal zone after MCAO are the main cellular source of ETs that may be involved in regulation of vascular constriction and glial chemokines/cytokines production. However, dissecting the role of individual component of the endothelin system in the various glial cells, notably activated microglia, would be vital in designing of an effective therapeutic strategy for clinical treatment of stroke in which microglial cells have been implicated. © 2010 IBRO.Publication Domoic acid-induced neuronal damage in the rat hippocampus: Changes in apoptosis related genes (Bcl-2, Bax, Caspase-3) and microglial response(2001) Ananth, C.; Thameem, Dheen S.; Gopalakrishnakone, P.; Kaur, C.; ANATOMYPublication Ultrastructural Changes of Macroglial Cells in the Rat Brain Following an Exposure to a Non-penetrative Blast(1997) Kaur, C.; Ling, E.A.; Singh, J.; Lim, M.K.; Yap, E.P.H.; Ng, B.L.; ANATOMYPublication Effects of melatonin on macrophages/microglia in postnatal rat brain(1999) Kaur, C.; Ling, E.A.; ANATOMYPublication 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(2008) Li, J.-J.; Wu, C.-Y.; Kaur, C.; Sivakumar, V.; Ling, E.-A.; Lu, J.; ANATOMYTransforming 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.