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,1
* Institute of Molecular Biology, The University of Hong Kong, Pokfulam;
Department of Biology, The Hong Kong University of Science and Technology, Clear Water Bays, Hong Kong, China;
Department of Cardiovascular Research, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
2Correspondence: Institute of Molecular Biology, The University of Hong Kong, South Wing, 8/F Kadoorie, Biological Science Bldg., Pokfulam Road, Hong Kong, China. E-mail: skchung{at}hkucc.hku.hk
Under pathological conditions such as ischemia (I), subarachnoid hemorrhage, and Alzheimer’s disease, astrocytes show a large increase in endothelin (ET) -like immunoreactivity. However, it is not clear whether ET is protective or destructive to these cells during brain injury. Using astrocytes from ET-1-deficient mice, we determined the effect of ET-1 on these cells under normal, hypoxic (H), and hypoxic/ischemic (H/I) conditions. Under normal culture conditions, astrocytes from wild-type and ET-1-deficient mice showed no difference in their morphology and cell proliferation rates. ET-3 and ETA receptor mRNAs were up-regulated whereas ETB receptor mRNA was down-regulated in ET-1-deficient astrocytes, suggesting that ET-1 and ET-3 may complement each other’s functions and that the expressions of these endothelins and their receptors are regulated by a complex feedback mechanism. Under H and H/I conditions, ET-1 peptide and mRNA were up-regulated in wild-type astrocytes, and the astrocytes without ET-1 died faster than the wild-type astrocytes, as indicated by greater efflux of lactate dehydrogenase. The present study suggests that astrocytes without ET-1 are more vulnerable to H and H/I injuries and that the up-regulation of astrocytic ET-1 is essential for the survival of astrocytes.—Ho, M. C. Y., Lo, A. C. Y., Kurihara, H., Yu, A. C. H., Chung, S. S. M., Chung, S. K. Endothelin-1 protects astrocytes from hypoxic/ischemic injury.
Key Words: Endothelin-3 • endothelin receptors • cell survival • lactate dehydrogenase • ET-1-deficient mice
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