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Brain ischemia induces serine phosphorylation of neuronal nitric oxide synthase by Ca2+/calmodulin-dependent protein kinase II in rat hippocampus

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Acta Pharmacologica Sinica 2004年第5期25卷 75-80页

作者： Xue-bo YAN, Fan-jie MENG, Bo SONG, Guang-yi ZHANG2Research Center for Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002, China Research Center for Biochemistry and Molecular Biology Xuzhou Medical College Xuzhou 221002

AIM: To investigate whether brain ischemia induces serine phosphorylation of neuronal nitric oxide synthase(nNOS) by Ca2+/calmodulin-dependent protein kinase II (CaMKII) and the interaction between CaMKIIa and nNOSin rat hippocampus. METHODS: Brain ischemia was induced by bilateral carotid artery occlusion *** and the interaction of proteins were studied by immunoprecipitation and immunoblotting. Weinvestigated during brain ischemia serine phosphorylation and amount of nNOS in crude membranes fraction (P)and cytosolic fraction (S), interaction between CaMKIIa and nNOS, and the effects of 1-[N,O-bis-(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN-62, a selective inhibitor of CaMKII) on phos-phorylation and the interaction of proteins in P. RESULTS: Serine phosphorylation of nNOS in P increased persis-tently during brain ischemia, and 15 min ischemia-induced serine phosphorylation of nNOS was attenuated signifi-cantly by KN-62. But there was no serine phosphorylation of nNOS in S. The distributions of nNOS were notaffected by ischemia and KN-62. However, the binding levels of both CaMKIIa with nNOS and Thr286autophosphorylated CaMKIIa with nNOS increased after ischemia, and were diminished by KN-62. CONCLUSION:CaMKII interacted with nNOS and regulated serine phosphorylation of nNOS during brain ischemia.

关键词： serine phosphorylation nitric oxide synthase calmodulin kinase KN 62 brain ischemia hippo-campus

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The potential of endogenous neurogenesis for brain repair and regeneration following traumatic brain injury

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Neural Regeneration Research 2014年第7期9卷 688-692页

作者： Dong Sun Department of Neurosurgery Medical College of Virginia Campus Virginia Commonwealth University

Traumatic brain injury （TBI） is the leading cause of death and disability of persons under 45 years old in the United States, affecting over 1.5 million individtials each year. It had been th ought that recovery from such injuries is severely limited due to the inability of the adult bra in to replace damaged neurons. However, recent studies indicate that the mature mammalian central nervous system （CNS） has the potential to replenish damaged neurons by proliferation and neuronal differentiation of adult neural stem/progenitor cells residing in the neurogenic regions in the brain. Furthermore, increasing evidence indicates that these endogenous stem/ progenitor cells may play regenerative and reparative roles in response to CNS injuries or diseases. In support of this notion, heightened levels of cell proliferation and neurogenesis have been ob- served in response to brain trauma or insults suggesting that the brain has the inherent potential to restore populations of damaged or destroyed neurons. This review will discuss the potential functions of adult neurogenesis and recent development of strategies aiming at harnessing this neurogenic capacity in order to repopulate and repair the injured brain.

关键词： traumatic brain injury adult neurogenesis neural stem cells cell proliferation hippo-campus subventricular zone learning and memory function regeneration cognition

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