Ischemic preconditioning-induced expression of gp130 and STAT3 in astrocytes of the rat hippocampus

Kim, Seong Yun; Park, Hyun Jung; Choi, Jeong Sun; Lee, Ju Eun; Ho, Jung; Choi, Yun Sik; Cho, Kyung-Ok; Chun, Myung-Hoon; Lee, Mun Yong

doi:10.1016/j.molbrainres.2004.06.025

Cited by 12 publications

(12 citation statements)

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“…1,2,3,4). In agreement with a previous study (Kim et al 2004), routine histological staining with cresyl violet revealed characteristic neuronal cell loss in the CA1 region of the hippocampus following 10-min ischemia, whereas the CA1 pyramidal neurons were preserved in the rat hippocampus after a short cerebral-ischemic preconditioning, and after a 10-min ischemia with ischemic preconditioning (data not shown).…”

Section: Resultssupporting

confidence: 92%

Expression of prostaglandin E2 receptor subtypes, EP2 and EP4, in the rat hippocampus after cerebral ischemia and ischemic tolerance

et al. 2006

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We investigated the distribution and time course of expression of two subtypes of prostaglandin E(2) (PGE(2)) receptors, EP2 and EP4, in a rat model of cerebral ischemia and ischemic tolerance. Adult male Sprague-Dawley rats were subjected to either lethal global ischemia (10 min) with or without sublethal ischemic preconditioning (3 min), or ischemia only (3 min). A short 3-min cerebral ischemia and a 3-min ischemia followed by a second lethal ischemia enhanced the expression of EP2 and EP4 receptors in CA1 pyramidal neurons of the hippocampus. In tolerance-acquired CA1 neurons, the immunoreactivities of EP2 and EP4 were upregulated after 4 h and 12 h, respectively. The immunoreactivities were most prominent at 3 days and were sustained for at least 14 days, consistent with results of immunoblotting experiments. However, immunoreactivities for these PGE(2) receptors increased in reactive glial cells in the vulnerable CA1 and hilar regions of rats subjected to lethal ischemia without ischemic preconditioning. Most of the EP2 immunoreactivity occurred in microglial cells and some astrocytes, whereas increased immunoreactivity for EP4 was found only in astrocytes. These data suggest that ischemia and the induction of ischemia tolerance have different regulatory effects on the expression of EP2 and EP4 receptors. Moreover, PGE(2) may exert its unique pathophysiological functions in relation to delayed neuronal death and ischemic tolerance induction in the rat hippocampus via specific PGE(2) receptors.

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Section: Resultssupporting

confidence: 92%

Expression of prostaglandin E2 receptor subtypes, EP2 and EP4, in the rat hippocampus after cerebral ischemia and ischemic tolerance

et al. 2006

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“…Therefore, STAT3 activation in astrocytes may indirectly be linked to neuronal survival. In support of this idea, ischemic preconditioning increases STAT3 expression in reactive astrocytes in the hippocampus [64], and STAT3 phosphorylation correlates with increased expression of cIAP2, a member of the inhibitor of apoptosis protein family, in glial cells in the penumbra [134]. Interestingly, STAT3 phosphorylation correlates with decreased gliosis in the most severely damaged part of the brain, the striatal core of the infarct.…”

Section: Role In Neuroprotectionmentioning

confidence: 77%

“…Robust nuclear P-STAT3 immunoreactivity is observed at 24 h, suggesting that STAT3 is functionally active and engaged in inducing gene transcription [36]. The majority of the data show that onset of glial STAT3 activation is most prevalent after 24 h of injury onset [64,112]. In some cases, however, STAT3 activation is observed in astrocytes at an earlier time.…”

Section: Stat3 Activation Following Ischemic Injurymentioning

confidence: 98%

Role of Signal Transducer and Activator of Transcription 3 in Neuronal Survival and Regeneration

Dziennis

Alkayed²

2008

Reviews in the Neurosciences

138

108

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SynopsisSignal Transducers and Activators of Transcription (STATs) comprise a family of transcription factors that mediate a wide variety of biological functions in the central and peripheral nervous systems. Injury to neural tissue induces STAT activation, and STATs are increasingly recognized for their role in neuronal survival. In this review, we discuss the role of STAT3 during neural development and following ischemic and traumatic injury in brain, spinal cord and peripheral nerves. We focus on STAT3 because of the expanding body of literature that investigates protective and regenerative effects of growth factors, hormones and cytokines that use STAT3 to mediate their effect, in part through transcriptional upregulation of neuroprotective and neurotrophic genes. Defining the endogenous molecular mechanisms that lead to neuroprotection by STAT3 after injury might identify novel therapeutic targets against acute neural tissue damage as well as chronic neurodegenerative disorders. KeywordsSTAT3; ischemia; neuroregeneration; neuroprotection; axotomy; spinal cord injury; neurodevelopment IntroductionSTATs are activated in the central nervous system (CNS) following injury in response to multiple signaling pathways (Fig. 1). The primary mechanism for STAT activation in brain and spinal cord is believed to be in response to the multiple cytokines and growth factors that are released after injury. However, STATs can also be activated by free radicals, excitatory neurotransmitters and other inflammatory mediators that are also produced in damaged neural tissue [3]. STATs comprise a family of seven transcription factors: STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b and STAT6 [119]. STATs are expressed during development in both neurons and glia. In adult brain, STATs are normally quiescent, but as summarized in Tables 1 and 2, several STAT family members, including STAT1, STAT3 and STAT5, have been shown to be activated after injury. Interestingly, however, different STATs seem to play different roles in injured tissue. For example, whereas STAT3 and STAT5 have been linked to neuroprotection by trophic factors and cytokines after ischemic brain or nerve injury, STAT1 activation has been associated with neuronal cell death. STAT3 and STAT5 promote neuronal survival by inducing neuroprotective genes, whereas STAT1 promotes neurodegeneration by inducing apoptotic and other cell death promoting genes. Finally, although several STAT Reprint address: Nabil J. Alkayed, M.D., Ph.D., Department of Anesthesiology & Peri-Operative Medicine, Oregon Health and Science University, 3181 S.W. Sam Jackson Park Rd., UHS-2, Portland, Oregon 97239-3098, USA, e-mail: E-mail: alkayedn@ohsu.edu. NIH Public Access Author ManuscriptRev Neurosci. Author manuscript; available in PMC 2009 May 13. Published in final edited form as:Rev Neurosci. 2008 ; 19(4-5): 341-361. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript family members influence neuronal survival during development and in response to trophic factors and cytok...

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“…4 4 nonreceptor-tyrosine kinases 16,17 . Some studies found that injury to neural cells could induce the activation of STAT3 18 , and others considered STAT3 activation caused neuroprotection [19][20][21] . The expression of NDRG2 modulates SOCS3 and STAT3 activity, ultimately leading to the suppression of IL-10 production in U937 cell line 22 .…”

Section: Page 3 Of 25mentioning

confidence: 99%

2-Arachidonylglycerol Protects Primary Astrocytes Exposed to Oxygen-Glucose Deprivation Through a Blockade of NDRG2 Signaling and STAT3 Phosphorylation

Wang

et al. 2016

Rejuvenation Research

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The human N-Myc downstream-regulated gene 2 (NDRG2) is expressed in astrocytes, and may be involved in the modulation of gliacyte function in the central nervous system. Our previous study found suppression of NDRG2 up-regulation in reactive astrocytes in cerebral ischemic tolerance. 2-Arachidonylglycerol (2-AG) can induce cerebral ischemic tolerance. However, the underlying mechanism of NDRG2 in cytoprotection induced by 2-AG in primary astrocytesis still unknown. In this study, we investigated the role of NDRG2 in cerebral ischemic tolerance induced by 2-AG after oxygen-glucose deprivation (OGD) in primary astrocytes. The results showed that primary astrocytes exposed to OGD resulted in marked increase of lactate dehydrogenase (LDH) release and decrease of methyl thiazolyl tetrazolium (MTT) reduction activity in comparison to control cultures. The levels of NDRG2 and phospho-signal transducer and activator of transcription 3 (pSTAT3) in the OGD group were comparably higher than those in the control group, and the up-regulation of NDRG2 and pSTAT3 was suppressed in NDRG2 siRNA group. The cell viability in the 2-AG group was higher than that in the OGD group, and transfecting the NDRG2 pSRL-CDH1-GFP vector reversed the protective effects of 2-AG. The levels of NDRG2 and pSTAT3 in the 2-AG group were lower than those in the OGD group. 2-AG suppressed STAT3 phosphorylation by decreased expression of NDRG2. In conclusion, 2-AG protects primary astrocytes exposed to oxygen-glucose deprivation through a blockade of NDRG2 signaling and STAT3 phosphorylation. These findings bring insight to the roles of NDRG2 in ischemic-hypoxic injury and provide novel potential targets for future potent clinical therapies on cerebral ischemia injury.

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Ischemic preconditioning-induced expression of gp130 and STAT3 in astrocytes of the rat hippocampus

Cited by 12 publications

References 37 publications

Expression of prostaglandin E2 receptor subtypes, EP2 and EP4, in the rat hippocampus after cerebral ischemia and ischemic tolerance

Expression of prostaglandin E2 receptor subtypes, EP2 and EP4, in the rat hippocampus after cerebral ischemia and ischemic tolerance

Role of Signal Transducer and Activator of Transcription 3 in Neuronal Survival and Regeneration

2-Arachidonylglycerol Protects Primary Astrocytes Exposed to Oxygen-Glucose Deprivation Through a Blockade of NDRG2 Signaling and STAT3 Phosphorylation

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