Induction of Rheb mRNA following middle cerebral artery occlusion in the rat

Kinouchi, Hiroyuki; Arai, Shouichi; Kamii, Hideyuki; Izaki, Kenji; Kunizuka, Hisanori; Mizoi, Kazuo; Yoshimoto, Takashi

doi:10.1097/00001756-199904060-00029

Cited by 8 publications

(3 citation statements)

References 8 publications

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“…Erythropoietin has been demonstrated to defend microglia from OGD by promoting the mTOR activity and inhibiting the release of mitochondrial cytochrome C because mTOR inhibition through rapamycin silences the cellprotective function of erythropoietin [31]. Rapamycin can also enlarge the brain infarct size and increase the neurological de cit score in rats with focal cerebral ischemia, indicating that promoting mTOR activation may lead to lighter ischemic brain injury and better behavior recovery.Rhebis a necessary protein in phosphorylating of mTOR for activation.Previous study found that Rheb mRNA levels were down-regulated in parietal cortex and Lateral striatum in MCAO rats after 24h, which wasconsistent with the results of the present study [32].Our study found that Rheb expression was decreased and miR155 expression was increased on 24 h after reperfusion in MCAO/R rats. Recent study has demonstrated thatmiR-155 might regulate the expression of Rheb at the post-transcriptional levels by directly act on Rheb mRNA in vitro [25].These results suggest that miR155 may inhibit mTOR signaling pathwayby targeting Rheb in IS.…”

Section: Discussionsupporting

confidence: 93%

MiR155 Affect the Cerebral Ischemic Injury by Rheb/mTOR Signaling Pathway

Chang¹,

Xue²,

Zhu³

et al. 2021

Preprint

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Ischemic stroke remains to be a leading cause of death and disability worldwide at present. Cerebral ischemia/reperfusion injury (CIRI) is a critical pathogenesis leading to a poor prognosis for ischemic stroke patients.Recent studies have found that miR155 may be involved in the occurrence of CIRI after stroke, but it’s role and specific mechanism are not completely clear.Therefore, this study investigated the effects of miR155 expression levels on mortality, cerebral infarction volume and neuronal apoptosis in MCAO/R rats by changing the expression level of miR155 in the ischemic penumbra (IP) region of rats. QRT-PCR and Western Blotting were used to detect the expression changes of Rheb, mTOR, 4EBP1 and S6K1 under different miR155 expression levels. The results showed that inhibition of miR155 could reduce the mortality, the volume of cerebral infarction and the number of neuronal apoptosis in MCAO/R rats.The mRNA and protein expressions of Rheb, mTOR, 4EBP1 and S6K1 were increased after inhibition of miR155, and vice versa. It suggested that inhibition the expression of miR155 could alleviate CIRI in the IP by activating Rheb/mTOR signaling at the transcriptional level. At the same time, we found that the phosphorylation level of mTOR signaling pathway were also increased after inhibition of miR155, indicating that autophagy level regulated by mTOR signaling pathway may be involved in the CIRI.

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Section: Discussionsupporting

confidence: 93%

MiR155 Affect the Cerebral Ischemic Injury by Rheb/mTOR Signaling Pathway

Chang¹,

Xue²,

Zhu³

et al. 2021

Preprint

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“…R as- h omology e nriched in b rain was identified as a gene whose expression was induced in rat brain by synaptic activity and growth factor stimulation [100, 101]. Rheb is a small GTPase that is structurally more close to Ras than to other small GTPases.…”

Section: Rhebmentioning

confidence: 99%

Key factors in mTOR regulation

Bai

Jiang

2009

Cell. Mol. Life Sci.

108

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Mammalian target of rapamycin (mTOR) is a protein serine/threonine kinase that controls a wide range of growth-related cellular processes. In the past several years, many factors have been identified that are involved in controlling mTOR activity. Those factors in turn are regulated by diverse signaling cascades responsive to changes in intracellular and environmental conditions. The molecular connections between mTOR and its regulators form a complex signaling network that governs cellular metabolism, growth and proliferation. In this review, we discuss some key factors in mTOR regulation and mechanisms by which these factors control mTOR activity.

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“…These genes include junB (Comelli et al, 1993;Hsu et al, 1993;Kamii et al, 1994a;, Zacl and PACAP (Gillardon et al, 1998), NGFIA,B,C (Lin et al, 1996;Honkaniemi et al, 1997), egr (Honkaniemi et al, 1997), Rheb (Kinouchi et al, 1999a), Arc (Kunizuka et al, 1999) and probably other lEGs. Hsp27, COX2, and PKC are induced by spreading depression (Plumier et al, 1997c;Miettinen et al, 1997;Koponen et al, 1999).…”

Section: Hemispheric Spreading Depressionmentioning

confidence: 99%

Signal Transduction and Gene Regulation During Hypoxia Stress: A Potential Role in Neurodegenerative Disease

Millhorn¹

2002

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Public reporting burden for this collection of infomiation is estimated to average 1 hour per response, including the time for reviewing instnjctions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway. Suite 1204, Arlington, VA 22202-4302, and PERFORMING ORGANIZATION NAIVIE(S) AND ADDRESS(ES)University of Cincinnati Cincinnati, Ohio 45267-0553 E-Mail: david.millhorn@uc.edu Soldiers deployed to high altitude terrain or exposed to chemical toxins that induce ischemia or impaired oxidative metabolism in the central nervous system (CNS) encounter sustained cellular hypoxia. This can compromise CNS function and lead to permanent neuronal injury, which is a precursor for neurodegenerative disorders such as Alzheimer's disease. The proposed research is designed to determine the role of stress-activated signal transduction systems in regulating a cellular phenotype that is tolerant to hypoxic stress. We hypothesize that de novo gene expression is a major component of the adaptative/protective response to hypoxia, and that the p38 kinase stress-activated pathway plays a major role in this response. We present novel preliminary findings, which show that genes involved in cell proliferation and differentiation are regulated by hypoxia and p38. We hypothesize that these genes and the genes that encode immediate early transcription factors, and the hypoxia-sensitive potassium channels are regulated by p38 during hypoxia and play a major role in protecting neurons form hypoxia injury and neurodegenerative disease. Studies are performed in PCI2 cells, which are extremely tolerant to reduced oxygen and a widely used model for elucidating the molecular mechanisms of neural function. SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES)UThe objectives of the proposed research are: 1) Identify the p38 isoforms that are activated by hypoxia. Determine the effects of hypoxia on the protein kinases and small G-proteins that lie upstream of p38. 2) Determine the role of the p38 kinase pathway on the unique hypoxia-induced regulation of cyclin A, and immediate early genes in thsfos and jun families. 3) Determine the role of the p38 kinase pathway in regulating the hypoxia-induced expression of the oxygen-sensitive Kvl.2 potassium channel.14. SUBJECT TERMS hypoxia, p38 kinase pathways, cyclin A, immediate early genes, potassium channels, signal transduction, pheochromocytoma cells, neurodegenerative disease References 10Appendices 10 IntroductionThe research in this project was undertaken to determine the role of stress-activated signal transduction systems in regulating a cellular phenotype that can survive and function during hypoxic stress. The general hypothesis is that reduced 02 c...

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Induction of Rheb mRNA following middle cerebral artery occlusion in the rat

Cited by 8 publications

References 8 publications

MiR155 Affect the Cerebral Ischemic Injury by Rheb/mTOR Signaling Pathway

MiR155 Affect the Cerebral Ischemic Injury by Rheb/mTOR Signaling Pathway

Key factors in mTOR regulation

Signal Transduction and Gene Regulation During Hypoxia Stress: A Potential Role in Neurodegenerative Disease

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