ArticleMolecular neurobiology2014
The roles of p38 MAPK/MSK1 signaling pathway in the neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in adult rats.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Hypoxic Postconditioning Offers Neuroprotection Against Transient Cerebral Ischemia via Down-Regulation of rno_piR_011022.CNS neuroscience & therapeutics · 2025Article
- Hypoxic postconditioning modulates neuroprotective glial reactivity in a 3D cortical ischemic-hypoxic injury model.Scientific reports · 2024Article
- Casein kinase 1α mediates eryptosis: a review.Apoptosis : an international journal on programmed cell death · 2023Review
- Remifentanil Promotes PDIA3 Expression by Activating p38MAPK to Inhibit Intestinal Ischemia/Reperfusion-Induced Oxidative and Endoplasmic Reticulum Stress.Frontiers in cell and developmental biology · 2022Article
- Hypoxic postconditioning-induced neuroprotection increases neuronal autophagy via activation of the SIRT1/FoxO1 signaling pathway in rats with global cerebral ischemia.Experimental and therapeutic medicine · 2021Article
- Remote Ischemic Postconditioning vs. Physical Exercise After Stroke: an Alternative Rehabilitation Strategy?Molecular neurobiology · 2021Article
- Hypoxic postconditioning promotes mitophagy against transient global cerebral ischemia via PINK1/Parkin-induced mitochondrial ubiquitination in adult rats.Cell death & disease · 2021Article
- Remote Ischemic Conditioning With Exercise (RICE)-Rehabilitative Strategy in Patients With Acute Ischemic Stroke: Rationale, Design, and Protocol for a Randomized Controlled Study.Frontiers in neurology · 2021Article
- Activation of p38 MAPK participates in the sulbactam-induced cerebral ischemic tolerance mediated by glial glutamate transporter-1 upregulation in rats.Scientific reports · 2020Article
- Neuroprotective Mechanism of Hypoxic Post-conditioning Involves HIF1-Associated Regulation of the Pentose Phosphate Pathway in Rat Brain.Neurochemical research · 2019Article
- Inhibition of MSK1 Promotes Inflammation and Apoptosis and Inhibits Functional Recovery After Spinal Cord Injury.Journal of molecular neuroscience : MN · 2019Article
- Treatment with MQA, a Derivative of Caffeoylquinic Acid, Provides Neuroprotective Effects against Cerebral Ischemia Through Suppression of the p38 Pathway and Oxidative Stress in Rats.Journal of molecular neuroscience : MN · 2019Article
- [Effect of lentivirus-mediated small interfering RNA on mitogen- and stress-activated protein kinase 1 in spinal cord injury of rats].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2018Article
- Neuroglobin mediates neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in rats through preserving the activity of NaCell death & disease · 2018Article
- Neuroprotection of hypoxic postconditioning against global cerebral ischemia through influencing posttranslational regulations of heat shock protein 27 in adult rats.Brain pathology (Zurich, Switzerland) · 2017Article
- Inhibiting purinergic P2X7 receptors with the antagonist brilliant blue G is neuroprotective in an intranigral lipopolysaccharide animal model of Parkinson's disease.Molecular medicine reports · 2017Article
- MicroRNA-128-3p Protects Mouse Against Cerebral Ischemia Through Reducing p38α Mitogen-Activated Protein Kinase Activity.Journal of molecular neuroscience : MN · 2017Article
- Electroacupuncture alleviates cerebral ischemia and reperfusion injury via modulation of the ERK1/2 signaling pathway.Neural regeneration research · 2016Article
- Electroacupuncture at different frequencies (5Hz and 25Hz) ameliorates cerebral ischemia-reperfusion injury in rats: possible involvement of p38 MAPK-mediated anti-apoptotic signaling pathways.BMC complementary and alternative medicine · 2015Article
- Timing is everything: Exercise therapy and remote ischemic conditioning for acute ischemic stroke patients.Brain circulationReview
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postconditioning has regenerated interest as a mechanical intervention against cerebral ischemia/reperfusion injury, but its molecular mechanisms remain unknown. We previously reported that hypoxic postconditioning (HPC) ameliorated neuronal death induced by transient global cerebral ischemia (tGCI) in hippocampal CA1 subregion of adult rats. This study tested the hypothesis that p38-mitogen-activated protein kinase (p38 MAPK)/mitogen- and stress-response kinase 1 (MSK1) signaling pathway plays a role in the HPC-induced neuroprotection. Male Wistar rats were subjected to 10 min ischemia induced by applying the four-vessel occlusion method. HPC with 120 min was applied at 24 h after reperfusion. Immunohistochemistry and Western blot were used to detect the expression of phosphorylation of p38 MAPK and MSK1, as well as cleaved caspase-3. We found that HPC induced a significant increase of phosphorylated p38 MAPK and MSK1 in neurons of hippocampal CA1 region and a significant decrease in glial cells after tGCI as well. Furthermore, HPC attenuated caspase-3 cleavation triggered by tGCI in CA1 region. Moreover, p38 MAPK inhibition by SB203580 significantly decreased the phosphorylation of MSK1, increased cleaved caspase-3 expression, and abolished the neuroprotection of HPC. These findings suggested that p38 MAPK/MSK1 signaling axis contributed to HPC-mediated neuroprotection against tGCI, at least in part, by regulating the activation of caspase-3.
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