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dc.contributor.authorChen, Jinghai
dc.contributor.authorBaydoun, A. R.
dc.contributor.authorXu, Ruixia
dc.contributor.authorDeng, Linzi
dc.contributor.authorLiu, Xuebin
dc.contributor.authorZhu, Weiquan
dc.contributor.authorShi, Linhui
dc.contributor.authorCong, Xiangfeng
dc.contributor.authorHu, Shengshou
dc.contributor.authorChen, Xi
dc.date.accessioned2013-01-11T08:59:09Z
dc.date.available2013-01-11T08:59:09Z
dc.date.issued2008-01
dc.identifier.citationChen , J , Baydoun , A R , Xu , R , Deng , L , Liu , X , Zhu , W , Shi , L , Cong , X , Hu , S & Chen , X 2008 , ' Lysophosphatidic acid protects mesenchymal stem cells against hypoxia and serum deprivation-induced apoptosis ' , Stem Cells , vol. 26 , no. 1 , pp. 135-45 . https://doi.org/10.1634/stemcells.2007-0098
dc.identifier.issn1549-4918
dc.identifier.otherPURE: 382106
dc.identifier.otherPURE UUID: fbb3029c-6d47-439a-8b8d-5cab6cbaa59b
dc.identifier.otherPubMed: 17932426
dc.identifier.otherScopus: 38349053358
dc.identifier.urihttp://hdl.handle.net/2299/9558
dc.descriptionFull text of this article is not available in UHRA
dc.description.abstractBone marrow-derived mesenchymal stem cells (MSCs) have shown great promise for cardiac repair. However, poor viability of transplanted MSCs within the ischemic heart has limited their therapeutic potential. Our previous studies have documented that hypoxia and serum deprivation (hypoxia/SD), induced MSCs apoptosis through the mitochondrial apoptotic pathway. Since serum lysophosphatidic acid (LPA) levels are known to be significantly elevated after acute myocardial infarction and that LPA enhanced survival of other cell systems, we embarked on determining whether LPA protects MSCs against hypoxia/SD-induced apoptosis. We have also investigated the potential mechanism(s) that may mediate such actions of LPA. All experiments were carried out on rat bone marrow MSCs. Apoptosis was induced by exposure of cells to hypoxia/SD in a sealed GENbox hypoxic chamber. Effects of LPA were investigated in the absence and presence of inhibitors that target either G(i)proteins, the mitogen activated protein kinases ERK1/2, or phosphoinositide 3-kinase (PI3K). The data obtained showed that hypoxia/SD-induced apoptosis was significantly attenuated by LPA through Gi-coupled LPA(1) receptors linked to the downstream ERK1/2 and PI3K/Akt signaling pathways that function in parallel. Additional studies have demonstrated that hypoxia/SD-induced activation of mitochondrial dysfunction was virtually abolished by LPA treatment and that inhibition of the LPA(1) receptor, Gi proteins, the PI3K/Akt pathway, or ERKs effectively reversed this protective action of LPA. Taken together, our findings indicate that LPA is a novel, potent survival factor for MSCs and this may prove to be of considerable therapeutic significance in terms of exploiting MSC-based therapy in the infracted myocardium.en
dc.format.extent11
dc.language.isoeng
dc.relation.ispartofStem Cells
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectBlotting, Western
dc.subjectCaspase 3
dc.subjectCell Hypoxia
dc.subjectCell Survival
dc.subjectCells, Cultured
dc.subjectExtracellular Signal-Regulated MAP Kinases
dc.subjectFlow Cytometry
dc.subjectGTP-Binding Protein alpha Subunits, Gi-Go
dc.subjectLysophospholipids
dc.subjectMembrane Potential, Mitochondrial
dc.subjectMesenchymal Stem Cells
dc.subjectPhosphatidylinositol 3-Kinases
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectSerum
dc.subjectSignal Transduction
dc.titleLysophosphatidic acid protects mesenchymal stem cells against hypoxia and serum deprivation-induced apoptosisen
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.contributor.institutionSchool of Life and Medical Sciences
dc.contributor.institutionDepartment of Human and Environmental Sciences
dc.contributor.institutionAgriculture, Veterinary and Food Sciences
dc.contributor.institutionPharmacology and Clinical Science Research
dc.contributor.institutionCardiovascular Pathologies
dc.contributor.institutionDiabetic neuropathies
dc.contributor.institutionBiochemistry and Bioinformatics
dc.description.statusPeer reviewed
rioxxterms.versionVoR
rioxxterms.versionofrecordhttps://doi.org/10.1634/stemcells.2007-0098
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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