Rab27a deletion impairs the therapeutic potential of endothelial progenitor cells for myocardial infarction
Endothelial progenitor cell (EPC) transplantation has shown advantages in the treatment of myocardial infarction (MI) in animal models and clinical trials through mechanisms of direct intercellular contacts, autocrine, and paracrine. However, the effects of EPC transplantation for MI treatment remai...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2021-02, Vol.476 (2), p.797-807 |
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| creator | Zhou, Wenyi Zheng, Xuefei Cheng, Chuanfang Guo, Guixian Zhong, Yun Liu, Weihua Liu, Kefeng Chen, Yanfang Liu, Shiming Liu, Shaojun |
| description | Endothelial progenitor cell (EPC) transplantation has shown advantages in the treatment of myocardial infarction (MI) in animal models and clinical trials through mechanisms of direct intercellular contacts, autocrine, and paracrine. However, the effects of EPC transplantation for MI treatment remain controversial and the underlying mechanisms have not been fully elucidated. Here, we explored the role of Rab27a in the therapeutic potential of EPC transplantation in MI. We found that Rab27a knockout impaired the viability, and reduced the proliferation and tube formation function of ECPs. The recovery of cardiac function and improvement of ventricular remodeling from EPCs transplantation were significantly damaged by Rab27a deletion in vivo. Rab27a deletion inhibited the protein expression of phosphoinositide 3-kinase (PI3K) and cyclin D1 and the phosphorylation levels of Akt and FoxO3a. Therefore, Rab27a knockout suppressed the PI3K-Akt-FoxO3a/cyclin D1 signaling pathway. Furthermore, Rab27a ablation dramatically reduced exosome release in EPCs. These results demonstrated that Rab27a plays an essential role in EPC functions. The elucidation of this mechanism provides novel insights into EPC transplantation as a promising treatment for post-MI injuries. |
| doi_str_mv | 10.1007/s11010-020-03945-x |
| format | Article |
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However, the effects of EPC transplantation for MI treatment remain controversial and the underlying mechanisms have not been fully elucidated. Here, we explored the role of Rab27a in the therapeutic potential of EPC transplantation in MI. We found that Rab27a knockout impaired the viability, and reduced the proliferation and tube formation function of ECPs. The recovery of cardiac function and improvement of ventricular remodeling from EPCs transplantation were significantly damaged by Rab27a deletion in vivo. Rab27a deletion inhibited the protein expression of phosphoinositide 3-kinase (PI3K) and cyclin D1 and the phosphorylation levels of Akt and FoxO3a. Therefore, Rab27a knockout suppressed the PI3K-Akt-FoxO3a/cyclin D1 signaling pathway. Furthermore, Rab27a ablation dramatically reduced exosome release in EPCs. These results demonstrated that Rab27a plays an essential role in EPC functions. The elucidation of this mechanism provides novel insights into EPC transplantation as a promising treatment for post-MI injuries.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-020-03945-x</identifier><identifier>PMID: 33095380</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>1-Phosphatidylinositol 3-kinase ; Ablation ; AKT protein ; Animal models ; Animals ; Autocrine signalling ; Biochemistry ; Biomedical and Life Sciences ; Bone Marrow Cells - metabolism ; Bone Marrow Cells - pathology ; Cardiology ; Cells (biology) ; Cells, Cultured ; Clinical trials ; Cyclin D1 ; Deletion ; Disease Models, Animal ; Endothelial Progenitor Cells - pathology ; Endothelial Progenitor Cells - transplantation ; Endothelium ; Exosomes - metabolism ; FOXO3 protein ; Gene Deletion ; Health aspects ; Heart ; Heart attack ; Heart attacks ; Kinases ; Life Sciences ; Male ; Medical Biochemistry ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial infarction ; Myocardial Infarction - genetics ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Infarction - therapy ; Oncology ; Paracrine signalling ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Progenitor cells ; Proto-Oncogene Proteins c-akt - metabolism ; rab27 GTP-Binding Proteins - deficiency ; rab27 GTP-Binding Proteins - genetics ; Signal Transduction ; Stem Cell Transplantation - methods ; Stem cells ; Transplantation ; Ventricle ; Ventricular Remodeling</subject><ispartof>Molecular and cellular biochemistry, 2021-02, Vol.476 (2), p.797-807</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>COPYRIGHT 2020 Springer</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-f95eda938bbc1e485dc29f5158e5179384c016f48929d28e314b53347d622ca43</citedby><cites>FETCH-LOGICAL-c508t-f95eda938bbc1e485dc29f5158e5179384c016f48929d28e314b53347d622ca43</cites><orcidid>0000-0001-7895-5577</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-020-03945-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-020-03945-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33095380$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Wenyi</creatorcontrib><creatorcontrib>Zheng, Xuefei</creatorcontrib><creatorcontrib>Cheng, Chuanfang</creatorcontrib><creatorcontrib>Guo, Guixian</creatorcontrib><creatorcontrib>Zhong, Yun</creatorcontrib><creatorcontrib>Liu, Weihua</creatorcontrib><creatorcontrib>Liu, Kefeng</creatorcontrib><creatorcontrib>Chen, Yanfang</creatorcontrib><creatorcontrib>Liu, Shiming</creatorcontrib><creatorcontrib>Liu, Shaojun</creatorcontrib><title>Rab27a deletion impairs the therapeutic potential of endothelial progenitor cells for myocardial infarction</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Endothelial progenitor cell (EPC) transplantation has shown advantages in the treatment of myocardial infarction (MI) in animal models and clinical trials through mechanisms of direct intercellular contacts, autocrine, and paracrine. However, the effects of EPC transplantation for MI treatment remain controversial and the underlying mechanisms have not been fully elucidated. Here, we explored the role of Rab27a in the therapeutic potential of EPC transplantation in MI. We found that Rab27a knockout impaired the viability, and reduced the proliferation and tube formation function of ECPs. The recovery of cardiac function and improvement of ventricular remodeling from EPCs transplantation were significantly damaged by Rab27a deletion in vivo. Rab27a deletion inhibited the protein expression of phosphoinositide 3-kinase (PI3K) and cyclin D1 and the phosphorylation levels of Akt and FoxO3a. Therefore, Rab27a knockout suppressed the PI3K-Akt-FoxO3a/cyclin D1 signaling pathway. Furthermore, Rab27a ablation dramatically reduced exosome release in EPCs. These results demonstrated that Rab27a plays an essential role in EPC functions. The elucidation of this mechanism provides novel insights into EPC transplantation as a promising treatment for post-MI injuries.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Ablation</subject><subject>AKT protein</subject><subject>Animal models</subject><subject>Animals</subject><subject>Autocrine signalling</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Bone Marrow Cells - pathology</subject><subject>Cardiology</subject><subject>Cells (biology)</subject><subject>Cells, Cultured</subject><subject>Clinical trials</subject><subject>Cyclin D1</subject><subject>Deletion</subject><subject>Disease Models, Animal</subject><subject>Endothelial Progenitor Cells - pathology</subject><subject>Endothelial Progenitor Cells - transplantation</subject><subject>Endothelium</subject><subject>Exosomes - metabolism</subject><subject>FOXO3 protein</subject><subject>Gene 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deletion impairs the therapeutic potential of endothelial progenitor cells for myocardial infarction</title><author>Zhou, Wenyi ; Zheng, Xuefei ; Cheng, Chuanfang ; Guo, Guixian ; Zhong, Yun ; Liu, Weihua ; Liu, Kefeng ; Chen, Yanfang ; Liu, Shiming ; Liu, Shaojun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-f95eda938bbc1e485dc29f5158e5179384c016f48929d28e314b53347d622ca43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Ablation</topic><topic>AKT protein</topic><topic>Animal models</topic><topic>Animals</topic><topic>Autocrine signalling</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Bone Marrow Cells - metabolism</topic><topic>Bone Marrow Cells - pathology</topic><topic>Cardiology</topic><topic>Cells (biology)</topic><topic>Cells, Cultured</topic><topic>Clinical 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Biochem</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>476</volume><issue>2</issue><spage>797</spage><epage>807</epage><pages>797-807</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Endothelial progenitor cell (EPC) transplantation has shown advantages in the treatment of myocardial infarction (MI) in animal models and clinical trials through mechanisms of direct intercellular contacts, autocrine, and paracrine. However, the effects of EPC transplantation for MI treatment remain controversial and the underlying mechanisms have not been fully elucidated. Here, we explored the role of Rab27a in the therapeutic potential of EPC transplantation in MI. We found that Rab27a knockout impaired the viability, and reduced the proliferation and tube formation function of ECPs. The recovery of cardiac function and improvement of ventricular remodeling from EPCs transplantation were significantly damaged by Rab27a deletion in vivo. Rab27a deletion inhibited the protein expression of phosphoinositide 3-kinase (PI3K) and cyclin D1 and the phosphorylation levels of Akt and FoxO3a. Therefore, Rab27a knockout suppressed the PI3K-Akt-FoxO3a/cyclin D1 signaling pathway. Furthermore, Rab27a ablation dramatically reduced exosome release in EPCs. These results demonstrated that Rab27a plays an essential role in EPC functions. The elucidation of this mechanism provides novel insights into EPC transplantation as a promising treatment for post-MI injuries.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33095380</pmid><doi>10.1007/s11010-020-03945-x</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-7895-5577</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Ablation AKT protein Animal models Animals Autocrine signalling Biochemistry Biomedical and Life Sciences Bone Marrow Cells - metabolism Bone Marrow Cells - pathology Cardiology Cells (biology) Cells, Cultured Clinical trials Cyclin D1 Deletion Disease Models, Animal Endothelial Progenitor Cells - pathology Endothelial Progenitor Cells - transplantation Endothelium Exosomes - metabolism FOXO3 protein Gene Deletion Health aspects Heart Heart attack Heart attacks Kinases Life Sciences Male Medical Biochemistry Mice Mice, Inbred C57BL Mice, Knockout Myocardial infarction Myocardial Infarction - genetics Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Infarction - therapy Oncology Paracrine signalling Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Progenitor cells Proto-Oncogene Proteins c-akt - metabolism rab27 GTP-Binding Proteins - deficiency rab27 GTP-Binding Proteins - genetics Signal Transduction Stem Cell Transplantation - methods Stem cells Transplantation Ventricle Ventricular Remodeling |
| title | Rab27a deletion impairs the therapeutic potential of endothelial progenitor cells for myocardial infarction |
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