microRNA-148a in Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviates Cardiomyocyte Apoptosis in Atrial Fibrillation by Inhibiting SMOC2
Exosomes-related microRNAs (miRNAs) have been considered to be the significant biomarkers contributing to the development of atrial fibrillation (AF). We observed the implicit mechanism of exosomes-miR-148a derived from bone marrow mesenchymal stem cells (BMSCs) in AF. The AF cell and mice models we...
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Veröffentlicht in: | Molecular biotechnology 2022-10, Vol.64 (10), p.1076-1087 |
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description | Exosomes-related microRNAs (miRNAs) have been considered to be the significant biomarkers contributing to the development of atrial fibrillation (AF). We observed the implicit mechanism of exosomes-miR-148a derived from bone marrow mesenchymal stem cells (BMSCs) in AF. The AF cell and mice models were established firstly. QRT-PCR and Western blot analysis were applied to detect the expression of miR-148a, SPARC-associated modular calcium-binding protein 2 (SMOC2), Bcl-2, Bax, and caspase-3. BMSCs were separated from healthy mice and exosomes were obtained from BMSCs. BMSCs were transfected with mimics and inhibitor, and HL-1 cells were treated with mimics and pcDNA3.1. MTT assay were used to detect cell viability of cells. Flow cytometric analysis and TUNEL analysis were used for detecting cell apoptosis of cells. In our study, exosomes derived from BMSCs inhibited the development of AF, and miR-148a acted a vital role in this segment. SMOC2 was a target gene of miR-148a and promoted apoptosis of HL-1 cells. Additionally, miR-148a mimics decreased cellular apoptosis, eliminated SMOC2 expression, and elevated Bcl-2 expression in AF-treated cells. Collectively, miR-148a overexpressed in BMSC-exosomes restrained cardiomyocytes apoptosis by inhibiting SMOC2. |
doi_str_mv | 10.1007/s12033-022-00487-z |
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We observed the implicit mechanism of exosomes-miR-148a derived from bone marrow mesenchymal stem cells (BMSCs) in AF. The AF cell and mice models were established firstly. QRT-PCR and Western blot analysis were applied to detect the expression of miR-148a, SPARC-associated modular calcium-binding protein 2 (SMOC2), Bcl-2, Bax, and caspase-3. BMSCs were separated from healthy mice and exosomes were obtained from BMSCs. BMSCs were transfected with mimics and inhibitor, and HL-1 cells were treated with mimics and pcDNA3.1. MTT assay were used to detect cell viability of cells. Flow cytometric analysis and TUNEL analysis were used for detecting cell apoptosis of cells. In our study, exosomes derived from BMSCs inhibited the development of AF, and miR-148a acted a vital role in this segment. SMOC2 was a target gene of miR-148a and promoted apoptosis of HL-1 cells. Additionally, miR-148a mimics decreased cellular apoptosis, eliminated SMOC2 expression, and elevated Bcl-2 expression in AF-treated cells. Collectively, miR-148a overexpressed in BMSC-exosomes restrained cardiomyocytes apoptosis by inhibiting SMOC2.</description><identifier>ISSN: 1073-6085</identifier><identifier>EISSN: 1559-0305</identifier><identifier>DOI: 10.1007/s12033-022-00487-z</identifier><identifier>PMID: 35397056</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animal models ; Apoptosis ; BAX protein ; Bcl-2 protein ; Biochemistry ; Biological Techniques ; Biomarkers ; Biotechnology ; Bone marrow ; Calcium-binding protein ; Cardiac arrhythmia ; Cardiomyocytes ; Caspase-3 ; Cell Biology ; Cell culture ; Cell viability ; Chemistry ; Chemistry and Materials Science ; Exosomes ; Fibrillation ; Flow cytometry ; Human Genetics ; Mesenchymal stem cells ; MicroRNAs ; miRNA ; Original Paper ; Osteonectin ; Protein Science ; Ribonucleic acid ; RNA ; Stem cell transplantation ; Stem cells</subject><ispartof>Molecular biotechnology, 2022-10, Vol.64 (10), p.1076-1087</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-b6e84a2b4a1d347bf67b95d663c9903496dbd2ffd52a7c83e1468683b2a23f873</citedby><cites>FETCH-LOGICAL-c375t-b6e84a2b4a1d347bf67b95d663c9903496dbd2ffd52a7c83e1468683b2a23f873</cites><orcidid>0000-0002-7824-9055</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/s12033-022-00487-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12033-022-00487-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35397056$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Weijuan</creatorcontrib><creatorcontrib>Man, Yilong</creatorcontrib><creatorcontrib>Chen, Zhanghu</creatorcontrib><title>microRNA-148a in Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviates Cardiomyocyte Apoptosis in Atrial Fibrillation by Inhibiting SMOC2</title><title>Molecular biotechnology</title><addtitle>Mol Biotechnol</addtitle><addtitle>Mol Biotechnol</addtitle><description>Exosomes-related microRNAs (miRNAs) have been considered to be the significant biomarkers contributing to the development of atrial fibrillation (AF). We observed the implicit mechanism of exosomes-miR-148a derived from bone marrow mesenchymal stem cells (BMSCs) in AF. The AF cell and mice models were established firstly. QRT-PCR and Western blot analysis were applied to detect the expression of miR-148a, SPARC-associated modular calcium-binding protein 2 (SMOC2), Bcl-2, Bax, and caspase-3. BMSCs were separated from healthy mice and exosomes were obtained from BMSCs. BMSCs were transfected with mimics and inhibitor, and HL-1 cells were treated with mimics and pcDNA3.1. MTT assay were used to detect cell viability of cells. Flow cytometric analysis and TUNEL analysis were used for detecting cell apoptosis of cells. In our study, exosomes derived from BMSCs inhibited the development of AF, and miR-148a acted a vital role in this segment. SMOC2 was a target gene of miR-148a and promoted apoptosis of HL-1 cells. Additionally, miR-148a mimics decreased cellular apoptosis, eliminated SMOC2 expression, and elevated Bcl-2 expression in AF-treated cells. Collectively, miR-148a overexpressed in BMSC-exosomes restrained cardiomyocytes apoptosis by inhibiting SMOC2.</description><subject>Animal models</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Biochemistry</subject><subject>Biological Techniques</subject><subject>Biomarkers</subject><subject>Biotechnology</subject><subject>Bone marrow</subject><subject>Calcium-binding protein</subject><subject>Cardiac arrhythmia</subject><subject>Cardiomyocytes</subject><subject>Caspase-3</subject><subject>Cell Biology</subject><subject>Cell culture</subject><subject>Cell viability</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Exosomes</subject><subject>Fibrillation</subject><subject>Flow cytometry</subject><subject>Human Genetics</subject><subject>Mesenchymal stem cells</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Original Paper</subject><subject>Osteonectin</subject><subject>Protein Science</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Stem cell transplantation</subject><subject>Stem 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in Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviates Cardiomyocyte Apoptosis in Atrial Fibrillation by Inhibiting SMOC2</title><author>Zhang, Weijuan ; Man, Yilong ; Chen, Zhanghu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-b6e84a2b4a1d347bf67b95d663c9903496dbd2ffd52a7c83e1468683b2a23f873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animal models</topic><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Biochemistry</topic><topic>Biological Techniques</topic><topic>Biomarkers</topic><topic>Biotechnology</topic><topic>Bone marrow</topic><topic>Calcium-binding protein</topic><topic>Cardiac arrhythmia</topic><topic>Cardiomyocytes</topic><topic>Caspase-3</topic><topic>Cell Biology</topic><topic>Cell culture</topic><topic>Cell viability</topic><topic>Chemistry</topic><topic>Chemistry and Materials 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in Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviates Cardiomyocyte Apoptosis in Atrial Fibrillation by Inhibiting SMOC2</atitle><jtitle>Molecular biotechnology</jtitle><stitle>Mol Biotechnol</stitle><addtitle>Mol Biotechnol</addtitle><date>2022-10-01</date><risdate>2022</risdate><volume>64</volume><issue>10</issue><spage>1076</spage><epage>1087</epage><pages>1076-1087</pages><issn>1073-6085</issn><eissn>1559-0305</eissn><abstract>Exosomes-related microRNAs (miRNAs) have been considered to be the significant biomarkers contributing to the development of atrial fibrillation (AF). We observed the implicit mechanism of exosomes-miR-148a derived from bone marrow mesenchymal stem cells (BMSCs) in AF. The AF cell and mice models were established firstly. QRT-PCR and Western blot analysis were applied to detect the expression of miR-148a, SPARC-associated modular calcium-binding protein 2 (SMOC2), Bcl-2, Bax, and caspase-3. BMSCs were separated from healthy mice and exosomes were obtained from BMSCs. BMSCs were transfected with mimics and inhibitor, and HL-1 cells were treated with mimics and pcDNA3.1. MTT assay were used to detect cell viability of cells. Flow cytometric analysis and TUNEL analysis were used for detecting cell apoptosis of cells. In our study, exosomes derived from BMSCs inhibited the development of AF, and miR-148a acted a vital role in this segment. SMOC2 was a target gene of miR-148a and promoted apoptosis of HL-1 cells. Additionally, miR-148a mimics decreased cellular apoptosis, eliminated SMOC2 expression, and elevated Bcl-2 expression in AF-treated cells. Collectively, miR-148a overexpressed in BMSC-exosomes restrained cardiomyocytes apoptosis by inhibiting SMOC2.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>35397056</pmid><doi>10.1007/s12033-022-00487-z</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-7824-9055</orcidid></addata></record> |
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subjects | Animal models Apoptosis BAX protein Bcl-2 protein Biochemistry Biological Techniques Biomarkers Biotechnology Bone marrow Calcium-binding protein Cardiac arrhythmia Cardiomyocytes Caspase-3 Cell Biology Cell culture Cell viability Chemistry Chemistry and Materials Science Exosomes Fibrillation Flow cytometry Human Genetics Mesenchymal stem cells MicroRNAs miRNA Original Paper Osteonectin Protein Science Ribonucleic acid RNA Stem cell transplantation Stem cells |
title | microRNA-148a in Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviates Cardiomyocyte Apoptosis in Atrial Fibrillation by Inhibiting SMOC2 |
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