MiR-221 and miR-26b Regulate Chemotactic Migration of MSCs Toward HGF Through Activation of Akt and FAK
ABSTRACT The chemotactic migration of mesenchymal stem cells (MSCs) is fundamental for their use in cell‐based therapies, but little is known about the molecular mechanisms that regulate their directed migration. MicroRNAs (miRNAs) participate in the regulation of a large variety of cellular process...
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| Veröffentlicht in: | Journal of cellular biochemistry 2016-06, Vol.117 (6), p.1370-1383 |
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| creator | Zhu, Aisi Kang, Naixin He, Lihong Li, Xianyang Xu, Xiaojing Zhang, Huanxiang |
| description | ABSTRACT
The chemotactic migration of mesenchymal stem cells (MSCs) is fundamental for their use in cell‐based therapies, but little is known about the molecular mechanisms that regulate their directed migration. MicroRNAs (miRNAs) participate in the regulation of a large variety of cellular processes. However, their roles in regulating the responses of MSCs to hepatocyte growth factor (HGF) remain elusive. Here, we found that microRNA‐221 (miR‐221) and microRNA‐26b (miR‐26b) were upregulated in MSCs subjected to HGF. Overexpression of miR‐221 or miR‐26b enhanced MSC migration through activation of PI3K/Akt signaling. Phosphatase and tensin homolog deleted on chromosome ten (PTEN) was identified as a potential target of miR‐221 and miR‐26b; overexpression of miR‐221 or miR‐26b decreased PTEN expression at both mRNA and protein levels. Overexpression of miR‐221 or miR‐26b in MSCs increased the phosphorylation of focal adhesion kinase (FAK), a downstream effector of PTEN, which regulates cell migration through assembly and distribution of focal adhesions (FAs), and more dot‐like FAs were localized at the periphery of these cells. Altering miR‐221 or miR‐26b expression influenced the directed migration of MSCs toward HGF. Inhibition of miR‐221 or miR‐26b suppressed the phosphorylation of Akt and FAK and upregulated PTEN expression, which was partly restored by HGF treatment. Collectively, these results demonstrate that miR‐221 and miR‐26b participate in regulating the chemotactic response of MSCs toward HGF. J. Cell. Biochem. 117: 1370–1383, 2016. © 2015 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/jcb.25428 |
| format | Article |
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The chemotactic migration of mesenchymal stem cells (MSCs) is fundamental for their use in cell‐based therapies, but little is known about the molecular mechanisms that regulate their directed migration. MicroRNAs (miRNAs) participate in the regulation of a large variety of cellular processes. However, their roles in regulating the responses of MSCs to hepatocyte growth factor (HGF) remain elusive. Here, we found that microRNA‐221 (miR‐221) and microRNA‐26b (miR‐26b) were upregulated in MSCs subjected to HGF. Overexpression of miR‐221 or miR‐26b enhanced MSC migration through activation of PI3K/Akt signaling. Phosphatase and tensin homolog deleted on chromosome ten (PTEN) was identified as a potential target of miR‐221 and miR‐26b; overexpression of miR‐221 or miR‐26b decreased PTEN expression at both mRNA and protein levels. Overexpression of miR‐221 or miR‐26b in MSCs increased the phosphorylation of focal adhesion kinase (FAK), a downstream effector of PTEN, which regulates cell migration through assembly and distribution of focal adhesions (FAs), and more dot‐like FAs were localized at the periphery of these cells. Altering miR‐221 or miR‐26b expression influenced the directed migration of MSCs toward HGF. Inhibition of miR‐221 or miR‐26b suppressed the phosphorylation of Akt and FAK and upregulated PTEN expression, which was partly restored by HGF treatment. Collectively, these results demonstrate that miR‐221 and miR‐26b participate in regulating the chemotactic response of MSCs toward HGF. J. Cell. Biochem. 117: 1370–1383, 2016. © 2015 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.25428</identifier><identifier>PMID: 26538296</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animals ; Cell migration ; Cell Movement - drug effects ; Chemotactic response ; Chemotaxis ; Chemotaxis - drug effects ; Chromosomes ; Focal adhesion kinase ; focal adhesion kinase (FAK) ; Focal Adhesion Kinase 1 - metabolism ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation - drug effects ; Growth factors ; Hepatocyte growth factor ; hepatocyte growth factor (HGF) ; Hepatocyte Growth Factor - pharmacology ; Homology ; Kinases ; Mesenchymal stem cells ; mesenchymal stem cells (MSCs) ; Mesenchymal Stromal Cells - cytology ; Mesenchymal Stromal Cells - drug effects ; Mesenchyme ; MicroRNAs ; MicroRNAs - genetics ; migration ; miR-221 and miR-26b ; miRNA ; Molecular modelling ; mRNA ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN ; PTEN protein ; Rats ; Ribonucleic acid ; RNA ; Signal Transduction ; Stem cells ; Target recognition ; Tensin</subject><ispartof>Journal of cellular biochemistry, 2016-06, Vol.117 (6), p.1370-1383</ispartof><rights>2015 Wiley Periodicals, Inc.</rights><rights>2016 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5188-14c61913f99eab5a6f656355a4e356bd3f7f738e75e3e0f8ac9118bf099d8ec93</citedby><cites>FETCH-LOGICAL-c5188-14c61913f99eab5a6f656355a4e356bd3f7f738e75e3e0f8ac9118bf099d8ec93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.25428$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.25428$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26538296$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Aisi</creatorcontrib><creatorcontrib>Kang, Naixin</creatorcontrib><creatorcontrib>He, Lihong</creatorcontrib><creatorcontrib>Li, Xianyang</creatorcontrib><creatorcontrib>Xu, Xiaojing</creatorcontrib><creatorcontrib>Zhang, Huanxiang</creatorcontrib><title>MiR-221 and miR-26b Regulate Chemotactic Migration of MSCs Toward HGF Through Activation of Akt and FAK</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem.</addtitle><description>ABSTRACT
The chemotactic migration of mesenchymal stem cells (MSCs) is fundamental for their use in cell‐based therapies, but little is known about the molecular mechanisms that regulate their directed migration. MicroRNAs (miRNAs) participate in the regulation of a large variety of cellular processes. However, their roles in regulating the responses of MSCs to hepatocyte growth factor (HGF) remain elusive. Here, we found that microRNA‐221 (miR‐221) and microRNA‐26b (miR‐26b) were upregulated in MSCs subjected to HGF. Overexpression of miR‐221 or miR‐26b enhanced MSC migration through activation of PI3K/Akt signaling. Phosphatase and tensin homolog deleted on chromosome ten (PTEN) was identified as a potential target of miR‐221 and miR‐26b; overexpression of miR‐221 or miR‐26b decreased PTEN expression at both mRNA and protein levels. Overexpression of miR‐221 or miR‐26b in MSCs increased the phosphorylation of focal adhesion kinase (FAK), a downstream effector of PTEN, which regulates cell migration through assembly and distribution of focal adhesions (FAs), and more dot‐like FAs were localized at the periphery of these cells. Altering miR‐221 or miR‐26b expression influenced the directed migration of MSCs toward HGF. Inhibition of miR‐221 or miR‐26b suppressed the phosphorylation of Akt and FAK and upregulated PTEN expression, which was partly restored by HGF treatment. Collectively, these results demonstrate that miR‐221 and miR‐26b participate in regulating the chemotactic response of MSCs toward HGF. J. Cell. Biochem. 117: 1370–1383, 2016. © 2015 Wiley Periodicals, Inc.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Chemotactic response</subject><subject>Chemotaxis</subject><subject>Chemotaxis - drug effects</subject><subject>Chromosomes</subject><subject>Focal adhesion kinase</subject><subject>focal adhesion kinase (FAK)</subject><subject>Focal Adhesion Kinase 1 - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Growth factors</subject><subject>Hepatocyte growth factor</subject><subject>hepatocyte growth factor (HGF)</subject><subject>Hepatocyte Growth Factor - pharmacology</subject><subject>Homology</subject><subject>Kinases</subject><subject>Mesenchymal stem cells</subject><subject>mesenchymal stem cells (MSCs)</subject><subject>Mesenchymal Stromal Cells - cytology</subject><subject>Mesenchymal Stromal Cells - drug effects</subject><subject>Mesenchyme</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>migration</subject><subject>miR-221 and miR-26b</subject><subject>miRNA</subject><subject>Molecular modelling</subject><subject>mRNA</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN</subject><subject>PTEN protein</subject><subject>Rats</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><subject>Target recognition</subject><subject>Tensin</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1vEzEQhi0EoqFw4A8gS1zgsK0_1l_HsCIpIQEUgjhaXq-dbLqbLfYupf8eJ2lzQKo4zRyeeWZGLwCvMbrACJHLrS0vCMuJfAJGGCmR5TzPn4IREhRlhGJyBl7EuEUIKUXJc3BGOKOSKD4C60W9zAjB0Owq2O57XsKlWw-N6R0sNq7temP72sJFvQ6mr7sd7DxcfC8iXHW3JlTwajqBq03ohvUGjhP6-0SNr_uDdzL-_BI886aJ7tV9PQc_Jh9XxVU2_zr9VIznmWVYygznlmOFqVfKmZIZ7jnjlDGTO8p4WVEvvKDSCeaoQ14aqzCWpU-PVdJZRc_Bu6P3JnS_Bhd73dbRuqYxO9cNUWOJWK4Yx-L_qBAKkZxKlNC3_6Dbbgi79Igm6W6a1h-Ej1LJJTGjguwvfH-kbOhiDM7rm1C3JtxpjPQ-Tp3i1Ic4E_vm3jiUratO5EN-Cbg8Ard14-4eN-lZ8eFBmR0n6ti7P6cJE641F1Qw_fPLVE-XeLb8ls_1jP4FWjmy5Q</recordid><startdate>201606</startdate><enddate>201606</enddate><creator>Zhu, Aisi</creator><creator>Kang, Naixin</creator><creator>He, Lihong</creator><creator>Li, Xianyang</creator><creator>Xu, Xiaojing</creator><creator>Zhang, Huanxiang</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201606</creationdate><title>MiR-221 and miR-26b Regulate Chemotactic Migration of MSCs Toward HGF Through Activation of Akt and FAK</title><author>Zhu, Aisi ; Kang, Naixin ; He, Lihong ; Li, Xianyang ; Xu, Xiaojing ; Zhang, Huanxiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5188-14c61913f99eab5a6f656355a4e356bd3f7f738e75e3e0f8ac9118bf099d8ec93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Chemotactic response</topic><topic>Chemotaxis</topic><topic>Chemotaxis - drug effects</topic><topic>Chromosomes</topic><topic>Focal adhesion kinase</topic><topic>focal adhesion kinase (FAK)</topic><topic>Focal Adhesion Kinase 1 - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Growth factors</topic><topic>Hepatocyte growth factor</topic><topic>hepatocyte growth factor (HGF)</topic><topic>Hepatocyte Growth Factor - pharmacology</topic><topic>Homology</topic><topic>Kinases</topic><topic>Mesenchymal stem cells</topic><topic>mesenchymal stem cells (MSCs)</topic><topic>Mesenchymal Stromal Cells - cytology</topic><topic>Mesenchymal Stromal Cells - drug effects</topic><topic>Mesenchyme</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>migration</topic><topic>miR-221 and miR-26b</topic><topic>miRNA</topic><topic>Molecular modelling</topic><topic>mRNA</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN</topic><topic>PTEN protein</topic><topic>Rats</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal Transduction</topic><topic>Stem cells</topic><topic>Target recognition</topic><topic>Tensin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Aisi</creatorcontrib><creatorcontrib>Kang, Naixin</creatorcontrib><creatorcontrib>He, Lihong</creatorcontrib><creatorcontrib>Li, Xianyang</creatorcontrib><creatorcontrib>Xu, Xiaojing</creatorcontrib><creatorcontrib>Zhang, Huanxiang</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Aisi</au><au>Kang, Naixin</au><au>He, Lihong</au><au>Li, Xianyang</au><au>Xu, Xiaojing</au><au>Zhang, Huanxiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-221 and miR-26b Regulate Chemotactic Migration of MSCs Toward HGF Through Activation of Akt and FAK</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem.</addtitle><date>2016-06</date><risdate>2016</risdate><volume>117</volume><issue>6</issue><spage>1370</spage><epage>1383</epage><pages>1370-1383</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>ABSTRACT
The chemotactic migration of mesenchymal stem cells (MSCs) is fundamental for their use in cell‐based therapies, but little is known about the molecular mechanisms that regulate their directed migration. MicroRNAs (miRNAs) participate in the regulation of a large variety of cellular processes. However, their roles in regulating the responses of MSCs to hepatocyte growth factor (HGF) remain elusive. Here, we found that microRNA‐221 (miR‐221) and microRNA‐26b (miR‐26b) were upregulated in MSCs subjected to HGF. Overexpression of miR‐221 or miR‐26b enhanced MSC migration through activation of PI3K/Akt signaling. Phosphatase and tensin homolog deleted on chromosome ten (PTEN) was identified as a potential target of miR‐221 and miR‐26b; overexpression of miR‐221 or miR‐26b decreased PTEN expression at both mRNA and protein levels. Overexpression of miR‐221 or miR‐26b in MSCs increased the phosphorylation of focal adhesion kinase (FAK), a downstream effector of PTEN, which regulates cell migration through assembly and distribution of focal adhesions (FAs), and more dot‐like FAs were localized at the periphery of these cells. Altering miR‐221 or miR‐26b expression influenced the directed migration of MSCs toward HGF. Inhibition of miR‐221 or miR‐26b suppressed the phosphorylation of Akt and FAK and upregulated PTEN expression, which was partly restored by HGF treatment. Collectively, these results demonstrate that miR‐221 and miR‐26b participate in regulating the chemotactic response of MSCs toward HGF. J. Cell. Biochem. 117: 1370–1383, 2016. © 2015 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>26538296</pmid><doi>10.1002/jcb.25428</doi><tpages>14</tpages></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animals Cell migration Cell Movement - drug effects Chemotactic response Chemotaxis Chemotaxis - drug effects Chromosomes Focal adhesion kinase focal adhesion kinase (FAK) Focal Adhesion Kinase 1 - metabolism Gene expression Gene Expression Profiling Gene Expression Regulation - drug effects Growth factors Hepatocyte growth factor hepatocyte growth factor (HGF) Hepatocyte Growth Factor - pharmacology Homology Kinases Mesenchymal stem cells mesenchymal stem cells (MSCs) Mesenchymal Stromal Cells - cytology Mesenchymal Stromal Cells - drug effects Mesenchyme MicroRNAs MicroRNAs - genetics migration miR-221 and miR-26b miRNA Molecular modelling mRNA Phosphorylation Proto-Oncogene Proteins c-akt - metabolism PTEN PTEN protein Rats Ribonucleic acid RNA Signal Transduction Stem cells Target recognition Tensin |
| title | MiR-221 and miR-26b Regulate Chemotactic Migration of MSCs Toward HGF Through Activation of Akt and FAK |
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