LIMK1 depletion enhances fasudil‐dependent inhibition of urethral fibroblast proliferation and migration
LIM kinase 1 (LIMK1) is an important regulator of the cell cytoskeleton. This study aimed to examine the role of LIMK1 in mediating the effects of the Rho kinase (ROCK) inhibitor fasudil. In vitro cultures of urethral fibroblasts were divided into LIMK1 knockdown (LIMK1 KD) and LIMK1 control (LIMK1...
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| Veröffentlicht in: | Journal of cellular biochemistry 2019-08, Vol.120 (8), p.12977-12988 |
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| creator | Liang, Ying‐Chun Li, Xiao‐Dong Wu, Yu‐Peng Ke, Zhi‐Bin Liu, Zhang‐Qi Chen, Shao‐Hao Wei, Yong Zheng, Qing‐Shui Xue, Xue‐Yi Xu, Ning |
| description | LIM kinase 1 (LIMK1) is an important regulator of the cell cytoskeleton. This study aimed to examine the role of LIMK1 in mediating the effects of the Rho kinase (ROCK) inhibitor fasudil. In vitro cultures of urethral fibroblasts were divided into LIMK1 knockdown (LIMK1 KD) and LIMK1 control (LIMK1 NC) experimental groups. Each group was incubated with fasudil (50 μmol/L) with or without transforming growth factor β1 (10 ng/mL) for 24 hours. Wound healing and Transwell assays were performed to determine cell migration. Flow cytometry was used to determine apoptosis. LIMK1, collagen I, collagen III, phospho‐myosin light chain (p‐MLC), alpha smooth muscle actin (α‐SMA), and phospho‐Cofilin (p‐Cofilin) expression was examined by Western blot analysis. The expression of LIMK1 was further validated in human urethral scar tissues. Transwell and wound healing assays revealed that the cells of the LIMK1 KD group exhibited significantly attenuated migration, when compared with those of the LIMK1 NC group (
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| doi_str_mv | 10.1002/jcb.28569 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2191005722</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2239141547</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3539-36e9a55050e7823ea72a12a66ae8fba639295a0e2df20f31378e056564bcde4f3</originalsourceid><addsrcrecordid>eNp10c1O3DAUBWCroirDtIu-AIrEhi7C-Cd24iWMKKUMYtOuLSe57jjyOIOdCM2OR-AZ-yR1J8ACiZVl3U9HV_cg9JXgM4IxXXRNfUYrLuQHNCNYlnkhiuIAzXDJcE4ZoYfoKMYOYywlo5_QIcOVIKSSM9Strm9vSNbC1sFge5-BX2vfQMyMjmNr3d_HpzQE34IfMuvXtrZ715tsDDCsg3aZsXXoa6fjkG1D76yBoPdI-zbb2D_T7zP6aLSL8OX5naPf3y9_LX_kq7ur6-X5Km8YZzJnAqTmHHMMZUUZ6JJqQrUQGipTa8EklVxjoK2h2DDCygowF1wUddNCYdgcnU65aZf7EeKgNjY24Jz20I9RUSLT1XhJaaInb2jXj8Gn7VSaSlIQXpRJfZtUE_oYAxi1DXajw04RrP4XoFIBal9AssfPiWO9gfZVvlw8gcUEHqyD3ftJ6ufyYor8ByAYkJg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2239141547</pqid></control><display><type>article</type><title>LIMK1 depletion enhances fasudil‐dependent inhibition of urethral fibroblast proliferation and migration</title><source>Access via Wiley Online Library</source><creator>Liang, Ying‐Chun ; Li, Xiao‐Dong ; Wu, Yu‐Peng ; Ke, Zhi‐Bin ; Liu, Zhang‐Qi ; Chen, Shao‐Hao ; Wei, Yong ; Zheng, Qing‐Shui ; Xue, Xue‐Yi ; Xu, Ning</creator><creatorcontrib>Liang, Ying‐Chun ; Li, Xiao‐Dong ; Wu, Yu‐Peng ; Ke, Zhi‐Bin ; Liu, Zhang‐Qi ; Chen, Shao‐Hao ; Wei, Yong ; Zheng, Qing‐Shui ; Xue, Xue‐Yi ; Xu, Ning</creatorcontrib><description>LIM kinase 1 (LIMK1) is an important regulator of the cell cytoskeleton. This study aimed to examine the role of LIMK1 in mediating the effects of the Rho kinase (ROCK) inhibitor fasudil. In vitro cultures of urethral fibroblasts were divided into LIMK1 knockdown (LIMK1 KD) and LIMK1 control (LIMK1 NC) experimental groups. Each group was incubated with fasudil (50 μmol/L) with or without transforming growth factor β1 (10 ng/mL) for 24 hours. Wound healing and Transwell assays were performed to determine cell migration. Flow cytometry was used to determine apoptosis. LIMK1, collagen I, collagen III, phospho‐myosin light chain (p‐MLC), alpha smooth muscle actin (α‐SMA), and phospho‐Cofilin (p‐Cofilin) expression was examined by Western blot analysis. The expression of LIMK1 was further validated in human urethral scar tissues. Transwell and wound healing assays revealed that the cells of the LIMK1 KD group exhibited significantly attenuated migration, when compared with those of the LIMK1 NC group (
P < 0.05). Cell migration was also attenuated in the LIMK1 KD group treated with fasudil (
P < 0.05). Flow cytometry analysis revealed that apoptosis was higher in the LIMK1 KD group than that in LIMK1 NC group (
P < 0.05). Apoptosis was also enhanced in the LIMK1 KD group treated with fasudil (
P < 0.05). Western blot analysis demonstrated that LIMK1, collagen I, collagen III, p‐MLC, α‐SMA, and p‐Cofilin expression was significantly attenuated in both the fasudil‐treated and untreated LIMK1 KD groups (
P < 0.05). LIMK1 was positively expressed in human urethral scar tissues while it was negatively expressed in normal urethra tissues. In conclusion, loss of LIMK1 expression inhibits the Rho/ROCK pathway‐dependent proliferation and migration via downregulation of collagen I, collagen III, p‐Cofilin, and α‐SMA. LIMK1 loss can also enhance the inhibitory effects of fasudil on the proliferation and migration of urethral fibroblasts.
Loss of LIMK1 expression inhibits the Rho/ROCK pathway‐dependent proliferation and migration via downregulation of collagen I, collagen III, p‐Cofilin, and α‐SMA,. LIMK1 loss can also enhance the inhibitory effects of fasudil on the proliferation and migration of urethral fibroblasts.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.28569</identifier><identifier>PMID: 30861189</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Actin ; Apoptosis ; Attenuation ; Cell adhesion & migration ; Cell migration ; Cofilin ; Collagen ; Collagen (type I) ; Collagen (type III) ; Cytoskeleton ; Depletion ; Enzyme inhibitors ; fasudil ; Fibroblasts ; Flow cytometry ; Growth factors ; Kinases ; LIM kinase ; LIMK1 ; Muscles ; Myosin ; p‐Cofilin ; Rho-associated kinase ; RNA interference ; Rocks ; Smooth muscle ; Tissues ; Transforming growth factor ; Urethra ; urethral fibroblast ; Wound healing</subject><ispartof>Journal of cellular biochemistry, 2019-08, Vol.120 (8), p.12977-12988</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3539-36e9a55050e7823ea72a12a66ae8fba639295a0e2df20f31378e056564bcde4f3</citedby><cites>FETCH-LOGICAL-c3539-36e9a55050e7823ea72a12a66ae8fba639295a0e2df20f31378e056564bcde4f3</cites><orcidid>0000-0002-6461-7435 ; 0000-0001-7909-7025 ; 0000-0001-5324-3733</orcidid></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.28569$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.28569$$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/30861189$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liang, Ying‐Chun</creatorcontrib><creatorcontrib>Li, Xiao‐Dong</creatorcontrib><creatorcontrib>Wu, Yu‐Peng</creatorcontrib><creatorcontrib>Ke, Zhi‐Bin</creatorcontrib><creatorcontrib>Liu, Zhang‐Qi</creatorcontrib><creatorcontrib>Chen, Shao‐Hao</creatorcontrib><creatorcontrib>Wei, Yong</creatorcontrib><creatorcontrib>Zheng, Qing‐Shui</creatorcontrib><creatorcontrib>Xue, Xue‐Yi</creatorcontrib><creatorcontrib>Xu, Ning</creatorcontrib><title>LIMK1 depletion enhances fasudil‐dependent inhibition of urethral fibroblast proliferation and migration</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>LIM kinase 1 (LIMK1) is an important regulator of the cell cytoskeleton. This study aimed to examine the role of LIMK1 in mediating the effects of the Rho kinase (ROCK) inhibitor fasudil. In vitro cultures of urethral fibroblasts were divided into LIMK1 knockdown (LIMK1 KD) and LIMK1 control (LIMK1 NC) experimental groups. Each group was incubated with fasudil (50 μmol/L) with or without transforming growth factor β1 (10 ng/mL) for 24 hours. Wound healing and Transwell assays were performed to determine cell migration. Flow cytometry was used to determine apoptosis. LIMK1, collagen I, collagen III, phospho‐myosin light chain (p‐MLC), alpha smooth muscle actin (α‐SMA), and phospho‐Cofilin (p‐Cofilin) expression was examined by Western blot analysis. The expression of LIMK1 was further validated in human urethral scar tissues. Transwell and wound healing assays revealed that the cells of the LIMK1 KD group exhibited significantly attenuated migration, when compared with those of the LIMK1 NC group (
P < 0.05). Cell migration was also attenuated in the LIMK1 KD group treated with fasudil (
P < 0.05). Flow cytometry analysis revealed that apoptosis was higher in the LIMK1 KD group than that in LIMK1 NC group (
P < 0.05). Apoptosis was also enhanced in the LIMK1 KD group treated with fasudil (
P < 0.05). Western blot analysis demonstrated that LIMK1, collagen I, collagen III, p‐MLC, α‐SMA, and p‐Cofilin expression was significantly attenuated in both the fasudil‐treated and untreated LIMK1 KD groups (
P < 0.05). LIMK1 was positively expressed in human urethral scar tissues while it was negatively expressed in normal urethra tissues. In conclusion, loss of LIMK1 expression inhibits the Rho/ROCK pathway‐dependent proliferation and migration via downregulation of collagen I, collagen III, p‐Cofilin, and α‐SMA. LIMK1 loss can also enhance the inhibitory effects of fasudil on the proliferation and migration of urethral fibroblasts.
Loss of LIMK1 expression inhibits the Rho/ROCK pathway‐dependent proliferation and migration via downregulation of collagen I, collagen III, p‐Cofilin, and α‐SMA,. LIMK1 loss can also enhance the inhibitory effects of fasudil on the proliferation and migration of urethral fibroblasts.</description><subject>Actin</subject><subject>Apoptosis</subject><subject>Attenuation</subject><subject>Cell adhesion & migration</subject><subject>Cell migration</subject><subject>Cofilin</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen (type III)</subject><subject>Cytoskeleton</subject><subject>Depletion</subject><subject>Enzyme inhibitors</subject><subject>fasudil</subject><subject>Fibroblasts</subject><subject>Flow cytometry</subject><subject>Growth factors</subject><subject>Kinases</subject><subject>LIM kinase</subject><subject>LIMK1</subject><subject>Muscles</subject><subject>Myosin</subject><subject>p‐Cofilin</subject><subject>Rho-associated kinase</subject><subject>RNA interference</subject><subject>Rocks</subject><subject>Smooth muscle</subject><subject>Tissues</subject><subject>Transforming growth factor</subject><subject>Urethra</subject><subject>urethral fibroblast</subject><subject>Wound healing</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp10c1O3DAUBWCroirDtIu-AIrEhi7C-Cd24iWMKKUMYtOuLSe57jjyOIOdCM2OR-AZ-yR1J8ACiZVl3U9HV_cg9JXgM4IxXXRNfUYrLuQHNCNYlnkhiuIAzXDJcE4ZoYfoKMYOYywlo5_QIcOVIKSSM9Strm9vSNbC1sFge5-BX2vfQMyMjmNr3d_HpzQE34IfMuvXtrZ715tsDDCsg3aZsXXoa6fjkG1D76yBoPdI-zbb2D_T7zP6aLSL8OX5naPf3y9_LX_kq7ur6-X5Km8YZzJnAqTmHHMMZUUZ6JJqQrUQGipTa8EklVxjoK2h2DDCygowF1wUddNCYdgcnU65aZf7EeKgNjY24Jz20I9RUSLT1XhJaaInb2jXj8Gn7VSaSlIQXpRJfZtUE_oYAxi1DXajw04RrP4XoFIBal9AssfPiWO9gfZVvlw8gcUEHqyD3ftJ6ufyYor8ByAYkJg</recordid><startdate>201908</startdate><enddate>201908</enddate><creator>Liang, Ying‐Chun</creator><creator>Li, Xiao‐Dong</creator><creator>Wu, Yu‐Peng</creator><creator>Ke, Zhi‐Bin</creator><creator>Liu, Zhang‐Qi</creator><creator>Chen, Shao‐Hao</creator><creator>Wei, Yong</creator><creator>Zheng, Qing‐Shui</creator><creator>Xue, Xue‐Yi</creator><creator>Xu, Ning</creator><general>Wiley Subscription Services, Inc</general><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><orcidid>https://orcid.org/0000-0002-6461-7435</orcidid><orcidid>https://orcid.org/0000-0001-7909-7025</orcidid><orcidid>https://orcid.org/0000-0001-5324-3733</orcidid></search><sort><creationdate>201908</creationdate><title>LIMK1 depletion enhances fasudil‐dependent inhibition of urethral fibroblast proliferation and migration</title><author>Liang, Ying‐Chun ; Li, Xiao‐Dong ; Wu, Yu‐Peng ; Ke, Zhi‐Bin ; Liu, Zhang‐Qi ; Chen, Shao‐Hao ; Wei, Yong ; Zheng, Qing‐Shui ; Xue, Xue‐Yi ; Xu, Ning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3539-36e9a55050e7823ea72a12a66ae8fba639295a0e2df20f31378e056564bcde4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Actin</topic><topic>Apoptosis</topic><topic>Attenuation</topic><topic>Cell adhesion & migration</topic><topic>Cell migration</topic><topic>Cofilin</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen (type III)</topic><topic>Cytoskeleton</topic><topic>Depletion</topic><topic>Enzyme inhibitors</topic><topic>fasudil</topic><topic>Fibroblasts</topic><topic>Flow cytometry</topic><topic>Growth factors</topic><topic>Kinases</topic><topic>LIM kinase</topic><topic>LIMK1</topic><topic>Muscles</topic><topic>Myosin</topic><topic>p‐Cofilin</topic><topic>Rho-associated kinase</topic><topic>RNA interference</topic><topic>Rocks</topic><topic>Smooth muscle</topic><topic>Tissues</topic><topic>Transforming growth factor</topic><topic>Urethra</topic><topic>urethral fibroblast</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liang, Ying‐Chun</creatorcontrib><creatorcontrib>Li, Xiao‐Dong</creatorcontrib><creatorcontrib>Wu, Yu‐Peng</creatorcontrib><creatorcontrib>Ke, Zhi‐Bin</creatorcontrib><creatorcontrib>Liu, Zhang‐Qi</creatorcontrib><creatorcontrib>Chen, Shao‐Hao</creatorcontrib><creatorcontrib>Wei, Yong</creatorcontrib><creatorcontrib>Zheng, Qing‐Shui</creatorcontrib><creatorcontrib>Xue, Xue‐Yi</creatorcontrib><creatorcontrib>Xu, Ning</creatorcontrib><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>Liang, Ying‐Chun</au><au>Li, Xiao‐Dong</au><au>Wu, Yu‐Peng</au><au>Ke, Zhi‐Bin</au><au>Liu, Zhang‐Qi</au><au>Chen, Shao‐Hao</au><au>Wei, Yong</au><au>Zheng, Qing‐Shui</au><au>Xue, Xue‐Yi</au><au>Xu, Ning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LIMK1 depletion enhances fasudil‐dependent inhibition of urethral fibroblast proliferation and migration</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2019-08</date><risdate>2019</risdate><volume>120</volume><issue>8</issue><spage>12977</spage><epage>12988</epage><pages>12977-12988</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>LIM kinase 1 (LIMK1) is an important regulator of the cell cytoskeleton. This study aimed to examine the role of LIMK1 in mediating the effects of the Rho kinase (ROCK) inhibitor fasudil. In vitro cultures of urethral fibroblasts were divided into LIMK1 knockdown (LIMK1 KD) and LIMK1 control (LIMK1 NC) experimental groups. Each group was incubated with fasudil (50 μmol/L) with or without transforming growth factor β1 (10 ng/mL) for 24 hours. Wound healing and Transwell assays were performed to determine cell migration. Flow cytometry was used to determine apoptosis. LIMK1, collagen I, collagen III, phospho‐myosin light chain (p‐MLC), alpha smooth muscle actin (α‐SMA), and phospho‐Cofilin (p‐Cofilin) expression was examined by Western blot analysis. The expression of LIMK1 was further validated in human urethral scar tissues. Transwell and wound healing assays revealed that the cells of the LIMK1 KD group exhibited significantly attenuated migration, when compared with those of the LIMK1 NC group (
P < 0.05). Cell migration was also attenuated in the LIMK1 KD group treated with fasudil (
P < 0.05). Flow cytometry analysis revealed that apoptosis was higher in the LIMK1 KD group than that in LIMK1 NC group (
P < 0.05). Apoptosis was also enhanced in the LIMK1 KD group treated with fasudil (
P < 0.05). Western blot analysis demonstrated that LIMK1, collagen I, collagen III, p‐MLC, α‐SMA, and p‐Cofilin expression was significantly attenuated in both the fasudil‐treated and untreated LIMK1 KD groups (
P < 0.05). LIMK1 was positively expressed in human urethral scar tissues while it was negatively expressed in normal urethra tissues. In conclusion, loss of LIMK1 expression inhibits the Rho/ROCK pathway‐dependent proliferation and migration via downregulation of collagen I, collagen III, p‐Cofilin, and α‐SMA. LIMK1 loss can also enhance the inhibitory effects of fasudil on the proliferation and migration of urethral fibroblasts.
Loss of LIMK1 expression inhibits the Rho/ROCK pathway‐dependent proliferation and migration via downregulation of collagen I, collagen III, p‐Cofilin, and α‐SMA,. LIMK1 loss can also enhance the inhibitory effects of fasudil on the proliferation and migration of urethral fibroblasts.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30861189</pmid><doi>10.1002/jcb.28569</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6461-7435</orcidid><orcidid>https://orcid.org/0000-0001-7909-7025</orcidid><orcidid>https://orcid.org/0000-0001-5324-3733</orcidid></addata></record> |
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| subjects | Actin Apoptosis Attenuation Cell adhesion & migration Cell migration Cofilin Collagen Collagen (type I) Collagen (type III) Cytoskeleton Depletion Enzyme inhibitors fasudil Fibroblasts Flow cytometry Growth factors Kinases LIM kinase LIMK1 Muscles Myosin p‐Cofilin Rho-associated kinase RNA interference Rocks Smooth muscle Tissues Transforming growth factor Urethra urethral fibroblast Wound healing |
| title | LIMK1 depletion enhances fasudil‐dependent inhibition of urethral fibroblast proliferation and migration |
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