IL-17A Recruits Rab35 to IL-17R to Mediate PKCα-Dependent Stress Fiber Formation and Airway Smooth Muscle Contractility
IL-17A is a critical proinflammatory cytokine for the pathogenesis of asthma including neutrophilic pulmonary inflammation and airway hyperresponsiveness. In this study, by cell type-specific deletion of IL-17R and adaptor Act1, we demonstrated that IL-17R/Act1 exerts a direct impact on the contract...
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| Veröffentlicht in: | The Journal of immunology (1950) 2019-03, Vol.202 (5), p.1540-1548 |
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| creator | Bulek, Katarzyna Chen, Xing Parron, Vandy Sundaram, Aparna Herjan, Tomasz Ouyang, Suidong Liu, Caini Majors, Alana Zepp, Jarod Gao, Ji Dongre, Ashok Bodaszewska-Lubas, Malgorzata Echard, Arnaud Aronica, Mark Carman, Julie Garantziotis, Stavros Sheppard, Dean Li, Xiaoxia |
| description | IL-17A is a critical proinflammatory cytokine for the pathogenesis of asthma including neutrophilic pulmonary inflammation and airway hyperresponsiveness. In this study, by cell type-specific deletion of IL-17R and adaptor Act1, we demonstrated that IL-17R/Act1 exerts a direct impact on the contraction of airway smooth muscle cells (ASMCs). Mechanistically, IL-17A induced the recruitment of Rab35 (a small monomeric GTPase) and DennD1C (guanine nucleotide exchange factor [GEF]) to the IL-17R/Act1 complex in ASMCs, resulting in activation of Rab35. Rab35 knockdown showed that IL-17A-induced Rab35 activation was essential for protein kinase Cα (PKCα) activation and phosphorylation of fascin at Ser39 in ASMCs, allowing F-actin to interact with myosin to form stress fibers and enhance the contraction induced by methacholine. PKCα inhibitor or Rab35 knockdown indeed substantially reduced IL-17A-induced stress fiber formation in ASMCs and attenuated IL-17A-enhanced, methacholine-induced contraction of airway smooth muscle. Taken together, these data indicate that IL-17A promotes airway smooth muscle contraction via direct recruitment of Rab35 to IL-17R, followed by PKCα activation and stress fiber formation. |
| doi_str_mv | 10.4049/jimmunol.1801025 |
| format | Article |
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In this study, by cell type-specific deletion of IL-17R and adaptor Act1, we demonstrated that IL-17R/Act1 exerts a direct impact on the contraction of airway smooth muscle cells (ASMCs). Mechanistically, IL-17A induced the recruitment of Rab35 (a small monomeric GTPase) and DennD1C (guanine nucleotide exchange factor [GEF]) to the IL-17R/Act1 complex in ASMCs, resulting in activation of Rab35. Rab35 knockdown showed that IL-17A-induced Rab35 activation was essential for protein kinase Cα (PKCα) activation and phosphorylation of fascin at Ser39 in ASMCs, allowing F-actin to interact with myosin to form stress fibers and enhance the contraction induced by methacholine. PKCα inhibitor or Rab35 knockdown indeed substantially reduced IL-17A-induced stress fiber formation in ASMCs and attenuated IL-17A-enhanced, methacholine-induced contraction of airway smooth muscle. Taken together, these data indicate that IL-17A promotes airway smooth muscle contraction via direct recruitment of Rab35 to IL-17R, followed by PKCα activation and stress fiber formation.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1801025</identifier><identifier>PMID: 30683702</identifier><language>eng</language><publisher>United States: Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists</publisher><subject>Animals ; Biochemistry, Molecular Biology ; Cancer ; Cellular Biology ; Immunology ; Innate Immunity and Inflammation ; Interleukin-17 - antagonists & inhibitors ; Interleukin-17 - deficiency ; Interleukin-17 - metabolism ; Life Sciences ; Mice ; Mice, Knockout ; Muscle Contraction - drug effects ; Muscle, Smooth - drug effects ; Muscle, Smooth - metabolism ; Protein Kinase C-alpha - antagonists & inhibitors ; Protein Kinase C-alpha - metabolism ; Protein Kinase Inhibitors - pharmacology ; rab GTP-Binding Proteins - antagonists & inhibitors ; rab GTP-Binding Proteins - metabolism ; Receptors, Interleukin-17 - antagonists & inhibitors ; Receptors, Interleukin-17 - metabolism ; Stress Fibers - drug effects ; Stress Fibers - metabolism</subject><ispartof>The Journal of immunology (1950), 2019-03, Vol.202 (5), p.1540-1548</ispartof><rights>Copyright © 2019 by The American Association of Immunologists, Inc.</rights><rights>Attribution - NonCommercial</rights><rights>Copyright © 2019 by The American Association of Immunologists, Inc. 2019 Copyright © 2019 by The American Association of Immunologists, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c360t-9d16941dbdd084fafd7082682e4afface3b5896940bed96549b30f0eaa137a733</citedby><cites>FETCH-LOGICAL-c360t-9d16941dbdd084fafd7082682e4afface3b5896940bed96549b30f0eaa137a733</cites><orcidid>0000-0002-9314-7145 ; 0000-0003-4007-375X ; 0000-0002-6277-2036 ; 0000-0001-9624-4584 ; 0000-0002-3698-1838 ; 0000-0003-3648-7941 ; 0000-0001-7402-1398</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30683702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-02394379$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Bulek, Katarzyna</creatorcontrib><creatorcontrib>Chen, Xing</creatorcontrib><creatorcontrib>Parron, Vandy</creatorcontrib><creatorcontrib>Sundaram, Aparna</creatorcontrib><creatorcontrib>Herjan, Tomasz</creatorcontrib><creatorcontrib>Ouyang, Suidong</creatorcontrib><creatorcontrib>Liu, Caini</creatorcontrib><creatorcontrib>Majors, Alana</creatorcontrib><creatorcontrib>Zepp, Jarod</creatorcontrib><creatorcontrib>Gao, Ji</creatorcontrib><creatorcontrib>Dongre, Ashok</creatorcontrib><creatorcontrib>Bodaszewska-Lubas, Malgorzata</creatorcontrib><creatorcontrib>Echard, Arnaud</creatorcontrib><creatorcontrib>Aronica, Mark</creatorcontrib><creatorcontrib>Carman, Julie</creatorcontrib><creatorcontrib>Garantziotis, Stavros</creatorcontrib><creatorcontrib>Sheppard, Dean</creatorcontrib><creatorcontrib>Li, Xiaoxia</creatorcontrib><title>IL-17A Recruits Rab35 to IL-17R to Mediate PKCα-Dependent Stress Fiber Formation and Airway Smooth Muscle Contractility</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>IL-17A is a critical proinflammatory cytokine for the pathogenesis of asthma including neutrophilic pulmonary inflammation and airway hyperresponsiveness. In this study, by cell type-specific deletion of IL-17R and adaptor Act1, we demonstrated that IL-17R/Act1 exerts a direct impact on the contraction of airway smooth muscle cells (ASMCs). Mechanistically, IL-17A induced the recruitment of Rab35 (a small monomeric GTPase) and DennD1C (guanine nucleotide exchange factor [GEF]) to the IL-17R/Act1 complex in ASMCs, resulting in activation of Rab35. Rab35 knockdown showed that IL-17A-induced Rab35 activation was essential for protein kinase Cα (PKCα) activation and phosphorylation of fascin at Ser39 in ASMCs, allowing F-actin to interact with myosin to form stress fibers and enhance the contraction induced by methacholine. PKCα inhibitor or Rab35 knockdown indeed substantially reduced IL-17A-induced stress fiber formation in ASMCs and attenuated IL-17A-enhanced, methacholine-induced contraction of airway smooth muscle. Taken together, these data indicate that IL-17A promotes airway smooth muscle contraction via direct recruitment of Rab35 to IL-17R, followed by PKCα activation and stress fiber formation.</description><subject>Animals</subject><subject>Biochemistry, Molecular Biology</subject><subject>Cancer</subject><subject>Cellular Biology</subject><subject>Immunology</subject><subject>Innate Immunity and Inflammation</subject><subject>Interleukin-17 - antagonists & inhibitors</subject><subject>Interleukin-17 - deficiency</subject><subject>Interleukin-17 - metabolism</subject><subject>Life Sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Muscle Contraction - drug effects</subject><subject>Muscle, Smooth - drug effects</subject><subject>Muscle, Smooth - metabolism</subject><subject>Protein Kinase C-alpha - antagonists & inhibitors</subject><subject>Protein Kinase C-alpha - metabolism</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>rab GTP-Binding Proteins - antagonists & inhibitors</subject><subject>rab GTP-Binding Proteins - metabolism</subject><subject>Receptors, Interleukin-17 - antagonists & inhibitors</subject><subject>Receptors, Interleukin-17 - metabolism</subject><subject>Stress Fibers - drug effects</subject><subject>Stress Fibers - metabolism</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFP3DAQhS0Egi1w51T5yiEwjhMnviCttl1AXVS0wNly4knXKIlXtpd2fxZ_pL-JbBcQ9DSjme89PekRcsLgLINMnj_arlv1rj1jJTBI8x0yYnkOiRAgdskIIE0TVojigHwJ4REABKTZPjngIEpeQDoif65nAzGmc6z9ysZA57riOY2O_nvMN9sNGqsj0tsfk7_PyTdcYm-wj_QuegyBTm2Fnk6d73S0rqe6N3Rs_W-9pnedc3FBb1ahbpFOXB-9rqNtbVwfkb1GtwGPX-cheZh-v59cJbOfl9eT8SypuYCYSMOEzJipjIEya3RjCihTUaaY6abRNfIqL-WAQIVGijyTFYcGUGvGC11wfkgutr7LVdWhqXGToVVLbzvt18ppqz5_ertQv9yTEryQJcjB4HRrsPhPdjWeqc0NUi6zAX5iAwtbtvYuBI_Nu4CB2jSm3hpTr40Nkq8f870L3iriL0wilJw</recordid><startdate>20190301</startdate><enddate>20190301</enddate><creator>Bulek, Katarzyna</creator><creator>Chen, Xing</creator><creator>Parron, Vandy</creator><creator>Sundaram, Aparna</creator><creator>Herjan, Tomasz</creator><creator>Ouyang, Suidong</creator><creator>Liu, Caini</creator><creator>Majors, Alana</creator><creator>Zepp, Jarod</creator><creator>Gao, Ji</creator><creator>Dongre, Ashok</creator><creator>Bodaszewska-Lubas, Malgorzata</creator><creator>Echard, Arnaud</creator><creator>Aronica, Mark</creator><creator>Carman, Julie</creator><creator>Garantziotis, Stavros</creator><creator>Sheppard, Dean</creator><creator>Li, Xiaoxia</creator><general>Publisher : Baltimore : Williams & Wilkins, c1950-. 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In this study, by cell type-specific deletion of IL-17R and adaptor Act1, we demonstrated that IL-17R/Act1 exerts a direct impact on the contraction of airway smooth muscle cells (ASMCs). Mechanistically, IL-17A induced the recruitment of Rab35 (a small monomeric GTPase) and DennD1C (guanine nucleotide exchange factor [GEF]) to the IL-17R/Act1 complex in ASMCs, resulting in activation of Rab35. Rab35 knockdown showed that IL-17A-induced Rab35 activation was essential for protein kinase Cα (PKCα) activation and phosphorylation of fascin at Ser39 in ASMCs, allowing F-actin to interact with myosin to form stress fibers and enhance the contraction induced by methacholine. PKCα inhibitor or Rab35 knockdown indeed substantially reduced IL-17A-induced stress fiber formation in ASMCs and attenuated IL-17A-enhanced, methacholine-induced contraction of airway smooth muscle. Taken together, these data indicate that IL-17A promotes airway smooth muscle contraction via direct recruitment of Rab35 to IL-17R, followed by PKCα activation and stress fiber formation.</abstract><cop>United States</cop><pub>Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists</pub><pmid>30683702</pmid><doi>10.4049/jimmunol.1801025</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-9314-7145</orcidid><orcidid>https://orcid.org/0000-0003-4007-375X</orcidid><orcidid>https://orcid.org/0000-0002-6277-2036</orcidid><orcidid>https://orcid.org/0000-0001-9624-4584</orcidid><orcidid>https://orcid.org/0000-0002-3698-1838</orcidid><orcidid>https://orcid.org/0000-0003-3648-7941</orcidid><orcidid>https://orcid.org/0000-0001-7402-1398</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biochemistry, Molecular Biology Cancer Cellular Biology Immunology Innate Immunity and Inflammation Interleukin-17 - antagonists & inhibitors Interleukin-17 - deficiency Interleukin-17 - metabolism Life Sciences Mice Mice, Knockout Muscle Contraction - drug effects Muscle, Smooth - drug effects Muscle, Smooth - metabolism Protein Kinase C-alpha - antagonists & inhibitors Protein Kinase C-alpha - metabolism Protein Kinase Inhibitors - pharmacology rab GTP-Binding Proteins - antagonists & inhibitors rab GTP-Binding Proteins - metabolism Receptors, Interleukin-17 - antagonists & inhibitors Receptors, Interleukin-17 - metabolism Stress Fibers - drug effects Stress Fibers - metabolism |
| title | IL-17A Recruits Rab35 to IL-17R to Mediate PKCα-Dependent Stress Fiber Formation and Airway Smooth Muscle Contractility |
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