The pro-proliferative effects of nicotine and its underlying mechanism on rat airway smooth muscle cells
Recent studies have shown that nicotine, a major component of cigarette smoke, can stimulate the proliferation of non-neuronal cells. Cigarette smoking can promote a variety of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease (COPD), atherosclerosis, and cancer. A...
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| Veröffentlicht in: | PloS one 2014-04, Vol.9 (4), p.e93508-e93508 |
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| creator | He, Fang Li, Bing Zhao, Zhuxiang Zhou, Yumin Hu, Guoping Zou, Weifeng Hong, Wei Zou, Yimin Jiang, Changbin Zhao, Dongxing Ran, Pixin |
| description | Recent studies have shown that nicotine, a major component of cigarette smoke, can stimulate the proliferation of non-neuronal cells. Cigarette smoking can promote a variety of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease (COPD), atherosclerosis, and cancer. A predominant feature of COPD is airway remodeling, which includes increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodeling in COPD have not yet been fully elucidated. Here, we show that nicotine induces a profound and time-dependent increase in DNA synthesis in rat airway smooth muscle cells (RASMCs) in vitro. Nicotine also significantly increased the number of RASMCs, which was associated with the increased expression of Cyclin D1, phosphorylation of the retinoblastoma protein (RB) and was dependent on the activation of Akt. The activation of Akt by nicotine occurred within minutes and depended upon the nicotinic acetylcholine receptors (nAchRs). Activated Akt increased the phosphorylation of downstream substrates such as GSK3β. Our data suggest that the binding of nicotine to the nAchRs on RASMCs can regulate cellular proliferation by activating the Akt pathway. |
| doi_str_mv | 10.1371/journal.pone.0093508 |
| format | Article |
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Cigarette smoking can promote a variety of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease (COPD), atherosclerosis, and cancer. A predominant feature of COPD is airway remodeling, which includes increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodeling in COPD have not yet been fully elucidated. Here, we show that nicotine induces a profound and time-dependent increase in DNA synthesis in rat airway smooth muscle cells (RASMCs) in vitro. Nicotine also significantly increased the number of RASMCs, which was associated with the increased expression of Cyclin D1, phosphorylation of the retinoblastoma protein (RB) and was dependent on the activation of Akt. The activation of Akt by nicotine occurred within minutes and depended upon the nicotinic acetylcholine receptors (nAchRs). Activated Akt increased the phosphorylation of downstream substrates such as GSK3β. Our data suggest that the binding of nicotine to the nAchRs on RASMCs can regulate cellular proliferation by activating the Akt pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0093508</identifier><identifier>PMID: 24690900</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acetylcholine receptors (nicotinic) ; Activation ; AKT protein ; Angiogenesis ; Animals ; Apoptosis ; Arteriosclerosis ; Atherosclerosis ; Biology and life sciences ; Cancer ; Cardiovascular diseases ; Care and treatment ; Cell cycle ; Cell growth ; Cell proliferation ; Cell Proliferation - drug effects ; Cells, Cultured ; Chronic obstructive pulmonary disease ; Cigarette smoke ; Cigarette smoking ; Cigarettes ; Cyclin D1 ; Cyclin D1 - metabolism ; Deoxyribonucleic acid ; Diagnosis ; Disease ; DNA ; DNA biosynthesis ; Epidermal growth factor ; Health aspects ; Heart diseases ; Hospitals ; Kinases ; Laboratory animals ; Lung cancer ; Lung diseases ; Lung diseases, Obstructive ; Medical research ; Medicine and Health Sciences ; Muscles ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; Nicotine ; Nicotine - pharmacology ; Obstructive lung disease ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Pulmonary arteries ; Rats ; Receptors ; Receptors, Nicotinic - metabolism ; Respiratory diseases ; Respiratory tract ; Retina ; Retinoblastoma ; Retinoblastoma protein ; Retinoblastoma Protein - metabolism ; Risk factors ; Rodents ; Signal Transduction - drug effects ; Smoke ; Smoking ; Smooth muscle ; Stem cells ; Substrates ; Trachea - cytology</subject><ispartof>PloS one, 2014-04, Vol.9 (4), p.e93508-e93508</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 He et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 He et al 2014 He et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-36845e437e857af2866a6c6404fb9f592e3d9f3c6494b21ece0d15d57f110e8c3</citedby><cites>FETCH-LOGICAL-c692t-36845e437e857af2866a6c6404fb9f592e3d9f3c6494b21ece0d15d57f110e8c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972239/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972239/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24690900$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Xiao, Qingzhong</contributor><creatorcontrib>He, Fang</creatorcontrib><creatorcontrib>Li, Bing</creatorcontrib><creatorcontrib>Zhao, Zhuxiang</creatorcontrib><creatorcontrib>Zhou, Yumin</creatorcontrib><creatorcontrib>Hu, Guoping</creatorcontrib><creatorcontrib>Zou, Weifeng</creatorcontrib><creatorcontrib>Hong, Wei</creatorcontrib><creatorcontrib>Zou, Yimin</creatorcontrib><creatorcontrib>Jiang, Changbin</creatorcontrib><creatorcontrib>Zhao, Dongxing</creatorcontrib><creatorcontrib>Ran, Pixin</creatorcontrib><title>The pro-proliferative effects of nicotine and its underlying mechanism on rat airway smooth muscle cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Recent studies have shown that nicotine, a major component of cigarette smoke, can stimulate the proliferation of non-neuronal cells. Cigarette smoking can promote a variety of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease (COPD), atherosclerosis, and cancer. A predominant feature of COPD is airway remodeling, which includes increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodeling in COPD have not yet been fully elucidated. Here, we show that nicotine induces a profound and time-dependent increase in DNA synthesis in rat airway smooth muscle cells (RASMCs) in vitro. Nicotine also significantly increased the number of RASMCs, which was associated with the increased expression of Cyclin D1, phosphorylation of the retinoblastoma protein (RB) and was dependent on the activation of Akt. The activation of Akt by nicotine occurred within minutes and depended upon the nicotinic acetylcholine receptors (nAchRs). Activated Akt increased the phosphorylation of downstream substrates such as GSK3β. Our data suggest that the binding of nicotine to the nAchRs on RASMCs can regulate cellular proliferation by activating the Akt pathway.</description><subject>Acetylcholine receptors (nicotinic)</subject><subject>Activation</subject><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Biology and life sciences</subject><subject>Cancer</subject><subject>Cardiovascular diseases</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Cigarette smoke</subject><subject>Cigarette smoking</subject><subject>Cigarettes</subject><subject>Cyclin D1</subject><subject>Cyclin D1 - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>Diagnosis</subject><subject>Disease</subject><subject>DNA</subject><subject>DNA biosynthesis</subject><subject>Epidermal growth factor</subject><subject>Health aspects</subject><subject>Heart diseases</subject><subject>Hospitals</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Lung diseases, Obstructive</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Muscles</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Obstructive lung disease</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Pulmonary arteries</subject><subject>Rats</subject><subject>Receptors</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Respiratory diseases</subject><subject>Respiratory tract</subject><subject>Retina</subject><subject>Retinoblastoma</subject><subject>Retinoblastoma protein</subject><subject>Retinoblastoma Protein - metabolism</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Smoke</subject><subject>Smoking</subject><subject>Smooth muscle</subject><subject>Stem cells</subject><subject>Substrates</subject><subject>Trachea - 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pro-proliferative effects of nicotine and its underlying mechanism on rat airway smooth muscle cells</title><author>He, Fang ; Li, Bing ; Zhao, Zhuxiang ; Zhou, Yumin ; Hu, Guoping ; Zou, Weifeng ; Hong, Wei ; Zou, Yimin ; Jiang, Changbin ; Zhao, Dongxing ; Ran, Pixin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-36845e437e857af2866a6c6404fb9f592e3d9f3c6494b21ece0d15d57f110e8c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acetylcholine receptors (nicotinic)</topic><topic>Activation</topic><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Biology and life sciences</topic><topic>Cancer</topic><topic>Cardiovascular diseases</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell 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Zhuxiang</au><au>Zhou, Yumin</au><au>Hu, Guoping</au><au>Zou, Weifeng</au><au>Hong, Wei</au><au>Zou, Yimin</au><au>Jiang, Changbin</au><au>Zhao, Dongxing</au><au>Ran, Pixin</au><au>Xiao, Qingzhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The pro-proliferative effects of nicotine and its underlying mechanism on rat airway smooth muscle cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-04-01</date><risdate>2014</risdate><volume>9</volume><issue>4</issue><spage>e93508</spage><epage>e93508</epage><pages>e93508-e93508</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Recent studies have shown that nicotine, a major component of cigarette smoke, can stimulate the proliferation of non-neuronal cells. Cigarette smoking can promote a variety of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease (COPD), atherosclerosis, and cancer. A predominant feature of COPD is airway remodeling, which includes increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodeling in COPD have not yet been fully elucidated. Here, we show that nicotine induces a profound and time-dependent increase in DNA synthesis in rat airway smooth muscle cells (RASMCs) in vitro. Nicotine also significantly increased the number of RASMCs, which was associated with the increased expression of Cyclin D1, phosphorylation of the retinoblastoma protein (RB) and was dependent on the activation of Akt. The activation of Akt by nicotine occurred within minutes and depended upon the nicotinic acetylcholine receptors (nAchRs). Activated Akt increased the phosphorylation of downstream substrates such as GSK3β. Our data suggest that the binding of nicotine to the nAchRs on RASMCs can regulate cellular proliferation by activating the Akt pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24690900</pmid><doi>10.1371/journal.pone.0093508</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acetylcholine receptors (nicotinic) Activation AKT protein Angiogenesis Animals Apoptosis Arteriosclerosis Atherosclerosis Biology and life sciences Cancer Cardiovascular diseases Care and treatment Cell cycle Cell growth Cell proliferation Cell Proliferation - drug effects Cells, Cultured Chronic obstructive pulmonary disease Cigarette smoke Cigarette smoking Cigarettes Cyclin D1 Cyclin D1 - metabolism Deoxyribonucleic acid Diagnosis Disease DNA DNA biosynthesis Epidermal growth factor Health aspects Heart diseases Hospitals Kinases Laboratory animals Lung cancer Lung diseases Lung diseases, Obstructive Medical research Medicine and Health Sciences Muscles Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism Nicotine Nicotine - pharmacology Obstructive lung disease Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Pulmonary arteries Rats Receptors Receptors, Nicotinic - metabolism Respiratory diseases Respiratory tract Retina Retinoblastoma Retinoblastoma protein Retinoblastoma Protein - metabolism Risk factors Rodents Signal Transduction - drug effects Smoke Smoking Smooth muscle Stem cells Substrates Trachea - cytology |
| title | The pro-proliferative effects of nicotine and its underlying mechanism on rat airway smooth muscle cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T04%3A21%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20pro-proliferative%20effects%20of%20nicotine%20and%20its%20underlying%20mechanism%20on%20rat%20airway%20smooth%20muscle%20cells&rft.jtitle=PloS%20one&rft.au=He,%20Fang&rft.date=2014-04-01&rft.volume=9&rft.issue=4&rft.spage=e93508&rft.epage=e93508&rft.pages=e93508-e93508&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0093508&rft_dat=%3Cgale_plos_%3EA375582828%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1511847532&rft_id=info:pmid/24690900&rft_galeid=A375582828&rft_doaj_id=oai_doaj_org_article_f5253a7aae7e48459b7dba2961ccb7bd&rfr_iscdi=true |