Nicotine induces upregulated expression of beta defensin-2 via the p38MAPK pathway in the HaCaT human keratinocyte cell line
Human beta-defensins (hBDs), a group of antimicrobial peptides, are involved in the protective barrier of the oral epithelium. Nicotine induces periodontal and oral epithelial diseases. The purpose of the present study was to investigate the effect of nicotine on the expression pattern of hBD-2 in k...
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| Veröffentlicht in: | Medical molecular morphology 2010-12, Vol.43 (4), p.204-210 |
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| creator | Nakamura, Sumiko Saitoh, Masato Yamazaki, Mami Nishimura, Michiko Kurashige, Yoshihito Arakawa, Toshiya Takuma, Taishin Kaku, Tohru Abiko, Yoshihiro |
| description | Human beta-defensins (hBDs), a group of antimicrobial peptides, are involved in the protective barrier of the oral epithelium. Nicotine induces periodontal and oral epithelial diseases. The purpose of the present study was to investigate the effect of nicotine on the expression pattern of hBD-2 in keratinocytes. HaCaT cells, a keratinocyte cell line, were incubated with 8, 15, 30, or 80 μM nicotine for 24 h. Expression of hBD-2 was observed by RT-PCR, qRTPCR, and ELISA assay. The cells were treated with inhibitors for intracellular pathways (p38MAP kinase, NF-κB, JNK, MAPK-ERK) and with nicotinic acetylcholine receptor (nAChR) inhibitors in a series of experiments. Data were analyzed using Student’s
t
test. qRT-PCR revealed that the expression level of hBD-2 mRNA was significantly higher at 30 and 80 μM nicotine than the control without nicotine (
P
< 0.05). The 80 μM cell extraction contained significantly higher hBD-2 peptide levels than the control (
P
< 0.05). The p38MAP kinase inhibitor abolished the upregulated expression of hBD-2 by nicotine. Both nAChR inhibitors also abolished the upregulation of hBD-2 by nicotine. The present study demonstrated that nicotine causes upregulated expression of hBD-2 via the p38MAP kinase pathway in keratinocytes. |
| doi_str_mv | 10.1007/s00795-010-0493-4 |
| format | Article |
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t
test. qRT-PCR revealed that the expression level of hBD-2 mRNA was significantly higher at 30 and 80 μM nicotine than the control without nicotine (
P
< 0.05). The 80 μM cell extraction contained significantly higher hBD-2 peptide levels than the control (
P
< 0.05). The p38MAP kinase inhibitor abolished the upregulated expression of hBD-2 by nicotine. Both nAChR inhibitors also abolished the upregulation of hBD-2 by nicotine. The present study demonstrated that nicotine causes upregulated expression of hBD-2 via the p38MAP kinase pathway in keratinocytes.</description><identifier>ISSN: 1860-1480</identifier><identifier>EISSN: 1860-1499</identifier><identifier>DOI: 10.1007/s00795-010-0493-4</identifier><identifier>PMID: 21267696</identifier><identifier>CODEN: MELMEJ</identifier><language>eng</language><publisher>Japan: Springer Japan</publisher><subject>Anatomy ; Antimicrobial agents ; beta-Defensins - biosynthesis ; beta-Defensins - genetics ; beta-Defensins - metabolism ; Cell Line ; Enzyme Inhibitors - pharmacology ; Epithelial Cells ; Gene expression ; Humans ; Intracellular Signaling Peptides and Proteins - antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Keratinocytes - drug effects ; Keratinocytes - metabolism ; Medicine ; Medicine & Public Health ; Molecular Medicine ; Nicotine ; Nicotine - pharmacology ; Nicotinic Antagonists - pharmacology ; Original Paper ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - genetics ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pathology ; Peptides ; Receptors, Nicotinic - drug effects ; Receptors, Nicotinic - genetics ; Receptors, Nicotinic - metabolism ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; Tubocurarine - pharmacology ; Up-Regulation - genetics</subject><ispartof>Medical molecular morphology, 2010-12, Vol.43 (4), p.204-210</ispartof><rights>The Japanese Society for Clinical Molecular Morphology 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-578bb57a39892a9eddf316dbe4ebb6066ed14ef45c20992ef6a2073c133b80d73</citedby><cites>FETCH-LOGICAL-c399t-578bb57a39892a9eddf316dbe4ebb6066ed14ef45c20992ef6a2073c133b80d73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00795-010-0493-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00795-010-0493-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21267696$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakamura, Sumiko</creatorcontrib><creatorcontrib>Saitoh, Masato</creatorcontrib><creatorcontrib>Yamazaki, Mami</creatorcontrib><creatorcontrib>Nishimura, Michiko</creatorcontrib><creatorcontrib>Kurashige, Yoshihito</creatorcontrib><creatorcontrib>Arakawa, Toshiya</creatorcontrib><creatorcontrib>Takuma, Taishin</creatorcontrib><creatorcontrib>Kaku, Tohru</creatorcontrib><creatorcontrib>Abiko, Yoshihiro</creatorcontrib><title>Nicotine induces upregulated expression of beta defensin-2 via the p38MAPK pathway in the HaCaT human keratinocyte cell line</title><title>Medical molecular morphology</title><addtitle>Med Mol Morphol</addtitle><addtitle>Med Mol Morphol</addtitle><description>Human beta-defensins (hBDs), a group of antimicrobial peptides, are involved in the protective barrier of the oral epithelium. Nicotine induces periodontal and oral epithelial diseases. The purpose of the present study was to investigate the effect of nicotine on the expression pattern of hBD-2 in keratinocytes. HaCaT cells, a keratinocyte cell line, were incubated with 8, 15, 30, or 80 μM nicotine for 24 h. Expression of hBD-2 was observed by RT-PCR, qRTPCR, and ELISA assay. The cells were treated with inhibitors for intracellular pathways (p38MAP kinase, NF-κB, JNK, MAPK-ERK) and with nicotinic acetylcholine receptor (nAChR) inhibitors in a series of experiments. Data were analyzed using Student’s
t
test. qRT-PCR revealed that the expression level of hBD-2 mRNA was significantly higher at 30 and 80 μM nicotine than the control without nicotine (
P
< 0.05). The 80 μM cell extraction contained significantly higher hBD-2 peptide levels than the control (
P
< 0.05). The p38MAP kinase inhibitor abolished the upregulated expression of hBD-2 by nicotine. Both nAChR inhibitors also abolished the upregulation of hBD-2 by nicotine. The present study demonstrated that nicotine causes upregulated expression of hBD-2 via the p38MAP kinase pathway in keratinocytes.</description><subject>Anatomy</subject><subject>Antimicrobial agents</subject><subject>beta-Defensins - biosynthesis</subject><subject>beta-Defensins - genetics</subject><subject>beta-Defensins - metabolism</subject><subject>Cell Line</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Epithelial Cells</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - antagonists & inhibitors</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular Medicine</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Antagonists - pharmacology</subject><subject>Original Paper</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - genetics</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pathology</subject><subject>Peptides</subject><subject>Receptors, Nicotinic - drug effects</subject><subject>Receptors, Nicotinic - genetics</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Tubocurarine - pharmacology</subject><subject>Up-Regulation - genetics</subject><issn>1860-1480</issn><issn>1860-1499</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kUtP3TAQhS1UBJTyA7qprG5YBcaPOPESXfGoeLQLWFtOPOGG5jqpnQBX6o-v0wtUqsTGY3u-OWekQ8hnBkcMoDiO6dB5BgwykFpkcovssVJBxqTWH97uJeySjzE-AIhC8XyH7HLGVaG02iO_b9q6H1uPtPVuqjHSaQh4P3V2REfxOT1ibHtP-4ZWOFrqsEEfW59x-thaOi6RDqK8PvlxSQc7Lp_sOin9_b6wC3tLl9PKevoTg00ufb0ekdbYdbRLnp_IdmO7iAcvdZ_cnZ3eLi6yq-_n3xYnV1kttB6zvCirKi-s0KXmVqNzjWDKVSixqhQohY5JbGRec9CaY6Msh0LUTIiqBFeIfXK40R1C_2vCOJpVG-ctrMd-iqaURa5zVkIiv_5HPvRT8Gm5GeKagZzl2AaqQx9jwMYMoV3ZsDYMzByM2QRjUjBmDsbINPPlRXiqVujeJl6TSADfADG1_D2Gf87vq_4B7EGYtQ</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>Nakamura, Sumiko</creator><creator>Saitoh, Masato</creator><creator>Yamazaki, Mami</creator><creator>Nishimura, Michiko</creator><creator>Kurashige, Yoshihito</creator><creator>Arakawa, Toshiya</creator><creator>Takuma, Taishin</creator><creator>Kaku, Tohru</creator><creator>Abiko, Yoshihiro</creator><general>Springer Japan</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20101201</creationdate><title>Nicotine induces upregulated expression of beta defensin-2 via the p38MAPK pathway in the HaCaT human keratinocyte cell line</title><author>Nakamura, Sumiko ; Saitoh, Masato ; Yamazaki, Mami ; Nishimura, Michiko ; Kurashige, Yoshihito ; Arakawa, Toshiya ; Takuma, Taishin ; Kaku, Tohru ; Abiko, Yoshihiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-578bb57a39892a9eddf316dbe4ebb6066ed14ef45c20992ef6a2073c133b80d73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Anatomy</topic><topic>Antimicrobial agents</topic><topic>beta-Defensins - biosynthesis</topic><topic>beta-Defensins - genetics</topic><topic>beta-Defensins - metabolism</topic><topic>Cell Line</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Epithelial Cells</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - antagonists & inhibitors</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular Medicine</topic><topic>Nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Antagonists - pharmacology</topic><topic>Original Paper</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - genetics</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pathology</topic><topic>Peptides</topic><topic>Receptors, Nicotinic - drug effects</topic><topic>Receptors, Nicotinic - genetics</topic><topic>Receptors, Nicotinic - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>Tubocurarine - pharmacology</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakamura, Sumiko</creatorcontrib><creatorcontrib>Saitoh, Masato</creatorcontrib><creatorcontrib>Yamazaki, Mami</creatorcontrib><creatorcontrib>Nishimura, Michiko</creatorcontrib><creatorcontrib>Kurashige, Yoshihito</creatorcontrib><creatorcontrib>Arakawa, Toshiya</creatorcontrib><creatorcontrib>Takuma, Taishin</creatorcontrib><creatorcontrib>Kaku, Tohru</creatorcontrib><creatorcontrib>Abiko, Yoshihiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Medical molecular morphology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakamura, Sumiko</au><au>Saitoh, Masato</au><au>Yamazaki, Mami</au><au>Nishimura, Michiko</au><au>Kurashige, Yoshihito</au><au>Arakawa, Toshiya</au><au>Takuma, Taishin</au><au>Kaku, Tohru</au><au>Abiko, Yoshihiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nicotine induces upregulated expression of beta defensin-2 via the p38MAPK pathway in the HaCaT human keratinocyte cell line</atitle><jtitle>Medical molecular morphology</jtitle><stitle>Med Mol Morphol</stitle><addtitle>Med Mol Morphol</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>43</volume><issue>4</issue><spage>204</spage><epage>210</epage><pages>204-210</pages><issn>1860-1480</issn><eissn>1860-1499</eissn><coden>MELMEJ</coden><abstract>Human beta-defensins (hBDs), a group of antimicrobial peptides, are involved in the protective barrier of the oral epithelium. Nicotine induces periodontal and oral epithelial diseases. The purpose of the present study was to investigate the effect of nicotine on the expression pattern of hBD-2 in keratinocytes. HaCaT cells, a keratinocyte cell line, were incubated with 8, 15, 30, or 80 μM nicotine for 24 h. Expression of hBD-2 was observed by RT-PCR, qRTPCR, and ELISA assay. The cells were treated with inhibitors for intracellular pathways (p38MAP kinase, NF-κB, JNK, MAPK-ERK) and with nicotinic acetylcholine receptor (nAChR) inhibitors in a series of experiments. Data were analyzed using Student’s
t
test. qRT-PCR revealed that the expression level of hBD-2 mRNA was significantly higher at 30 and 80 μM nicotine than the control without nicotine (
P
< 0.05). The 80 μM cell extraction contained significantly higher hBD-2 peptide levels than the control (
P
< 0.05). The p38MAP kinase inhibitor abolished the upregulated expression of hBD-2 by nicotine. Both nAChR inhibitors also abolished the upregulation of hBD-2 by nicotine. The present study demonstrated that nicotine causes upregulated expression of hBD-2 via the p38MAP kinase pathway in keratinocytes.</abstract><cop>Japan</cop><pub>Springer Japan</pub><pmid>21267696</pmid><doi>10.1007/s00795-010-0493-4</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
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| subjects | Anatomy Antimicrobial agents beta-Defensins - biosynthesis beta-Defensins - genetics beta-Defensins - metabolism Cell Line Enzyme Inhibitors - pharmacology Epithelial Cells Gene expression Humans Intracellular Signaling Peptides and Proteins - antagonists & inhibitors Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Keratinocytes - drug effects Keratinocytes - metabolism Medicine Medicine & Public Health Molecular Medicine Nicotine Nicotine - pharmacology Nicotinic Antagonists - pharmacology Original Paper p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - genetics p38 Mitogen-Activated Protein Kinases - metabolism Pathology Peptides Receptors, Nicotinic - drug effects Receptors, Nicotinic - genetics Receptors, Nicotinic - metabolism Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - biosynthesis RNA, Messenger - genetics Tubocurarine - pharmacology Up-Regulation - genetics |
| title | Nicotine induces upregulated expression of beta defensin-2 via the p38MAPK pathway in the HaCaT human keratinocyte cell line |
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