1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients
Reduced neutrophil apoptosis plays an important role in the pathogenesis of acute exacerbation chronic obstructive pulmonary disease (AECOPD). The p38 mitogen-activated protein kinase (MAPK) signaling pathway is involved in neutrophil apoptosis. 1α,25-Dihydroxyvitamin D3 (1α,25VitD3) can induce tumo...
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creator | Yang, Haihua Long, Feng Zhang, Youzhi Yu, Ronghuan Zhang, Peng Li, Wenjing Li, Shuijun Jin, Xianqiao Xia, Jingwen Dong, Liang Zhu, Ning Huang, Ying Gong, Yi Chen, Xiaodong |
description | Reduced neutrophil apoptosis plays an important role in the pathogenesis of acute exacerbation chronic obstructive pulmonary disease (AECOPD). The p38 mitogen-activated protein kinase (MAPK) signaling pathway is involved in neutrophil apoptosis. 1α,25-Dihydroxyvitamin D3 (1α,25VitD3) can induce tumor cell apoptosis. The aim of this study was to assess the effects of 1α,25VitD3 on peripheral blood neutrophil apoptosis in AECOPD and examine the role of the p38 MAPK signaling pathway.
The study enrolled 36 AECOPD patients and 36 healthy volunteers. Venous blood samples were obtained from both groups. Serum 25-hydroxyvitamin D (25-(OH) D) levels in peripheral venous blood were assayed using liquid chromatography-tandem mass spectrometry (LC-MS/MS); the neutrophils were separated and cultured with SB203580 (a p38 inhibitor) and 1α,25VitD3. Neutrophil apoptosis was measured using flow cytometry, and phospho-p38 MAPK protein expression was detected by Western blot. Statistical analysis was performed using analysis of variance. Student's t-test and Pearson's correlation coefficient were used for the between-group differences and correlation analysis, respectively.
The 25-(OH) D levels were lower in AECOPD patients than in healthy controls, and the peripheral blood neutrophil apoptosis results were similar. 1α,25VitD3 increased the apoptosis rate and the level of phospho-p38 MAPK in peripheral blood neutrophils of AECOPD patients. SB203580 partly inhibited 1α,25VitD3-induced peripheral blood neutrophil apoptosis and phospho-p38 MAPK overexpression. The 25-(OH) D levels were positively correlated with increased peripheral blood neutrophil apoptosis and phospho-p38 MAPK levels. In addition, expression of the phospho-p38 MAPK protein was also positively correlated with peripheral blood neutrophil apoptosis.
Our results suggest that 1α,25VitD3 induces peripheral blood neutrophil apoptosis through the p38 MAPK signaling pathway in AECOPD patients. |
doi_str_mv | 10.1371/journal.pone.0120515 |
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fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1675171959</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_28504654fb5340c0ab8a727a68ab39f7</doaj_id><sourcerecordid>1675876569</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4925-14d5a49fbbc9ab3405fbc2c6ab15be36562a84eea0af14500a2495c5cb318343</originalsourceid><addsrcrecordid>eNptksuO0zAYhSMEYi7wBggssWFBix3buWyQqpZLxcBUYvbWb8dJXKVxxk7K9C14FV6EZ8KhmdEMYmXLPuf4-60TRS8InhOakndbO7gWmnlnWz3HJMac8EfRKclpPEtiTB_f259EZ95vMeY0S5Kn0UnMc8wTyk-jn-T3r7cxn61MfSicvTnsTQ8706IVReu2GJT26Jseeme72jRo0dmut9541NfODlUdVo06mqGvi80X9N1UAcm0FdpAX_-AAwpJy6BsjUKX0vduUL3Za7QZmp1twR3QyngNXo8Go9veP4uelNB4_Xxaz6Orjx-ulp9nF5ef1svFxUyxPPASVnBgeSmlykFShnkpVawSkIRLTROexJAxrQFDSRjHGGKWc8WVpCSjjJ5Hr46xXWO9mP7SC5KknKQk53lQrI-KwsJWdM7sAq6wYMTfA-sqAa43qtEizjhmCWel5IFEYZAZpHEKSRbQ8jINWe-n1wa504UKgzpoHoQ-vGlNLSq7F4zhNMvGgDdTgLPXg_a92BmvdNNAq-1w5M7SMPXI_fof6f-nY0eVctZ7p8s7GILF2K9blxj7JaZ-BdvL-4PcmW4LRf8A86XQTA</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1675171959</pqid></control><display><type>article</type><title>1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>Public Library of Science (PLoS)</source><creator>Yang, Haihua ; Long, Feng ; Zhang, Youzhi ; Yu, Ronghuan ; Zhang, Peng ; Li, Wenjing ; Li, Shuijun ; Jin, Xianqiao ; Xia, Jingwen ; Dong, Liang ; Zhu, Ning ; Huang, Ying ; Gong, Yi ; Chen, Xiaodong</creator><creatorcontrib>Yang, Haihua ; Long, Feng ; Zhang, Youzhi ; Yu, Ronghuan ; Zhang, Peng ; Li, Wenjing ; Li, Shuijun ; Jin, Xianqiao ; Xia, Jingwen ; Dong, Liang ; Zhu, Ning ; Huang, Ying ; Gong, Yi ; Chen, Xiaodong</creatorcontrib><description>Reduced neutrophil apoptosis plays an important role in the pathogenesis of acute exacerbation chronic obstructive pulmonary disease (AECOPD). The p38 mitogen-activated protein kinase (MAPK) signaling pathway is involved in neutrophil apoptosis. 1α,25-Dihydroxyvitamin D3 (1α,25VitD3) can induce tumor cell apoptosis. The aim of this study was to assess the effects of 1α,25VitD3 on peripheral blood neutrophil apoptosis in AECOPD and examine the role of the p38 MAPK signaling pathway.
The study enrolled 36 AECOPD patients and 36 healthy volunteers. Venous blood samples were obtained from both groups. Serum 25-hydroxyvitamin D (25-(OH) D) levels in peripheral venous blood were assayed using liquid chromatography-tandem mass spectrometry (LC-MS/MS); the neutrophils were separated and cultured with SB203580 (a p38 inhibitor) and 1α,25VitD3. Neutrophil apoptosis was measured using flow cytometry, and phospho-p38 MAPK protein expression was detected by Western blot. Statistical analysis was performed using analysis of variance. Student's t-test and Pearson's correlation coefficient were used for the between-group differences and correlation analysis, respectively.
The 25-(OH) D levels were lower in AECOPD patients than in healthy controls, and the peripheral blood neutrophil apoptosis results were similar. 1α,25VitD3 increased the apoptosis rate and the level of phospho-p38 MAPK in peripheral blood neutrophils of AECOPD patients. SB203580 partly inhibited 1α,25VitD3-induced peripheral blood neutrophil apoptosis and phospho-p38 MAPK overexpression. The 25-(OH) D levels were positively correlated with increased peripheral blood neutrophil apoptosis and phospho-p38 MAPK levels. In addition, expression of the phospho-p38 MAPK protein was also positively correlated with peripheral blood neutrophil apoptosis.
Our results suggest that 1α,25VitD3 induces peripheral blood neutrophil apoptosis through the p38 MAPK signaling pathway in AECOPD patients.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0120515</identifier><identifier>PMID: 25905635</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>25-Hydroxyvitamin D ; Aged ; Apoptosis ; Apoptosis - drug effects ; Blood ; Case-Control Studies ; Chromatography ; Chronic obstructive pulmonary disease ; Correlation ; Correlation analysis ; Correlation coefficient ; Correlation coefficients ; Dihydroxyvitamin D3 ; Female ; Flow cytometry ; Flow mapping ; Humans ; Imidazoles - therapeutic use ; Kinases ; Leukocytes (neutrophilic) ; Liquid chromatography ; Lung diseases ; Male ; MAP kinase ; Mass spectrometry ; Mass spectroscopy ; Neutrophils - drug effects ; Neutrophils - metabolism ; Obstructive lung disease ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pathogenesis ; Patients ; Peripheral blood ; Phosphorylation - drug effects ; Protein kinase ; Proteins ; Pulmonary Disease, Chronic Obstructive - drug therapy ; Pulmonary Disease, Chronic Obstructive - metabolism ; Pyridines - therapeutic use ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Statistical analysis ; Statistical methods ; Studies ; Variance analysis ; Vitamin D ; Vitamin D - analogs & derivatives ; Vitamin D - therapeutic use ; Vitamin D3</subject><ispartof>PloS one, 2015-04, Vol.10 (4), p.e0120515-e0120515</ispartof><rights>2015 Yang 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>2015 Yang et al 2015 Yang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4925-14d5a49fbbc9ab3405fbc2c6ab15be36562a84eea0af14500a2495c5cb318343</citedby><cites>FETCH-LOGICAL-c4925-14d5a49fbbc9ab3405fbc2c6ab15be36562a84eea0af14500a2495c5cb318343</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/PMC4407887/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407887/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25905635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Haihua</creatorcontrib><creatorcontrib>Long, Feng</creatorcontrib><creatorcontrib>Zhang, Youzhi</creatorcontrib><creatorcontrib>Yu, Ronghuan</creatorcontrib><creatorcontrib>Zhang, Peng</creatorcontrib><creatorcontrib>Li, Wenjing</creatorcontrib><creatorcontrib>Li, Shuijun</creatorcontrib><creatorcontrib>Jin, Xianqiao</creatorcontrib><creatorcontrib>Xia, Jingwen</creatorcontrib><creatorcontrib>Dong, Liang</creatorcontrib><creatorcontrib>Zhu, Ning</creatorcontrib><creatorcontrib>Huang, Ying</creatorcontrib><creatorcontrib>Gong, Yi</creatorcontrib><creatorcontrib>Chen, Xiaodong</creatorcontrib><title>1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Reduced neutrophil apoptosis plays an important role in the pathogenesis of acute exacerbation chronic obstructive pulmonary disease (AECOPD). The p38 mitogen-activated protein kinase (MAPK) signaling pathway is involved in neutrophil apoptosis. 1α,25-Dihydroxyvitamin D3 (1α,25VitD3) can induce tumor cell apoptosis. The aim of this study was to assess the effects of 1α,25VitD3 on peripheral blood neutrophil apoptosis in AECOPD and examine the role of the p38 MAPK signaling pathway.
The study enrolled 36 AECOPD patients and 36 healthy volunteers. Venous blood samples were obtained from both groups. Serum 25-hydroxyvitamin D (25-(OH) D) levels in peripheral venous blood were assayed using liquid chromatography-tandem mass spectrometry (LC-MS/MS); the neutrophils were separated and cultured with SB203580 (a p38 inhibitor) and 1α,25VitD3. Neutrophil apoptosis was measured using flow cytometry, and phospho-p38 MAPK protein expression was detected by Western blot. Statistical analysis was performed using analysis of variance. Student's t-test and Pearson's correlation coefficient were used for the between-group differences and correlation analysis, respectively.
The 25-(OH) D levels were lower in AECOPD patients than in healthy controls, and the peripheral blood neutrophil apoptosis results were similar. 1α,25VitD3 increased the apoptosis rate and the level of phospho-p38 MAPK in peripheral blood neutrophils of AECOPD patients. SB203580 partly inhibited 1α,25VitD3-induced peripheral blood neutrophil apoptosis and phospho-p38 MAPK overexpression. The 25-(OH) D levels were positively correlated with increased peripheral blood neutrophil apoptosis and phospho-p38 MAPK levels. In addition, expression of the phospho-p38 MAPK protein was also positively correlated with peripheral blood neutrophil apoptosis.
Our results suggest that 1α,25VitD3 induces peripheral blood neutrophil apoptosis through the p38 MAPK signaling pathway in AECOPD patients.</description><subject>25-Hydroxyvitamin D</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Blood</subject><subject>Case-Control Studies</subject><subject>Chromatography</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Correlation</subject><subject>Correlation analysis</subject><subject>Correlation coefficient</subject><subject>Correlation coefficients</subject><subject>Dihydroxyvitamin D3</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Flow mapping</subject><subject>Humans</subject><subject>Imidazoles - therapeutic use</subject><subject>Kinases</subject><subject>Leukocytes (neutrophilic)</subject><subject>Liquid chromatography</subject><subject>Lung diseases</subject><subject>Male</subject><subject>MAP kinase</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - metabolism</subject><subject>Obstructive lung disease</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Peripheral blood</subject><subject>Phosphorylation - drug effects</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Pulmonary Disease, Chronic Obstructive - drug therapy</subject><subject>Pulmonary Disease, Chronic Obstructive - metabolism</subject><subject>Pyridines - therapeutic use</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Statistical analysis</subject><subject>Statistical methods</subject><subject>Studies</subject><subject>Variance analysis</subject><subject>Vitamin D</subject><subject>Vitamin D - analogs & derivatives</subject><subject>Vitamin D - therapeutic use</subject><subject>Vitamin D3</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptksuO0zAYhSMEYi7wBggssWFBix3buWyQqpZLxcBUYvbWb8dJXKVxxk7K9C14FV6EZ8KhmdEMYmXLPuf4-60TRS8InhOakndbO7gWmnlnWz3HJMac8EfRKclpPEtiTB_f259EZ95vMeY0S5Kn0UnMc8wTyk-jn-T3r7cxn61MfSicvTnsTQ8706IVReu2GJT26Jseeme72jRo0dmut9541NfODlUdVo06mqGvi80X9N1UAcm0FdpAX_-AAwpJy6BsjUKX0vduUL3Za7QZmp1twR3QyngNXo8Go9veP4uelNB4_Xxaz6Orjx-ulp9nF5ef1svFxUyxPPASVnBgeSmlykFShnkpVawSkIRLTROexJAxrQFDSRjHGGKWc8WVpCSjjJ5Hr46xXWO9mP7SC5KknKQk53lQrI-KwsJWdM7sAq6wYMTfA-sqAa43qtEizjhmCWel5IFEYZAZpHEKSRbQ8jINWe-n1wa504UKgzpoHoQ-vGlNLSq7F4zhNMvGgDdTgLPXg_a92BmvdNNAq-1w5M7SMPXI_fof6f-nY0eVctZ7p8s7GILF2K9blxj7JaZ-BdvL-4PcmW4LRf8A86XQTA</recordid><startdate>20150423</startdate><enddate>20150423</enddate><creator>Yang, Haihua</creator><creator>Long, Feng</creator><creator>Zhang, Youzhi</creator><creator>Yu, Ronghuan</creator><creator>Zhang, Peng</creator><creator>Li, Wenjing</creator><creator>Li, Shuijun</creator><creator>Jin, Xianqiao</creator><creator>Xia, Jingwen</creator><creator>Dong, Liang</creator><creator>Zhu, Ning</creator><creator>Huang, Ying</creator><creator>Gong, Yi</creator><creator>Chen, Xiaodong</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150423</creationdate><title>1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients</title><author>Yang, Haihua ; Long, Feng ; Zhang, Youzhi ; Yu, Ronghuan ; Zhang, Peng ; Li, Wenjing ; Li, Shuijun ; Jin, Xianqiao ; Xia, Jingwen ; Dong, Liang ; Zhu, Ning ; Huang, Ying ; Gong, Yi ; Chen, Xiaodong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4925-14d5a49fbbc9ab3405fbc2c6ab15be36562a84eea0af14500a2495c5cb318343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>25-Hydroxyvitamin D</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Blood</topic><topic>Case-Control Studies</topic><topic>Chromatography</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Correlation</topic><topic>Correlation analysis</topic><topic>Correlation coefficient</topic><topic>Correlation coefficients</topic><topic>Dihydroxyvitamin D3</topic><topic>Female</topic><topic>Flow cytometry</topic><topic>Flow mapping</topic><topic>Humans</topic><topic>Imidazoles - therapeutic use</topic><topic>Kinases</topic><topic>Leukocytes (neutrophilic)</topic><topic>Liquid chromatography</topic><topic>Lung diseases</topic><topic>Male</topic><topic>MAP kinase</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - metabolism</topic><topic>Obstructive lung disease</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Peripheral blood</topic><topic>Phosphorylation - drug effects</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Pulmonary Disease, Chronic Obstructive - drug therapy</topic><topic>Pulmonary Disease, Chronic Obstructive - metabolism</topic><topic>Pyridines - therapeutic use</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Statistical analysis</topic><topic>Statistical methods</topic><topic>Studies</topic><topic>Variance analysis</topic><topic>Vitamin D</topic><topic>Vitamin D - analogs & derivatives</topic><topic>Vitamin D - therapeutic use</topic><topic>Vitamin D3</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Haihua</creatorcontrib><creatorcontrib>Long, Feng</creatorcontrib><creatorcontrib>Zhang, Youzhi</creatorcontrib><creatorcontrib>Yu, Ronghuan</creatorcontrib><creatorcontrib>Zhang, Peng</creatorcontrib><creatorcontrib>Li, Wenjing</creatorcontrib><creatorcontrib>Li, Shuijun</creatorcontrib><creatorcontrib>Jin, Xianqiao</creatorcontrib><creatorcontrib>Xia, Jingwen</creatorcontrib><creatorcontrib>Dong, Liang</creatorcontrib><creatorcontrib>Zhu, Ning</creatorcontrib><creatorcontrib>Huang, Ying</creatorcontrib><creatorcontrib>Gong, Yi</creatorcontrib><creatorcontrib>Chen, Xiaodong</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Haihua</au><au>Long, Feng</au><au>Zhang, Youzhi</au><au>Yu, Ronghuan</au><au>Zhang, Peng</au><au>Li, Wenjing</au><au>Li, Shuijun</au><au>Jin, Xianqiao</au><au>Xia, Jingwen</au><au>Dong, Liang</au><au>Zhu, Ning</au><au>Huang, Ying</au><au>Gong, Yi</au><au>Chen, Xiaodong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-04-23</date><risdate>2015</risdate><volume>10</volume><issue>4</issue><spage>e0120515</spage><epage>e0120515</epage><pages>e0120515-e0120515</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Reduced neutrophil apoptosis plays an important role in the pathogenesis of acute exacerbation chronic obstructive pulmonary disease (AECOPD). The p38 mitogen-activated protein kinase (MAPK) signaling pathway is involved in neutrophil apoptosis. 1α,25-Dihydroxyvitamin D3 (1α,25VitD3) can induce tumor cell apoptosis. The aim of this study was to assess the effects of 1α,25VitD3 on peripheral blood neutrophil apoptosis in AECOPD and examine the role of the p38 MAPK signaling pathway.
The study enrolled 36 AECOPD patients and 36 healthy volunteers. Venous blood samples were obtained from both groups. Serum 25-hydroxyvitamin D (25-(OH) D) levels in peripheral venous blood were assayed using liquid chromatography-tandem mass spectrometry (LC-MS/MS); the neutrophils were separated and cultured with SB203580 (a p38 inhibitor) and 1α,25VitD3. Neutrophil apoptosis was measured using flow cytometry, and phospho-p38 MAPK protein expression was detected by Western blot. Statistical analysis was performed using analysis of variance. Student's t-test and Pearson's correlation coefficient were used for the between-group differences and correlation analysis, respectively.
The 25-(OH) D levels were lower in AECOPD patients than in healthy controls, and the peripheral blood neutrophil apoptosis results were similar. 1α,25VitD3 increased the apoptosis rate and the level of phospho-p38 MAPK in peripheral blood neutrophils of AECOPD patients. SB203580 partly inhibited 1α,25VitD3-induced peripheral blood neutrophil apoptosis and phospho-p38 MAPK overexpression. The 25-(OH) D levels were positively correlated with increased peripheral blood neutrophil apoptosis and phospho-p38 MAPK levels. In addition, expression of the phospho-p38 MAPK protein was also positively correlated with peripheral blood neutrophil apoptosis.
Our results suggest that 1α,25VitD3 induces peripheral blood neutrophil apoptosis through the p38 MAPK signaling pathway in AECOPD patients.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25905635</pmid><doi>10.1371/journal.pone.0120515</doi><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2015-04, Vol.10 (4), p.e0120515-e0120515 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1675171959 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
subjects | 25-Hydroxyvitamin D Aged Apoptosis Apoptosis - drug effects Blood Case-Control Studies Chromatography Chronic obstructive pulmonary disease Correlation Correlation analysis Correlation coefficient Correlation coefficients Dihydroxyvitamin D3 Female Flow cytometry Flow mapping Humans Imidazoles - therapeutic use Kinases Leukocytes (neutrophilic) Liquid chromatography Lung diseases Male MAP kinase Mass spectrometry Mass spectroscopy Neutrophils - drug effects Neutrophils - metabolism Obstructive lung disease p38 Mitogen-Activated Protein Kinases - metabolism Pathogenesis Patients Peripheral blood Phosphorylation - drug effects Protein kinase Proteins Pulmonary Disease, Chronic Obstructive - drug therapy Pulmonary Disease, Chronic Obstructive - metabolism Pyridines - therapeutic use Signal transduction Signal Transduction - drug effects Signaling Statistical analysis Statistical methods Studies Variance analysis Vitamin D Vitamin D - analogs & derivatives Vitamin D - therapeutic use Vitamin D3 |
title | 1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients |
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