Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats
Background: Maternal nicotine exposure increases lung collagen in fetal and newborn animals. Connective tissue growth factor (CTGF) plays a role in hyperoxia-induced pulmonary fibrosis. Objective: To determine whether pre- and postnatal nicotine exposure can augment CTGF expression and postnatal hyp...
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| Veröffentlicht in: | Neonatology (Basel, Switzerland) Switzerland), 2014-01, Vol.106 (2), p.94-101 |
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| creator | Huang, Liang-Ti Chou, Hsiu-Chu Lin, Chun-Mao Yeh, Tsu-Fu Chen, Chung-Ming |
| description | Background: Maternal nicotine exposure increases lung collagen in fetal and newborn animals. Connective tissue growth factor (CTGF) plays a role in hyperoxia-induced pulmonary fibrosis. Objective: To determine whether pre- and postnatal nicotine exposure can augment CTGF expression and postnatal hyperoxia-induced lung fibrosis. Methods: Nicotine was administered to pregnant Sprague-Dawley rats at a dose of 6 mg/kg/day from gestational days 7-21 (prenatal nicotine-treated group) and gestational day 7 to postnatal day 14 (pre- and postnatal nicotine-treated group). A control group of pregnant dams was injected with an equal volume of saline. Within 12 h of birth, rats were exposed to room air or 1 week of >95% O 2 and an additional 2 weeks of 60% O 2 (3 weeks of hyperoxia). Lungs were taken for total collagen, CTGF expression and histological analyses. Results: In each maternal treatment group, the rats reared in hyperoxia had a higher total collagen compared with rats reared in room air on postnatal days 7 and 21. Collagen content was significantly higher in rats born to pre- and postnatal nicotine-treated dams than rats born to saline-treated and prenatal nicotine-treated dams on postnatal days 7 and 21. Pre- and postnatal nicotine exposure and neonatal hyperoxia exposure increased CTGF expression on postnatal days 7 and 21. Conclusions: CTGF may be involved in the pathogenesis of lung fibrosis induced by maternal nicotine and neonatal hyperoxia, and maternal nicotine exposure exacerbates neonatal hyperoxia-induced lung fibrosis. These results are relevant to neonates who require supplemental oxygen and are exposed to the breast milk of smoking mothers during infancy. |
| doi_str_mv | 10.1159/000362153 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmed_primary_24851831</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1553320052</sourcerecordid><originalsourceid>FETCH-LOGICAL-c334t-ab24e72c6007ed48432e72dd1200c9b8f6dd8f8c5a45b0816ac33ef687425c943</originalsourceid><addsrcrecordid>eNpd0M9LwzAUB_AgipvTg3eRghc9VPOzzY4yNjeYE0TxWNIkHZldU5MWtv_elM0ePOUFPu_7eA-AawQfEWLjJwghSTBi5AQMUZKgOOVofNrXEA7AhfcbCBljCT4HA0w5Q5ygIfh6FY12lSijlZG2MZWOprva-tZ1hZDa5QH4aKVtJZrA5vtaO7szIl5UqpVaRcu2WkczkzvrjY9MFb2Lxl-Cs0KUXl8d3xH4nE0_JvN4-faymDwvY0kIbWKRY6pTLBMIU60opwSHr1IIQyjHOS8SpXjBJROU5ZCjRIQ-XSQ8pZjJMSUjcH_IrZ39abVvsq3xUpelqLRtfYYYIySEMRzo3T-6sW23elApCbMpTLvAh4OSYR_vdJHVzmyF22cIZt21s_7awd4eE9t8q1Uv_84bwM0BfAu31q4Hx_5fldGBSA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1734844074</pqid></control><display><type>article</type><title>Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats</title><source>Karger电子期刊和电子书数据库</source><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Huang, Liang-Ti ; Chou, Hsiu-Chu ; Lin, Chun-Mao ; Yeh, Tsu-Fu ; Chen, Chung-Ming</creator><creatorcontrib>Huang, Liang-Ti ; Chou, Hsiu-Chu ; Lin, Chun-Mao ; Yeh, Tsu-Fu ; Chen, Chung-Ming</creatorcontrib><description>Background: Maternal nicotine exposure increases lung collagen in fetal and newborn animals. Connective tissue growth factor (CTGF) plays a role in hyperoxia-induced pulmonary fibrosis. Objective: To determine whether pre- and postnatal nicotine exposure can augment CTGF expression and postnatal hyperoxia-induced lung fibrosis. Methods: Nicotine was administered to pregnant Sprague-Dawley rats at a dose of 6 mg/kg/day from gestational days 7-21 (prenatal nicotine-treated group) and gestational day 7 to postnatal day 14 (pre- and postnatal nicotine-treated group). A control group of pregnant dams was injected with an equal volume of saline. Within 12 h of birth, rats were exposed to room air or 1 week of >95% O 2 and an additional 2 weeks of 60% O 2 (3 weeks of hyperoxia). Lungs were taken for total collagen, CTGF expression and histological analyses. Results: In each maternal treatment group, the rats reared in hyperoxia had a higher total collagen compared with rats reared in room air on postnatal days 7 and 21. Collagen content was significantly higher in rats born to pre- and postnatal nicotine-treated dams than rats born to saline-treated and prenatal nicotine-treated dams on postnatal days 7 and 21. Pre- and postnatal nicotine exposure and neonatal hyperoxia exposure increased CTGF expression on postnatal days 7 and 21. Conclusions: CTGF may be involved in the pathogenesis of lung fibrosis induced by maternal nicotine and neonatal hyperoxia, and maternal nicotine exposure exacerbates neonatal hyperoxia-induced lung fibrosis. These results are relevant to neonates who require supplemental oxygen and are exposed to the breast milk of smoking mothers during infancy.</description><identifier>ISSN: 1661-7800</identifier><identifier>EISSN: 1661-7819</identifier><identifier>DOI: 10.1159/000362153</identifier><identifier>PMID: 24851831</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Animals, Newborn ; Collagen - metabolism ; Connective Tissue Growth Factor - genetics ; Connective Tissue Growth Factor - metabolism ; Disease Models, Animal ; Female ; Gestational Age ; Hyperoxia - complications ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Maternal Exposure - adverse effects ; Nicotine - administration & dosage ; Nicotine - toxicity ; Nicotinic Agonists - administration & dosage ; Nicotinic Agonists - toxicity ; Original Paper ; Pregnancy ; Prenatal Exposure Delayed Effects ; Pulmonary Fibrosis - chemically induced ; Pulmonary Fibrosis - etiology ; Pulmonary Fibrosis - genetics ; Pulmonary Fibrosis - metabolism ; Pulmonary Fibrosis - pathology ; Rats, Sprague-Dawley ; Risk Factors ; Time Factors</subject><ispartof>Neonatology (Basel, Switzerland), 2014-01, Vol.106 (2), p.94-101</ispartof><rights>2014 S. Karger AG, Basel</rights><rights>2014 S. Karger AG, Basel.</rights><rights>Copyright S. Karger AG Aug 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c334t-ab24e72c6007ed48432e72dd1200c9b8f6dd8f8c5a45b0816ac33ef687425c943</citedby><cites>FETCH-LOGICAL-c334t-ab24e72c6007ed48432e72dd1200c9b8f6dd8f8c5a45b0816ac33ef687425c943</cites><orcidid>0000-0002-9454-6842 ; 0000-0001-8762-8957</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24851831$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Liang-Ti</creatorcontrib><creatorcontrib>Chou, Hsiu-Chu</creatorcontrib><creatorcontrib>Lin, Chun-Mao</creatorcontrib><creatorcontrib>Yeh, Tsu-Fu</creatorcontrib><creatorcontrib>Chen, Chung-Ming</creatorcontrib><title>Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats</title><title>Neonatology (Basel, Switzerland)</title><addtitle>Neonatology</addtitle><description>Background: Maternal nicotine exposure increases lung collagen in fetal and newborn animals. Connective tissue growth factor (CTGF) plays a role in hyperoxia-induced pulmonary fibrosis. Objective: To determine whether pre- and postnatal nicotine exposure can augment CTGF expression and postnatal hyperoxia-induced lung fibrosis. Methods: Nicotine was administered to pregnant Sprague-Dawley rats at a dose of 6 mg/kg/day from gestational days 7-21 (prenatal nicotine-treated group) and gestational day 7 to postnatal day 14 (pre- and postnatal nicotine-treated group). A control group of pregnant dams was injected with an equal volume of saline. Within 12 h of birth, rats were exposed to room air or 1 week of >95% O 2 and an additional 2 weeks of 60% O 2 (3 weeks of hyperoxia). Lungs were taken for total collagen, CTGF expression and histological analyses. Results: In each maternal treatment group, the rats reared in hyperoxia had a higher total collagen compared with rats reared in room air on postnatal days 7 and 21. Collagen content was significantly higher in rats born to pre- and postnatal nicotine-treated dams than rats born to saline-treated and prenatal nicotine-treated dams on postnatal days 7 and 21. Pre- and postnatal nicotine exposure and neonatal hyperoxia exposure increased CTGF expression on postnatal days 7 and 21. Conclusions: CTGF may be involved in the pathogenesis of lung fibrosis induced by maternal nicotine and neonatal hyperoxia, and maternal nicotine exposure exacerbates neonatal hyperoxia-induced lung fibrosis. These results are relevant to neonates who require supplemental oxygen and are exposed to the breast milk of smoking mothers during infancy.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Collagen - metabolism</subject><subject>Connective Tissue Growth Factor - genetics</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Gestational Age</subject><subject>Hyperoxia - complications</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Maternal Exposure - adverse effects</subject><subject>Nicotine - administration & dosage</subject><subject>Nicotine - toxicity</subject><subject>Nicotinic Agonists - administration & dosage</subject><subject>Nicotinic Agonists - toxicity</subject><subject>Original Paper</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Pulmonary Fibrosis - chemically induced</subject><subject>Pulmonary Fibrosis - etiology</subject><subject>Pulmonary Fibrosis - genetics</subject><subject>Pulmonary Fibrosis - metabolism</subject><subject>Pulmonary Fibrosis - pathology</subject><subject>Rats, Sprague-Dawley</subject><subject>Risk Factors</subject><subject>Time Factors</subject><issn>1661-7800</issn><issn>1661-7819</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpd0M9LwzAUB_AgipvTg3eRghc9VPOzzY4yNjeYE0TxWNIkHZldU5MWtv_elM0ePOUFPu_7eA-AawQfEWLjJwghSTBi5AQMUZKgOOVofNrXEA7AhfcbCBljCT4HA0w5Q5ygIfh6FY12lSijlZG2MZWOprva-tZ1hZDa5QH4aKVtJZrA5vtaO7szIl5UqpVaRcu2WkczkzvrjY9MFb2Lxl-Cs0KUXl8d3xH4nE0_JvN4-faymDwvY0kIbWKRY6pTLBMIU60opwSHr1IIQyjHOS8SpXjBJROU5ZCjRIQ-XSQ8pZjJMSUjcH_IrZ39abVvsq3xUpelqLRtfYYYIySEMRzo3T-6sW23elApCbMpTLvAh4OSYR_vdJHVzmyF22cIZt21s_7awd4eE9t8q1Uv_84bwM0BfAu31q4Hx_5fldGBSA</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Huang, Liang-Ti</creator><creator>Chou, Hsiu-Chu</creator><creator>Lin, Chun-Mao</creator><creator>Yeh, Tsu-Fu</creator><creator>Chen, Chung-Ming</creator><general>S. Karger AG</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9454-6842</orcidid><orcidid>https://orcid.org/0000-0001-8762-8957</orcidid></search><sort><creationdate>20140101</creationdate><title>Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats</title><author>Huang, Liang-Ti ; Chou, Hsiu-Chu ; Lin, Chun-Mao ; Yeh, Tsu-Fu ; Chen, Chung-Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c334t-ab24e72c6007ed48432e72dd1200c9b8f6dd8f8c5a45b0816ac33ef687425c943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Collagen - metabolism</topic><topic>Connective Tissue Growth Factor - genetics</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Gestational Age</topic><topic>Hyperoxia - complications</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Maternal Exposure - adverse effects</topic><topic>Nicotine - administration & dosage</topic><topic>Nicotine - toxicity</topic><topic>Nicotinic Agonists - administration & dosage</topic><topic>Nicotinic Agonists - toxicity</topic><topic>Original Paper</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects</topic><topic>Pulmonary Fibrosis - chemically induced</topic><topic>Pulmonary Fibrosis - etiology</topic><topic>Pulmonary Fibrosis - genetics</topic><topic>Pulmonary Fibrosis - metabolism</topic><topic>Pulmonary Fibrosis - pathology</topic><topic>Rats, Sprague-Dawley</topic><topic>Risk Factors</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Liang-Ti</creatorcontrib><creatorcontrib>Chou, Hsiu-Chu</creatorcontrib><creatorcontrib>Lin, Chun-Mao</creatorcontrib><creatorcontrib>Yeh, Tsu-Fu</creatorcontrib><creatorcontrib>Chen, Chung-Ming</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>ProQuest 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>Science 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Research Library</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Neonatology (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Liang-Ti</au><au>Chou, Hsiu-Chu</au><au>Lin, Chun-Mao</au><au>Yeh, Tsu-Fu</au><au>Chen, Chung-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats</atitle><jtitle>Neonatology (Basel, Switzerland)</jtitle><addtitle>Neonatology</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>106</volume><issue>2</issue><spage>94</spage><epage>101</epage><pages>94-101</pages><issn>1661-7800</issn><eissn>1661-7819</eissn><abstract>Background: Maternal nicotine exposure increases lung collagen in fetal and newborn animals. Connective tissue growth factor (CTGF) plays a role in hyperoxia-induced pulmonary fibrosis. Objective: To determine whether pre- and postnatal nicotine exposure can augment CTGF expression and postnatal hyperoxia-induced lung fibrosis. Methods: Nicotine was administered to pregnant Sprague-Dawley rats at a dose of 6 mg/kg/day from gestational days 7-21 (prenatal nicotine-treated group) and gestational day 7 to postnatal day 14 (pre- and postnatal nicotine-treated group). A control group of pregnant dams was injected with an equal volume of saline. Within 12 h of birth, rats were exposed to room air or 1 week of >95% O 2 and an additional 2 weeks of 60% O 2 (3 weeks of hyperoxia). Lungs were taken for total collagen, CTGF expression and histological analyses. Results: In each maternal treatment group, the rats reared in hyperoxia had a higher total collagen compared with rats reared in room air on postnatal days 7 and 21. Collagen content was significantly higher in rats born to pre- and postnatal nicotine-treated dams than rats born to saline-treated and prenatal nicotine-treated dams on postnatal days 7 and 21. Pre- and postnatal nicotine exposure and neonatal hyperoxia exposure increased CTGF expression on postnatal days 7 and 21. Conclusions: CTGF may be involved in the pathogenesis of lung fibrosis induced by maternal nicotine and neonatal hyperoxia, and maternal nicotine exposure exacerbates neonatal hyperoxia-induced lung fibrosis. These results are relevant to neonates who require supplemental oxygen and are exposed to the breast milk of smoking mothers during infancy.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>24851831</pmid><doi>10.1159/000362153</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-9454-6842</orcidid><orcidid>https://orcid.org/0000-0001-8762-8957</orcidid></addata></record> |
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| source | Karger电子期刊和电子书数据库; MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Animals, Newborn Collagen - metabolism Connective Tissue Growth Factor - genetics Connective Tissue Growth Factor - metabolism Disease Models, Animal Female Gestational Age Hyperoxia - complications Lung - drug effects Lung - metabolism Lung - pathology Maternal Exposure - adverse effects Nicotine - administration & dosage Nicotine - toxicity Nicotinic Agonists - administration & dosage Nicotinic Agonists - toxicity Original Paper Pregnancy Prenatal Exposure Delayed Effects Pulmonary Fibrosis - chemically induced Pulmonary Fibrosis - etiology Pulmonary Fibrosis - genetics Pulmonary Fibrosis - metabolism Pulmonary Fibrosis - pathology Rats, Sprague-Dawley Risk Factors Time Factors |
| title | Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats |
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