Prenatal exposure to tobacco smoke sex dependently influences methylation and mRNA levels of the Igf axis in lungs of mouse offspring
Prenatal smoke exposure is a risk factor for abnormal lung development and increased sex-dependent susceptibility for asthma and chronic obstructive pulmonary disease (COPD). Birth cohort studies show genome-wide DNA methylation changes in children from smoking mothers, but evidence for sex-dependen...
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creator | Meyer, K F Krauss-Etschmann, S Kooistra, W Reinders-Luinge, M Timens, W Kobzik, L Plösch, T Hylkema, M N |
description | Prenatal smoke exposure is a risk factor for abnormal lung development and increased sex-dependent susceptibility for asthma and chronic obstructive pulmonary disease (COPD). Birth cohort studies show genome-wide DNA methylation changes in children from smoking mothers, but evidence for sex-dependent smoke-induced effects is limited. The insulin-like growth factor (IGF) system plays an important role in lung development. We hypothesized that prenatal exposure to smoke induces lasting changes in promoter methylation patterns of
and
, thus influencing transcriptional activity and contributing to abnormal lung development. We measured and compared mRNA levels along with promoter methylation of
and
and their protein concentrations in lung tissue of 30-day-old mice that had been prenatally exposed to cigarette smoke (PSE) or filtered air (control). Body weight at 30 days after birth was measured as global indicator of normal development. Female PSE mice showed lower mRNA levels of
and its receptor (
:
= 0.05;
:
= 0.03). Furthermore, CpG-site-specific methylation changes were detected in
in a sex-dependent manner and the body weight of female offspring was reduced after prenatal exposure to smoke, while protein concentrations were unaffected. Prenatal exposure to smoke induces a CpG-site-specific loss of
promoter methylation, which can be associated with body weight. These findings highlight the sex-dependent and potentially detrimental effects of in utero smoke exposure on DNA methylation and
and
mRNA levels. The observations support a role for
and
in abnormal development. |
doi_str_mv | 10.1152/ajplung.00271.2016 |
format | Article |
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and
, thus influencing transcriptional activity and contributing to abnormal lung development. We measured and compared mRNA levels along with promoter methylation of
and
and their protein concentrations in lung tissue of 30-day-old mice that had been prenatally exposed to cigarette smoke (PSE) or filtered air (control). Body weight at 30 days after birth was measured as global indicator of normal development. Female PSE mice showed lower mRNA levels of
and its receptor (
:
= 0.05;
:
= 0.03). Furthermore, CpG-site-specific methylation changes were detected in
in a sex-dependent manner and the body weight of female offspring was reduced after prenatal exposure to smoke, while protein concentrations were unaffected. Prenatal exposure to smoke induces a CpG-site-specific loss of
promoter methylation, which can be associated with body weight. These findings highlight the sex-dependent and potentially detrimental effects of in utero smoke exposure on DNA methylation and
and
mRNA levels. The observations support a role for
and
in abnormal development.</description><identifier>ISSN: 1040-0605</identifier><identifier>ISSN: 1522-1504</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.00271.2016</identifier><identifier>PMID: 28130259</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Animals, Newborn ; Body Weight ; Chronic obstructive pulmonary disease ; CpG Islands - genetics ; DNA methylation ; DNA Methylation - genetics ; Female ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - metabolism ; Lung - metabolism ; Male ; Mice, Inbred BALB C ; Pregnancy ; Prenatal Exposure Delayed Effects - metabolism ; Promoter Regions, Genetic ; Proteins ; Receptor, IGF Type 1 - genetics ; Receptor, IGF Type 1 - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Rodents ; Sex Characteristics ; Signal Transduction - genetics ; Smoking ; Smoking - adverse effects ; Tobacco Products ; Tobacco smoke</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2017-04, Vol.312 (4), p.L542-L555</ispartof><rights>Copyright © 2017 the American Physiological Society.</rights><rights>Copyright American Physiological Society Apr 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-bdffc63c2f8bb22774a35a143ef7746976c8836b7c3b94d7ef40a35f5e770a9b3</citedby><cites>FETCH-LOGICAL-c408t-bdffc63c2f8bb22774a35a143ef7746976c8836b7c3b94d7ef40a35f5e770a9b3</cites><orcidid>0000-0002-6732-8903</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3040,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28130259$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meyer, K F</creatorcontrib><creatorcontrib>Krauss-Etschmann, S</creatorcontrib><creatorcontrib>Kooistra, W</creatorcontrib><creatorcontrib>Reinders-Luinge, M</creatorcontrib><creatorcontrib>Timens, W</creatorcontrib><creatorcontrib>Kobzik, L</creatorcontrib><creatorcontrib>Plösch, T</creatorcontrib><creatorcontrib>Hylkema, M N</creatorcontrib><title>Prenatal exposure to tobacco smoke sex dependently influences methylation and mRNA levels of the Igf axis in lungs of mouse offspring</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>Prenatal smoke exposure is a risk factor for abnormal lung development and increased sex-dependent susceptibility for asthma and chronic obstructive pulmonary disease (COPD). Birth cohort studies show genome-wide DNA methylation changes in children from smoking mothers, but evidence for sex-dependent smoke-induced effects is limited. The insulin-like growth factor (IGF) system plays an important role in lung development. We hypothesized that prenatal exposure to smoke induces lasting changes in promoter methylation patterns of
and
, thus influencing transcriptional activity and contributing to abnormal lung development. We measured and compared mRNA levels along with promoter methylation of
and
and their protein concentrations in lung tissue of 30-day-old mice that had been prenatally exposed to cigarette smoke (PSE) or filtered air (control). Body weight at 30 days after birth was measured as global indicator of normal development. Female PSE mice showed lower mRNA levels of
and its receptor (
:
= 0.05;
:
= 0.03). Furthermore, CpG-site-specific methylation changes were detected in
in a sex-dependent manner and the body weight of female offspring was reduced after prenatal exposure to smoke, while protein concentrations were unaffected. Prenatal exposure to smoke induces a CpG-site-specific loss of
promoter methylation, which can be associated with body weight. These findings highlight the sex-dependent and potentially detrimental effects of in utero smoke exposure on DNA methylation and
and
mRNA levels. The observations support a role for
and
in abnormal development.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Body Weight</subject><subject>Chronic obstructive pulmonary disease</subject><subject>CpG Islands - genetics</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>Female</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Lung - metabolism</subject><subject>Male</subject><subject>Mice, Inbred BALB C</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>Receptor, IGF Type 1 - genetics</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Sex Characteristics</subject><subject>Signal Transduction - genetics</subject><subject>Smoking</subject><subject>Smoking - adverse effects</subject><subject>Tobacco Products</subject><subject>Tobacco smoke</subject><issn>1040-0605</issn><issn>1522-1504</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9O3DAQxq2KqvxpX6AHZIkLlyxjJ7GdI0IUkBBUiJ4jxxkv2Tp2GifV7gPw3nhhy6EnJEv-pPl9o5n5CPnOYMFYyc_0anCzXy4AuGQLDkx8IgepwDNWQrGXNBSQgYBynxzGuAKAEkB8IftcsRx4WR2Q558jej1pR3E9hDiPSKeQXqONCTT24TfSiGva4oC-RT-5De28dTN6g5H2OD1tnJ664Kn2Le0f7s6pw7_oIg2WTk9Ib5aW6nUXk41ux30t9GGOmISNw9j55Vfy2WoX8dvuPyK_flw-Xlxnt_dXNxfnt5kpQE1Z01prRG64VU3DuZSFzkvNihxt0qKSwiiVi0aavKmKVqItIBG2RClBV01-RE7f-g5j-DNjnOq-iwad0x7TRDVTFVNSKS4-gAou02kLmdCT_9BVmEefFkmUEkKlgFSi-BtlxhDjiLZOq_d63NQM6m2e9S7P-jXPeptnMh3vWs9Nj-275V-A-QsXTJ5i</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>Meyer, K F</creator><creator>Krauss-Etschmann, S</creator><creator>Kooistra, W</creator><creator>Reinders-Luinge, M</creator><creator>Timens, W</creator><creator>Kobzik, L</creator><creator>Plösch, T</creator><creator>Hylkema, M N</creator><general>American Physiological Society</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>7QP</scope><scope>7TS</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><scope>7TM</scope><orcidid>https://orcid.org/0000-0002-6732-8903</orcidid></search><sort><creationdate>20170401</creationdate><title>Prenatal exposure to tobacco smoke sex dependently influences methylation and mRNA levels of the Igf axis in lungs of mouse offspring</title><author>Meyer, K F ; Krauss-Etschmann, S ; Kooistra, W ; Reinders-Luinge, M ; Timens, W ; Kobzik, L ; Plösch, T ; Hylkema, M N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-bdffc63c2f8bb22774a35a143ef7746976c8836b7c3b94d7ef40a35f5e770a9b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Body Weight</topic><topic>Chronic obstructive pulmonary disease</topic><topic>CpG Islands - genetics</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>Female</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Lung - metabolism</topic><topic>Male</topic><topic>Mice, Inbred BALB C</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>Receptor, IGF Type 1 - genetics</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Sex Characteristics</topic><topic>Signal Transduction - genetics</topic><topic>Smoking</topic><topic>Smoking - adverse effects</topic><topic>Tobacco Products</topic><topic>Tobacco smoke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meyer, K F</creatorcontrib><creatorcontrib>Krauss-Etschmann, S</creatorcontrib><creatorcontrib>Kooistra, W</creatorcontrib><creatorcontrib>Reinders-Luinge, M</creatorcontrib><creatorcontrib>Timens, W</creatorcontrib><creatorcontrib>Kobzik, L</creatorcontrib><creatorcontrib>Plösch, T</creatorcontrib><creatorcontrib>Hylkema, M N</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>Nucleic Acids Abstracts</collection><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meyer, K F</au><au>Krauss-Etschmann, S</au><au>Kooistra, W</au><au>Reinders-Luinge, M</au><au>Timens, W</au><au>Kobzik, L</au><au>Plösch, T</au><au>Hylkema, M N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prenatal exposure to tobacco smoke sex dependently influences methylation and mRNA levels of the Igf axis in lungs of mouse offspring</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2017-04-01</date><risdate>2017</risdate><volume>312</volume><issue>4</issue><spage>L542</spage><epage>L555</epage><pages>L542-L555</pages><issn>1040-0605</issn><issn>1522-1504</issn><eissn>1522-1504</eissn><abstract>Prenatal smoke exposure is a risk factor for abnormal lung development and increased sex-dependent susceptibility for asthma and chronic obstructive pulmonary disease (COPD). Birth cohort studies show genome-wide DNA methylation changes in children from smoking mothers, but evidence for sex-dependent smoke-induced effects is limited. The insulin-like growth factor (IGF) system plays an important role in lung development. We hypothesized that prenatal exposure to smoke induces lasting changes in promoter methylation patterns of
and
, thus influencing transcriptional activity and contributing to abnormal lung development. We measured and compared mRNA levels along with promoter methylation of
and
and their protein concentrations in lung tissue of 30-day-old mice that had been prenatally exposed to cigarette smoke (PSE) or filtered air (control). Body weight at 30 days after birth was measured as global indicator of normal development. Female PSE mice showed lower mRNA levels of
and its receptor (
:
= 0.05;
:
= 0.03). Furthermore, CpG-site-specific methylation changes were detected in
in a sex-dependent manner and the body weight of female offspring was reduced after prenatal exposure to smoke, while protein concentrations were unaffected. Prenatal exposure to smoke induces a CpG-site-specific loss of
promoter methylation, which can be associated with body weight. These findings highlight the sex-dependent and potentially detrimental effects of in utero smoke exposure on DNA methylation and
and
mRNA levels. The observations support a role for
and
in abnormal development.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>28130259</pmid><doi>10.1152/ajplung.00271.2016</doi><orcidid>https://orcid.org/0000-0002-6732-8903</orcidid><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Animals Animals, Newborn Body Weight Chronic obstructive pulmonary disease CpG Islands - genetics DNA methylation DNA Methylation - genetics Female Insulin-Like Growth Factor I - genetics Insulin-Like Growth Factor I - metabolism Lung - metabolism Male Mice, Inbred BALB C Pregnancy Prenatal Exposure Delayed Effects - metabolism Promoter Regions, Genetic Proteins Receptor, IGF Type 1 - genetics Receptor, IGF Type 1 - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Rodents Sex Characteristics Signal Transduction - genetics Smoking Smoking - adverse effects Tobacco Products Tobacco smoke |
title | Prenatal exposure to tobacco smoke sex dependently influences methylation and mRNA levels of the Igf axis in lungs of mouse offspring |
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