Michael R Hussey, James MacDonald, Theo K Bammler, Fasil Tekola-Ayele, Kathleen F Kerr, Alison G Paquette, Carmen J Marsit, Kaja Z LeWinn, Qi Zhao, Catherine J Karr, Sheela Sathyanarayana, Daniel A Enquobahrie
{"title":"在两个出生队列中，胎盘lncRNA表达与母亲孕前BMI和婴儿出生体重的关系","authors":"Michael R Hussey, James MacDonald, Theo K Bammler, Fasil Tekola-Ayele, Kathleen F Kerr, Alison G Paquette, Carmen J Marsit, Kaja Z LeWinn, Qi Zhao, Catherine J Karr, Sheela Sathyanarayana, Daniel A Enquobahrie","doi":"10.1017/S204017442500011X","DOIUrl":null,"url":null,"abstract":"<p><p>Pre-pregnancy obesity (ppOB) is linked to pregnancy complications and abnormal fetal growth through placental mechanisms, and long non-coding RNAs (lncRNAs) may play an epigenetic role in these processes. We investigated overall and sex-specific associations of pre-pregnancy body mass index (ppBMI), ppOB, and birthweight with placental lncRNA transcripts in two birth cohorts. Study participants were mother-child dyads recruited to the CANDLE (Memphis, TN)(<i>n</i> = 725) and GAPPS (Seattle and Yakima, WA)(<i>n</i> = 159) cohorts. Maternal ppBMI was assessed at enrollment using interviewer-administered questionnaires. LncRNAs (1,077 and 1,033 for CANDLE and GAPPS, respectively) were sequenced from placental samples collected at birth. Placental lncRNA was regressed on ppBMI, ppOB (ppBMI ≥30kg/m<sup>2</sup>), or continuous birthweight in cohort-specific weighted linear models controlling for <i>a priori</i>-specified confounders and experimental variables. Potential effect modification by infant-sex was examined in sex-stratified analyses and models including BMI-infant-sex interaction terms. No lncRNA transcripts were significantly associated with ppBMI, ppOB, or birthweight in primary models. Among male infants in CANDLE, expression of three lncRNA transcripts (<i>ERVH48-1</i>, <i>AC139099.1</i>, <i>CEBPA-DT</i>) was associated with ppBMI and one transcript (<i>AC104083.1</i>) with birthweight. In GAPPS, ppBMI was associated with two lncRNA transcripts (<i>AP000879.1</i> and <i>AL365203.2</i>) among males, and birthweight was associated with 17 lncRNA transcripts (including <i>LINC02709</i>, <i>KANSL1-AS1, DANCR, EPB41L4A-AS1</i>, and <i>GABPB1-AS1</i>) among females. No BMI-infant-sex interactions were observed. Though many of these potential associations are for uncharacterized transcripts, several identified lncRNAs (e.g., <i>ERVH48-1</i> and <i>CEBPA-DT</i>) have been linked to pathways controlling cancer or placental growth, trophoblast differentiation, and gene expression. These associations warrant validation in future studies.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"16 ","pages":"e20"},"PeriodicalIF":1.8000,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097519/pdf/","citationCount":"0","resultStr":"{\"title\":\"Associations of placental lncRNA expression with maternal pre-pregnancy BMI and infant birthweight in two birth cohorts.\",\"authors\":\"Michael R Hussey, James MacDonald, Theo K Bammler, Fasil Tekola-Ayele, Kathleen F Kerr, Alison G Paquette, Carmen J Marsit, Kaja Z LeWinn, Qi Zhao, Catherine J Karr, Sheela Sathyanarayana, Daniel A Enquobahrie\",\"doi\":\"10.1017/S204017442500011X\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Pre-pregnancy obesity (ppOB) is linked to pregnancy complications and abnormal fetal growth through placental mechanisms, and long non-coding RNAs (lncRNAs) may play an epigenetic role in these processes. We investigated overall and sex-specific associations of pre-pregnancy body mass index (ppBMI), ppOB, and birthweight with placental lncRNA transcripts in two birth cohorts. Study participants were mother-child dyads recruited to the CANDLE (Memphis, TN)(<i>n</i> = 725) and GAPPS (Seattle and Yakima, WA)(<i>n</i> = 159) cohorts. Maternal ppBMI was assessed at enrollment using interviewer-administered questionnaires. LncRNAs (1,077 and 1,033 for CANDLE and GAPPS, respectively) were sequenced from placental samples collected at birth. Placental lncRNA was regressed on ppBMI, ppOB (ppBMI ≥30kg/m<sup>2</sup>), or continuous birthweight in cohort-specific weighted linear models controlling for <i>a priori</i>-specified confounders and experimental variables. Potential effect modification by infant-sex was examined in sex-stratified analyses and models including BMI-infant-sex interaction terms. No lncRNA transcripts were significantly associated with ppBMI, ppOB, or birthweight in primary models. Among male infants in CANDLE, expression of three lncRNA transcripts (<i>ERVH48-1</i>, <i>AC139099.1</i>, <i>CEBPA-DT</i>) was associated with ppBMI and one transcript (<i>AC104083.1</i>) with birthweight. In GAPPS, ppBMI was associated with two lncRNA transcripts (<i>AP000879.1</i> and <i>AL365203.2</i>) among males, and birthweight was associated with 17 lncRNA transcripts (including <i>LINC02709</i>, <i>KANSL1-AS1, DANCR, EPB41L4A-AS1</i>, and <i>GABPB1-AS1</i>) among females. No BMI-infant-sex interactions were observed. Though many of these potential associations are for uncharacterized transcripts, several identified lncRNAs (e.g., <i>ERVH48-1</i> and <i>CEBPA-DT</i>) have been linked to pathways controlling cancer or placental growth, trophoblast differentiation, and gene expression. 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Associations of placental lncRNA expression with maternal pre-pregnancy BMI and infant birthweight in two birth cohorts.
Pre-pregnancy obesity (ppOB) is linked to pregnancy complications and abnormal fetal growth through placental mechanisms, and long non-coding RNAs (lncRNAs) may play an epigenetic role in these processes. We investigated overall and sex-specific associations of pre-pregnancy body mass index (ppBMI), ppOB, and birthweight with placental lncRNA transcripts in two birth cohorts. Study participants were mother-child dyads recruited to the CANDLE (Memphis, TN)(n = 725) and GAPPS (Seattle and Yakima, WA)(n = 159) cohorts. Maternal ppBMI was assessed at enrollment using interviewer-administered questionnaires. LncRNAs (1,077 and 1,033 for CANDLE and GAPPS, respectively) were sequenced from placental samples collected at birth. Placental lncRNA was regressed on ppBMI, ppOB (ppBMI ≥30kg/m2), or continuous birthweight in cohort-specific weighted linear models controlling for a priori-specified confounders and experimental variables. Potential effect modification by infant-sex was examined in sex-stratified analyses and models including BMI-infant-sex interaction terms. No lncRNA transcripts were significantly associated with ppBMI, ppOB, or birthweight in primary models. Among male infants in CANDLE, expression of three lncRNA transcripts (ERVH48-1, AC139099.1, CEBPA-DT) was associated with ppBMI and one transcript (AC104083.1) with birthweight. In GAPPS, ppBMI was associated with two lncRNA transcripts (AP000879.1 and AL365203.2) among males, and birthweight was associated with 17 lncRNA transcripts (including LINC02709, KANSL1-AS1, DANCR, EPB41L4A-AS1, and GABPB1-AS1) among females. No BMI-infant-sex interactions were observed. Though many of these potential associations are for uncharacterized transcripts, several identified lncRNAs (e.g., ERVH48-1 and CEBPA-DT) have been linked to pathways controlling cancer or placental growth, trophoblast differentiation, and gene expression. These associations warrant validation in future studies.
期刊介绍：
JDOHaD publishes leading research in the field of Developmental Origins of Health and Disease (DOHaD). The Journal focuses on the environment during early pre-natal and post-natal animal and human development, interactions between environmental and genetic factors, including environmental toxicants, and their influence on health and disease risk throughout the lifespan. JDOHaD publishes work on developmental programming, fetal and neonatal biology and physiology, early life nutrition, especially during the first 1,000 days of life, human ecology and evolution and Gene-Environment Interactions.
JDOHaD also accepts manuscripts that address the social determinants or education of health and disease risk as they relate to the early life period, as well as the economic and health care costs of a poor start to life. Accordingly, JDOHaD is multi-disciplinary, with contributions from basic scientists working in the fields of physiology, biochemistry and nutrition, endocrinology and metabolism, developmental biology, molecular biology/ epigenetics, human biology/ anthropology, and evolutionary developmental biology. Moreover clinicians, nutritionists, epidemiologists, social scientists, economists, public health specialists and policy makers are very welcome to submit manuscripts.
The journal includes original research articles, short communications and reviews, and has regular themed issues, with guest editors; it is also a platform for conference/workshop reports, and for opinion, comment and interaction.
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