PMID- 28859286 OWN - NLM STAT- MEDLINE DCOM- 20180510 LR - 20220316 IS - 1529-7268 (Electronic) IS - 0006-3363 (Linking) VI - 97 IP - 1 DP - 2017 Jul 1 TI - Persistence of risk factors associated with maternal cardiovascular disease following aberrant inflammation in rat pregnancy. PG - 143-152 LID - 10.1093/biolre/iox072 [doi] AB - INTRODUCTION: Pre-eclampsia is associated with increased risk of subsequent cardiovascular and metabolic disease in the affected mothers. While aberrant inflammation contributes to the pathophysiology of pre-eclampsia, it is unclear whether maternal inflammation contributes to the increased risk of disease. Here, we determined the effect of aberrant inflammation in pregnancy on cardiovascular and metabolic disease risk factors. METHODS: Wistar rats were administered low doses of lipopolysaccharide (LPS) on gestational days (GD) 13.5-16.5 to induce inflammation. Controls included pregnant rats treated with saline and nonpregnant rats treated with LPS or saline. We previously showed that LPS-treated pregnant rats exhibit key features of pre-eclampsia. Echocardiographic parameters, heart weight, blood pressure, blood lipids, pulse-wave velocity, and glucose tolerance, were assessed at 16 weeks postpartum. Messenger RNA levels of transcription factors associated with cardiac growth were measured in left ventricular tissue; histone modifications and global DNA methylation were determined in hearts and livers at GD 17.5 and at 16 weeks postpartum. RESULTS: Compared with saline-treated pregnant rats and nonpregnant rats treated with LPS or saline, LPS-treated pregnant rats exhibited left ventricular hypertrophy and increased blood cholesterol and low-density lipoprotein levels at 16 weeks postdelivery. LPS-treated rats had increased left ventricular mRNA levels of hypertrophy-associated transcription factors at GD 17.5 and increased levels of modified histones in hearts and livers at GD 17.5 and 16 weeks postpartum. Other parameters remained unchanged. CONCLUSION: Aberrant inflammation during pregnancy results in persistent alterations in maternal physiological parameters and epigenetic modifications that could contribute to the pathophysiology of cardiovascular disease. CI - (c) The Authors 2017. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com FAU - Ushida, Takafumi AU - Ushida T AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. AD - Department of Gynecology and Obstetrics, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Japan. FAU - Macdonald-Goodfellow, Shannyn K AU - Macdonald-Goodfellow SK AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. FAU - Quadri, Allegra AU - Quadri A AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. FAU - Tse, M Yat AU - Tse MY AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. FAU - Winn, Louise M AU - Winn LM AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. FAU - Pang, Stephen C AU - Pang SC AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. FAU - Adams, Michael A AU - Adams MA AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. FAU - Kotani, Tomomi AU - Kotani T AD - Department of Gynecology and Obstetrics, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Japan. FAU - Kikkawa, Fumitaka AU - Kikkawa F AD - Department of Gynecology and Obstetrics, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Japan. FAU - Graham, Charles H AU - Graham CH AD - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. LA - eng PT - Journal Article PL - United States TA - Biol Reprod JT - Biology of reproduction JID - 0207224 RN - 0 (Histones) RN - 0 (Lipopolysaccharides) RN - 9007-49-2 (DNA) SB - IM MH - Animals MH - Blood Pressure MH - DNA/genetics/metabolism MH - Echocardiography MH - Female MH - Gene Expression Regulation MH - Heart MH - Histones/genetics/metabolism MH - Inflammation/*chemically induced/complications MH - Lipopolysaccharides/*toxicity MH - Pregnancy MH - *Pregnancy Complications, Cardiovascular MH - Rats MH - Rats, Wistar MH - Risk Factors OTO - NOTNLM OT - cardiac hypertrophy OT - cardiovascular disease OT - epigenetics OT - hyperlipidemia OT - intrauterine growth restriction OT - maternal inflammation OT - pre-eclampsia EDAT- 2017/09/02 06:00 MHDA- 2018/05/11 06:00 CRDT- 2017/09/02 06:00 PHST- 2017/04/19 00:00 [received] PHST- 2017/07/04 00:00 [accepted] PHST- 2017/09/02 06:00 [entrez] PHST- 2017/09/02 06:00 [pubmed] PHST- 2018/05/11 06:00 [medline] AID - 3950272 [pii] AID - 10.1093/biolre/iox072 [doi] PST - ppublish SO - Biol Reprod. 2017 Jul 1;97(1):143-152. doi: 10.1093/biolre/iox072.