Long-Term Effect of Lactation on Maternal Cardiovascular Function and Adiposity in a Murine Model

Herrera, Sandra; Vincent, Kathleen L.; Poole, Aaron; Olson, Gayle; Patrikeev, Igor; Saada, Jamal I.; Gamble, Phyllis; Motamedi, Massoud; Saade, George R.; Stuebe, Alison M.; Prewit, Egle Bytautiene

doi:10.1055/s-0038-1669443

Cited by 8 publications

(4 citation statements)

References 46 publications

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“…For postpartum groups, dams were allowed to deliver, and pups were removed within 12 h to avoid lactation. Lactation was controlled for as it significantly impacts total peripheral resistance, cardiac output, and blood pressure at 2 and 9 mo postpartum (22,36) and would, therefore, differentially affect outcomes in the present study based on litter characteristics. Postpartum mice were multihoused with ad libitum access to standard chow and water in a temperature-controlled room with a 12:12-h light-dark cycle until experiment day (6 or 10 mo of age).…”

Section: Animalsmentioning

confidence: 99%

Paternal deficiency of complement component C1q leads to a preeclampsia-like pregnancy in wild-type female mice and vascular adaptations postpartum

Sutton

Gemmel

Brands

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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Preeclampsia is a spontaneously occurring, pregnancy-specific syndrome that is clinically diagnosed by new onset hypertension and proteinuria. Epidemiological evidence describes an association between a history of preeclampsia and increased risk for cardiovascular disease in later life; however, the mechanism(s) driving this relationship are unclear. Our study aims to leverage a novel preeclampsia-like mouse model, the C1q−/− model, to help elucidate the acute and persistent vascular changes during and following a preeclampsia-like pregnancy. Female C57BL/6J mice were mated to C1q−/− male mice to model a preeclampsia-like pregnancy (“PE-like”), and the maternal cardiovascular phenotype (blood pressure, renal function, systemic glycocalyx, and ex vivo vascular function) was assessed in late pregnancy and postpartum at 6 and 10 mo of age. Uncomplicated, normotensive pregnancies (female C57BL/6J bred to male C57BL/6J mice) served as age-matched controls. In pregnancy, PE-like dams exhibited increased systolic and diastolic pressure during mid- and late gestation, renal dysfunction, fetal growth restriction, and reduced placental efficiency. Ex vivo wire myography studies of mesenteric arteries revealed severe pregnancy-specific endothelial-dependent and -independent vascular dysfunction. At 3 and 7 mo postpartum (6 and 10 mo old, respectively), hypertension resolved in PE-like dams, whereas mild vascular dysfunction persisted at 3 mo postpartum. In conclusion, the female C57BL/6J-by-male C57BL/6J C1q−/− model recapitulates many aspects of the human preeclampsia syndrome in a low-risk, wild-type female mouse. The pregnancy-specific phenotype results in systemic maternal endothelial-dependent and -independent vascular dysfunction that persists postpartum.

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Section: Animalsmentioning

confidence: 99%

Paternal deficiency of complement component C1q leads to a preeclampsia-like pregnancy in wild-type female mice and vascular adaptations postpartum

Sutton

Gemmel

Brands

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The exact mechanisms of the association between hypertension and breastfeeding remain unknown. However, it is known that lactation improves the cardiometabolic risk profile [ 24 – 26 ]. Breastfeeding has been reported to be associated with less postpartum weight retention in mothers who had a normal weight before pregnancy [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

“…In a meta-analysis, Nguyen and Ding reported protective effects of breastfeeding on cardiovascular health (metabolic syndrome, inflammatory markers, hypertension and cardiovascular disease) [ 28 ]. A previous animal study showed that at 9 months post-delivery, non-lactating mice had a significantly lower cardiac output, ejection fraction, fasting glucose level, and low-density lipoprotein level [ 26 ]. In addition, breastfeeding may affect factors that influence systolic blood pressure (arterial stiffness and compliance) [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Association between breastfeeding and preeclampsia in parous women: a case –control study

et al. 2021

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Background Preeclampsia is a global health problem and it is the main cause of maternal and perinatal morbidity and mortality. Breastfeeding has been reported to be associated with lower postpartum blood pressure in women with gestational hypertension. However, there is no published data on the role that breastfeeding might play in preventing preeclampsia. The aim of the current study was to investigate if breastfeeding was associated with preeclampsia in parous women. Method A case-control study was conducted in Saad Abualila Maternity Hospital in Khartoum, Sudan, from May to December 2019. The cases (n = 116) were parous women with preeclampsia. Two consecutive healthy pregnant women served as controls for each case (n = 232). The sociodemographic, medical, and obstetric histories were gathered using a questionnaire. Breastfeeding practices and duration were assessed. Results A total of 98 (84.5%) women with preeclampsia and 216 (93.1%) women in the control group had breastfed their previous children. The unadjusted odds ratio (OR) of preeclampsia (no breastfeeding vs breastfeeding) was 3.55, 95% confidence interval (CI) 1.64,7.70 and p value = 0.001 based on these numbers. After adjusting for age, parity, education level, occupation, history of preeclampsia, history of miscarriage, body mass index groups the adjusted OR was 3.19, 95% CI 1.49, 6.82 (p value = 0.006). Conclusion Breastfeeding might reduce the risk for preeclampsia. Further larger studies are required.

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“…Echocardiography was performed using a Vevo 2,100 high-resolution ultrasound system (VisualSonics, Toronto, ON, Canada) to measure changes in cardiac and physiology over time in a non-invasive manner, with the protocol adapted from Herrera et al (2018) ( Herrera et al, 2019 ). A total of 9 mice ( n = 3 for normal pregnancy, n = 3 for ascending infection, n = 3 for nonpregnant control) were used for the study, evaluated on days 7, 14, 21, 28, and 60 postpartum.…”

Section: Methodsmentioning

confidence: 99%

Characterization of fetal microchimeric immune cells in mouse maternal hearts during physiologic and pathologic pregnancies

Lintao,

Kammala,

Radnaa

et al. 2023

Front. Cell Dev. Biol.

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Introduction: During pregnancy, fetal cells can be incorporated into maternal tissues (fetal microchimerism), where they can persist postpartum. Whether these fetal cells are beneficial or detrimental to maternal health is unknown. This study aimed to characterize fetal microchimeric immune cells in the maternal heart during pregnancy and postpartum, and to identify differences in these fetal microchimeric subpopulations between normal and pregnancies complicated by spontaneous preterm induced by ascending infection.Methods: A Cre reporter mouse model, which when mated with wild-type C57BL/6J females resulted in cells and tissues of progeny expressing red fluorescent protein tandem dimer Tomato (mT+), was used to detect fetal microchimeric cells. On embryonic day (E)15, 104 colony-forming units (CFU) E. coli was administered intravaginally to mimic ascending infection, with delivery on or before E18.5 considered as preterm delivery. A subset of pregnant mice was sacrificed at E16 and postpartum day 28 to harvest maternal hearts. Heart tissues were processed for immunofluorescence microscopy and high-dimensional mass cytometry by time-of-flight (CyTOF) using an antibody panel of immune cell markers. Changes in cardiac physiologic parameters were measured up to 60 days postpartum via two-dimensional echocardiography.Results: Intravaginal E. coli administration resulted in preterm delivery of live pups in 70% of the cases. mT + expressing cells were detected in maternal uterus and heart, implying that fetal cells can migrate to different maternal compartments. During ascending infection, more fetal antigen-presenting cells (APCs) and less fetal hematopoietic stem cells (HSCs) and fetal double-positive (DP) thymocytes were observed in maternal hearts at E16 compared to normal pregnancy. These HSCs were cleared while DP thymocytes persisted 28 days postpartum following an ascending infection. No significant changes in cardiac physiologic parameters were observed postpartum except a trend in lowering the ejection fraction rate in preterm delivered mothers.Conclusion: Both normal pregnancy and ascending infection revealed distinct compositions of fetal microchimeric immune cells within the maternal heart, which could potentially influence the maternal cardiac microenvironment via (1) modulation of cardiac reverse modeling processes by fetal stem cells, and (2) differential responses to recognition of fetal APCs by maternal T cells.

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Long-Term Effect of Lactation on Maternal Cardiovascular Function and Adiposity in a Murine Model

Abstract: Our results show the benefit of lactation is not just limited to the immediate postpartum period but it also extends into midlife in a murine model.

Cited by 8 publications

References 46 publications

Paternal deficiency of complement component C1q leads to a preeclampsia-like pregnancy in wild-type female mice and vascular adaptations postpartum

Paternal deficiency of complement component C1q leads to a preeclampsia-like pregnancy in wild-type female mice and vascular adaptations postpartum

Association between breastfeeding and preeclampsia in parous women: a case –control study

Characterization of fetal microchimeric immune cells in mouse maternal hearts during physiologic and pathologic pregnancies

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