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The role of maternal obesity-driven inflammation and adverse pregnancy outcomes in a mouse model of preeclampsia

孕产妇肥胖驱动的炎症和不良妊娠结局在先兆子痫小鼠模型中的作用

基本信息

批准号：
10569517
负责人：
Jennifer Liford Sones
金额：
$ 18.5万
依托单位：
LSU PENNINGTON BIOMEDICAL RESEARCH CTR
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-03-01 至 2025-01-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10569517
关键词：
Abnormal placentation Adipose tissue Adult Affect Angiogenic Factor Birth Weight Blood Pressure Blood Vessels Blood flow Body Weight decreased Body mass index Cell Count Cell Separation Cells Characteristics Clinical Conceptions Cytokine Gene Data Decidua Defect Development Disease Eating Eclampsia Embryo Etiology Event Exhibits Female Fetal Death Fetal Growth Retardation Fetus Gene Expression Genetic Models Goals Growth Health Hypertension Immune Impairment Inbreeding Infant Inflammation Inflammation Mediators Inflammatory Interleukin-6 Intervention Ischemia Laboratories Life Link Macrophage Maternal Mortality Maternal-Fetal Exchange Measures Messenger RNA Metabolic Modeling Monitor Mothers Mus Natural Killer Cells Necrosis Obesity Ovary PGF gene Pathogenesis Phenotype Physiological Placenta Placentation Play Population Pre-Eclampsia Pregnancy Pregnancy Outcome Premature Birth Prevalence Prevention Protein Tyrosine Kinase Proteinuria Recommendation Risk Risk Factors Role Signal Transduction Source Syndrome Testing Thinness United States Uterus Vascular Endothelial Growth Factors Woman adverse outcome adverse pregnancy outcome angiogenesis attenuation cell type comorbidity cytokine early pregnancy experimental study fetal food surveillance gestational weight gain improved inflammatory milieu maternal hypertension maternal morbidity maternal obesity mortality mouse model offspring perinatal morbidity pregnancy disorder pregnancy hypertension pregnant prepregnancy prevent reproductive transcriptome sequencing tumor

项目摘要

Project Summary: Pregnancy is a physiological state of inflammation. However, heightened inflammation during pregnancy is linked to adverse outcomes, such as preeclampsia (PE). The clinical signs of PE include maternal hypertension and proteinuria during the second half of gestation. While PE presents later in pregnancy, its origins are thought to begin early in pregnancy or even before conception. Importantly, maternal hypertension only resolves after delivery of the placenta; therefore, it is widely accepted that abnormal placentation plays a causal role in PE pathogenesis, though the etiology of this is unknown. A number of maternal characteristics, including obesity, are known risk factors for developing PE. It is hypothesized maternal adiposity may contribute to heightened inflammation and subsequent abnormal placental vascular development. The overarching goal of these proposed studies is to test the hypothesis that pro-inflammatory mediators produced by specific immune cells within maternal adipose tissue reduce pro-angiogenic factors at the maternal-fetal interface. We will conduct our studies using the BPH/5 mouse model of PE.

项目概要：怀孕是一种炎症的生理状态。然而，怀孕期间炎症加剧与不良后果，如先兆子痫（PE）。PE的临床体征包括母体高血压和妊娠后半期出现蛋白尿。虽然PE在怀孕后期出现，但其起源被认为是开始在怀孕早期或甚至在受孕之前。重要的是，母亲的高血压只有在胎盘的分娩;因此，人们普遍认为胎盘形成异常在PE中起着因果作用发病机制，尽管其病因尚不清楚。一些母亲的特征，包括肥胖，是已知的发生PE的危险因素。据推测，母亲肥胖可能有助于提高炎症和随后的异常胎盘血管发育。其总体目标是，提出的研究是为了验证这一假设，即由特定的免疫细胞产生的促炎介质母体脂肪组织内的促血管生成因子减少母体-胎儿界面处的促血管生成因子。我们将进行我们的使用BPH/5小鼠PE模型的研究。