Maternal nutrition influences angiogenesis in the placenta through peroxisome proliferator activated receptors: A novel hypothesis

Meher, Akshaya; Sundrani, Deepali; Joshi, Sadhana

doi:10.1002/mrd.22518

Cited by 38 publications

(28 citation statements)

References 95 publications

(107 reference statements)

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“…VEGF, acting as a key angiogenesis promoter, plays a significant role in physiological and pathophysiological vascular development and maintenance 23 . It has been shown that VEGF expression is found in the decidua cells of early pregnancy, and it participates in physiological placental angiogenesis during embryogenesis and reproductive functions during the initial stages of pregnancy 24 . Dysregulation of VEGF expression has been linked to the onset of placental pathologies including preeclampsia, early pregnancy loss and intrauterine growth restriction and is deeply implicated in multiple steps of RSA occurrence and development 25 26 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-16 inhibits feto-maternal angiogenesis and causes recurrent spontaneous abortion by targeting vascular endothelial growth factor

Zhu

Huo

et al. 2016

Sci Rep

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Recurrent spontaneous abortion (RSA) is a common health problem that affects women of reproductive age. Recent studies have indicated that microRNAs are important factors in miscarriage. This study investigated the role of miR-16 in regulating vascular endothelial growth factor (VEGF) expression and the pathogenesis of RSA. In this report, clinical samples revealed that miR-16 expression was significantly elevated in the villi and decidua of RSA patients. In vitro, miR-16 upregulation inhibited human umbilical vein endothelial cell proliferation, migration and tube formation. Conversely, the downregulation of miR-16 reversed these effects. In vivo, we demonstrated that abnormal miR-16 levels affect the weights of the placenta and embryo and the number of progeny and microvascular density, as well as cause recurrent abortions by controlling VEGF expression in pregnant mice. VEGF, a potential target gene of miR-16, was inversely correlated with miR-16 expression in the decidua of clinical samples. Furthermore, the luciferase reporter system demonstrated that miR-16 was found to directly downregulate the expression of VEGF by binding a specific sequence of its 3′-untranslated region (3′UTR). Collectively, these data strongly suggest that miR-16 regulates placental angiogenesis and development by targeting VEGF expression and is involved in the pathogenesis of RSA.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-16 inhibits feto-maternal angiogenesis and causes recurrent spontaneous abortion by targeting vascular endothelial growth factor

Zhu

Huo

et al. 2016

Sci Rep

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“…PPARs are nuclear transcription factor and nutrient-sensing signaling that regulate metabolic and tissue developmental processes. Studies focusing on the mechanisms of such metabolic programming have implicated PPARs as a candidate gatekeeper pathway of developmental programming [ 21 , 22 , 23 ], although their relationship with programmed hypertension and metabolic syndrome remains to be established.…”

Section: The Impact Of Renal Programming In Programmed Hypertensiomentioning

confidence: 99%

PPARs Link Early Life Nutritional Insults to Later Programmed Hypertension and Metabolic Syndrome

Tain

Hsu

Chan

2015

IJMS

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Hypertension is an important component of metabolic syndrome. Adulthood hypertension and metabolic syndrome can be programmed in response to nutritional insults in early life. Peroxisome proliferator-activated receptors (PPARs) serve as a nutrient-sensing signaling linking nutritional programming to hypertension and metabolic syndrome. All three members of PPARs, PPARα, PPARβ/δ, and PPARγ, are expressed in the kidney and involved in blood pressure control. This review provides an overview of potential clinical applications of targeting on the PPARs in the kidney to prevent programmed hypertension and metabolic syndrome, with an emphasis on the following areas: mechanistic insights to interpret programmed hypertension; the link between the PPARs, nutritional insults, and programmed hypertension and metabolic syndrome; the impact of PPAR signaling pathway in a maternal high-fructose model; and current experimental studies on early intervention by PPAR modulators to prevent programmed hypertension and metabolic syndrome. Animal studies employing a reprogramming strategy via targeting PPARs to prevent hypertension have demonstrated interesting results. It is critical that the observed effects on developmental reprogramming in animal models are replicated in human studies, to halt the globally-growing epidemic of metabolic syndrome-related diseases.

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“…Obesity in pregnancy has been associated with an increased risk of metabolic disorders and adverse pregnancy outcomes, including gestational diabetes mellitus (GDM), gestational hypertension, preeclampsia, and preterm delivery . The placenta is the organ responsible for mammalian embryo survival.…”

Section: Introductionmentioning

confidence: 99%

Maternal Eicosapentaenoic Acid Feeding Decreases Placental Lipid Deposition and Improves the Homeostasis of Oxidative Stress Through a Sirtuin‐1 (SIRT1) Independent Manner

Peng

Xiong

Cui

et al. 2019

Molecular Nutrition Food Res

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Scope: Maternal obesity has been associated with increased placental lipotoxicity and impaired mitochondrial function. Sirtuin-1 (SIRT1) is an important regulator of both lipid metabolism and mitochondrial biogenesis. The present study aims to determine whether supplementation of the maternal diet with eicosapentaenoic acid (EPA) can decrease placental lipid deposition and improve antioxidant ability, in a SIRT1-dependent manner. Methods and results: Pregnant SIRT1 +/− mice (mated with male SIRT1 +/− ) are fed a high-fat diet consisting of 60% of the kcal from fat, or an equienergy EPA diet for 18.5 d. Supplementation with EPA significantly changes maternal plasma, placental and fetal fatty acid composition, and decreases placental and fetal lipid content. In addition, placental antioxidant capacity and lipid peroxidation products are increased, placental uncoupling protein 1 (UCP1) and PPAR coactivator-1 (PGC1 ) expression are activated, and mitochondrial swelling decreases. While SIRT1 deficiency has little effect on placental fatty acid composition and lipid content, decreased fetal lipid deposition is observed, placental PGC1 expression decreases, mitochondrial swelling increases, and placental total superoxide dismutase (T-SOD) activity increases. Both EPA and SIRT1 have no effect on BODIPY-FL-C16 uptake. Interestingly, there is no significant interaction between diet and genotype. Conclusion: Maternal EPA feeding decreases placental lipid deposition and improves placental oxidative stress homeostasis independent of SIRT1.

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Maternal nutrition influences angiogenesis in the placenta through peroxisome proliferator activated receptors: A novel hypothesis

Cited by 38 publications

References 95 publications

MicroRNA-16 inhibits feto-maternal angiogenesis and causes recurrent spontaneous abortion by targeting vascular endothelial growth factor

MicroRNA-16 inhibits feto-maternal angiogenesis and causes recurrent spontaneous abortion by targeting vascular endothelial growth factor

PPARs Link Early Life Nutritional Insults to Later Programmed Hypertension and Metabolic Syndrome

Maternal Eicosapentaenoic Acid Feeding Decreases Placental Lipid Deposition and Improves the Homeostasis of Oxidative Stress Through a Sirtuin‐1 (SIRT1) Independent Manner

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