Long-term effects of maternal undernutrition on offspring carotid artery remodeling: role of miR-29c

Khorram, Omid; Chuang, Tsai‐Der; Pearce, William J.

doi:10.1017/s2040174415001208

Cited by 19 publications

(17 citation statements)

References 48 publications

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“…Clinical and experimental data have revealed deleterious adaptations in the vasculature as a hallmark of the fetal programming process. [1][2][3][4][5][6][7][8][9][10][11] These responses are attributed to insults (e.g. maternal diet manipulation, hypoxia, and uteroplacental insufficiency) that occur during the critical window of fetal development.…”

Section: Introductionmentioning

confidence: 99%

Intrauterine growth restriction-induced deleterious adaptations in endothelial progenitor cells: possible mechanism to impair endothelial function

Oliveira

Souza

Fernandes

et al. 2017

J Dev Orig Health Dis

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Intrauterine growth restriction (IUGR) can induce deleterious changes in the modulatory ability of the vascular endothelium, contributing to an increased risk of developing cardiovascular diseases in the long term. However, the mechanisms involved are not fully understood. Emerging evidence has suggested the potential role of endothelial progenitor cells (EPCs) in vascular health and repair. Therefore, we aimed to evaluate the effects of IUGR on vascular reactivity and EPCs derived from the peripheral blood (PB) and bone marrow (BM) in vitro. Pregnant Wistar rats were fed an ad libitum diet (control group) or 50% of the ad libitum diet (restricted group) throughout gestation. We determined vascular reactivity, nitric oxide (NO) concentration, and endothelial nitric oxide synthase (eNOS) protein expression by evaluating the thoracic aorta of adult male offspring from both groups (aged: 19-20 weeks). Moreover, the amount, functional capacity, and senescence of EPCs were assessed in vitro. Our results indicated that IUGR reduced vasodilation via acetylcholine in aorta rings, decreased NO levels, and increased eNOS phosphorylation at Thr495. The amount of EPCs was similar between both groups; however, IUGR decreased the functional capacity of EPCs from the PB and BM. Furthermore, the senescence process was accelerated in BM-derived EPCs from IUGR rats. In summary, our findings demonstrated the deleterious changes in EPCs from IUGR rats, such as reduced EPC function and accelerated senescence in vitro. These findings may contribute towards elucidating the possible mechanisms involved in endothelial dysfunction induced by fetal programming.

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Section: Introductionmentioning

confidence: 99%

Intrauterine growth restriction-induced deleterious adaptations in endothelial progenitor cells: possible mechanism to impair endothelial function

Oliveira

Souza

Fernandes

et al. 2017

J Dev Orig Health Dis

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“…Additionally, miR-29c could inhibit endotheliocyte migration and angiogenesis of human endothelial cells by suppressing the insulin like growth factor 1 [30]. Khorram O et al also found that miR-29 played vital roles in atherosclerosis by regulating the expression of extracellular matrix [31]. These preclinical studies indicated that miR-29c could play several distinct roles during atherosclerosis development; thus, they provide underlying molecular mechanisms for our results.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 60%

“…Finally, we studied only miR-29c in our research. But many previous basic studies from references indicated that miR-29c may play an important role in the development of atherosclerosis through many mechanisms [14,30,31]. Therefore, those basic researches mentioned in the previous literatures provided a certain theoretical guarantee for our conclusion.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 63%

Plasma MicroRNA-29c Levels Are Associated with Carotid Intima-Media Thickness and is a Potential Biomarker for the Early Detection of Atherosclerosis

Huang¹,

Li²,

Huang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Atherosclerosis is a serious disease that increases the risk of myocardial infarction and ischemic stroke. Previous studies have demonstrated that microRNA (miR)-29c could play significant roles in atherosclerosis via regulating inflammatory processes. However, the relationship between miR-29c and carotid intima-media thickness (CIMT) remains unknown. This study investigated associations between miR-29c and atherosclerosis and tested whether plasma miR-29c levels could be used to detect atherosclerosis. Methods: Plasma miR-29c levels were estimated by quantitative real-time PCR, and CIMT was measured by carotid ultrasound. Associations between miR-29c and CIMT were assessed by Spearman’s correlation coefficient and multiple linear regression analyses. Results: In total, 170 participants were divided into the study (CIMT ≥0.9 mm) and control (CIMT < 0.9 mm) groups. The study group showed higher C-reactive protein (CRP) and miR-29c relative expression levels compared with the control group. CIMT was positively correlated with miR-29c (r=0.659, p< 0.001) and CRP (r=0.447, p< 0.001), and miR-29c levels were also correlated with CRP (r=0.512, p< 0.001). Furthermore, multiple linear regression analysis showed that CIMT was significantly correlated with miR-29c (β=0.573, 95% confidence interval [CI]: 0.315-0.839; p< 0.001) and CRP (β=0.439, 95%CI: 0.186–0.825; p< 0.001). After age, body mass index, systolic blood pressure, total cholesterol and fasting blood-glucose were adjusted for, CIMT was still closely associated with miR-29c (β=0.529, 95%CI: 0.354–0.812; p< 0.001) and CRP (β=0.417, 95%CI: 0.198–0.724; p< 0.001). Evaluating CRP and miR-29c together (AUC=0.900, p< 0.001) achieved a better prognostic value for atherosclerosis than miR-29c (AUC=0.870, p< 0.001) or CRP (AUC=0.722, p< 0.001) alone. Conclusion: Increased miR-29c was closely associated with CIMT and may serve as a biomarker for identifying atherosclerotic patients.

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“…The hypertension may be associated with salt sensitivity [67]. Undernutrition in sheep dams leads to increased expression of several extracellular matrix proteins in the carotid arteries, related in part to suppression of miR-29c that may involve glucocorticoids [68•]. Low-protein diet during pregnancy has been reported to lead to enhanced responsiveness to angiotensin II [69], especially in male off-spring [70], and exaggerated proliferative response to vascular injury in the offspring with increased expression of genes related to oxidative stress [71].…”

Section: Pathogenesis Of Primary Pediatric Hypertensionmentioning

confidence: 99%

Primary Pediatric Hypertension: Current Understanding and Emerging Concepts

et al. 2017

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The rising prevalence of primary pediatric hypertension and its tracking into adult hypertension point to the importance of determining its pathogenesis to gain insights into its current and emerging management. Considering that the intricate control of BP is governed by a myriad of anatomical, molecular biological, biochemical, and physiological systems, multiple genes are likely to influence an individual's BP and susceptibility to develop hypertension. The long-term regulation of BP rests on renal and non-renal mechanisms. One renal mechanism relates to sodium transport. The impaired renal sodium handling in primary hypertension and salt sensitivity may be caused by aberrant counter-regulatory natriuretic and anti-natriuretic pathways. The sympathetic nervous and renin-angiotensin-aldosterone systems are examples of antinatriuretic pathways. An important counter-regulatory natriuretic pathway is afforded by the renal autocrine/paracrine dopamine system, aberrations of which are involved in the pathogenesis of hypertension, including that associated with obesity. We present updates on the complex interactions of these two systems with dietary salt intake in relation to obesity, insulin resistance, inflammation, and oxidative stress. We review how insults during pregnancy such as maternal and paternal malnutrition, glucocorticoid exposure, infection, placental insufficiency, and treatments during the neonatal period have long-lasting effects in the regulation of renal function and BP. Moreover, these effects have sex differences. There is a need for early diagnosis, frequent monitoring, and timely management due to increasing evidence of premature target organ damage. Large controlled studies are needed to evaluate the long-term consequences of the treatment of elevated BP during childhood, especially to establish the validity of the current definition and treatment of pediatric hypertension.

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Long-term effects of maternal undernutrition on offspring carotid artery remodeling: role of miR-29c

Cited by 19 publications

References 48 publications

Intrauterine growth restriction-induced deleterious adaptations in endothelial progenitor cells: possible mechanism to impair endothelial function

Intrauterine growth restriction-induced deleterious adaptations in endothelial progenitor cells: possible mechanism to impair endothelial function

Plasma MicroRNA-29c Levels Are Associated with Carotid Intima-Media Thickness and is a Potential Biomarker for the Early Detection of Atherosclerosis

Primary Pediatric Hypertension: Current Understanding and Emerging Concepts

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