Late‐gestation ventricular myocardial reduction in fetuses of hyperglycemic CD1 mice is associated with increased apoptosis

Gutierrez, Juan Claudio; Prater, M. Renée; Smith, Bonnie J.; Freeman, Lisa C.; Mallela, Murali K.; Holladay, Steven D.

doi:10.1002/bdrb.20212

Cited by 14 publications

(10 citation statements)

References 24 publications

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“…Available data in the literature are limited but support the idea that hyperglycemia may increase adult heart myocardial apoptosis [23]. There has been extensive evidence: maternal hyperglycemia is an inducer of birth defects that include a high incidence of cardiovascular malformations [21,23].…”

Section: Issn 2475-5451mentioning

confidence: 99%

“…The rate of heart myocardial apoptosis may increase in adult mice under a hyperglycemic environment, and it's observed both increased apoptosis and necrosis in myocytes, endothelial cells and fibroblasts of the human adult diabetic heart [35][36][37]. In the fetal context, Gutierrez et al detected ventricular chamber dilation and myocardial reduction in late gestation fetal hearts, collected from hyperglycemic pregnant CD-1 mouse dams [16,23].…”

Section: In Late Gestationmentioning

confidence: 99%

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Paracetamol and Cardiac Congenital Malformations in Prediabetic Pregnancy Women

2018

IJDMD

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Hyperglycemia can influence the development of the fetal heart, affecting both its structure and its function. Prospective and retrospective cohort studies have demonstrated an increased risk of congenital abnormalities with gestational diabetes. This observation is probably related to the inclusion of women with unrecognized type 2 diabetes [1,2]. Substantial literature indicates that diabetes in pregnant rats and mice induces embryo lethality, growth retardation and a variable incidence of birth defects. Then, the maintenance of normal concentrations of metabolites from all nutrient classes may be important for prevention of adverse fetal outcome in diabetic pregnancy.Acetaminophen overdose is the most often cause of acute liver injury and obese women are in particular risk, because is able to induce mitochondrial oxidative stress [3]. Acetaminophen (Paracetamol) over doses decreased embryonic low-molecularweight thiols (glutathione and cysteine), compounds that play a vital role in the detoxication of exogenous and endogenous chemicals [3][4][5].The apparent safety of Paracetamol drug, a useful analgesic only (with no anti-inflammatory properties) is compromised by its widespread and extensive chronic use, particularly in Peruvian population, where its analgesic is doing without control [6][7][8][9]. In fact, paracetamol though considered safe at a considerable low dose, especially in women could cause kidney derangement and cardiac malformations during pregnant state if the drug is ingested in the first trimester [8]. Major congenital malformations, including those affecting the cardiovascular system, remain the leading cause of mortality and morbidity in infants of diabetic mothers [10]. Thus, there is overcome potential maternal acetaminophen (paracetamol) toxicity [11].

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Section: Issn 2475-5451mentioning

confidence: 99%

Section: In Late Gestationmentioning

confidence: 99%

Paracetamol and Cardiac Congenital Malformations in Prediabetic Pregnancy Women

2018

IJDMD

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“…These authors later associated diabetes-related fetal mouse myocardial reduction with increased myocardial apoptosis, and suggested that maternal immune stimulation may restore normal myocardial apoptosis rates during development. 19 Punareewattana et al used STZ-induced diabetes in pregnant mice to induce craniofacial and neural tube defects (NTDs). These authors identified 36 out of 151 maternal splenic cytokine/growth factor genes studied as significantly different (either upregulated or downregulated) between immune-stimulated diabetic dams and non-stimulated diabetic dams.…”

Section: Immune Protection During Development 133mentioning

confidence: 99%

Diverse ability of maternal immune stimulation to reduce birth defects in mice exposed to teratogens: a review

Hrubec

Prater

Mallela

et al. 2011

J Devel Orig Health Dis

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Stimulating the maternal immune system before or during pregnancy can dramatically improve morphologic outcome in mice that have been exposed to teratogens. For example, maternal immune stimulation in mice reduced craniofacial and palate defects, heart defects, digit and limb defects, tail malformations and neural tube defects caused by diverse teratogens that included chemical agents, hyperthermia, X-rays and diabetes mellitus. Several different procedures of immune stimulation were effective and included footpad injection with Freund's Complete Adjuvant, intraperitoneal (IP) injection with inert particles or attenuated Bacillus Calmette-Guerin, intrauterine injection with allogenic or xenogenic lymphocytes, or intravascular, intrauterine or IP injection with immunomodulatory cytokines. Limited information is available regarding mechanisms by which such immune stimulation reduces fetal dysmorphogenesis; however, cytokines of maternal origin have been suggested as effector molecules that act on the placenta or fetus to improve development. These collective data raise novel questions about the possibility of unrecognized maternal immune system regulatory activity in normal fetal development. This manuscript reviews the literature showing maternal immune protection against morphologic birth defects. Potential operating mechanisms are discussed, and the possibility is considered that a suppressed maternal immune system may negatively impact fetal development.

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“…Maternal hyperglycemia might potentially inhibit cardiomyocyte proliferation and promote cell apoptosis during fetal heart development (Han et al 2015 ; Su et al 2016 ). Decreased cell proliferation and increased apoptosis are the two key factors leading to a reduction in the number of cardiomyocytes (Gutierrez et al 2009 ; Su et al 2017 ; Su et al 2019 ). Immature cardiomyocytes actively proliferate in the fetuses of mammals but cease to proliferate shortly after birth.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miRNA-23a-3p rescues high glucose-induced cell apoptosis and proliferation inhibition in cardiomyocytes

Wang

Yang

et al. 2020

In Vitro Cell.Dev.Biol.-Animal

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Maternal hyperglycemia potentially inhibits the development of the fetal heart by suppressing cardiomyocyte proliferation and promoting apoptosis. Different studies have indicated that miRNAs are key regulators of cardiomyocyte proliferation, differentiation, and apoptosis and play a protective role in a variety of cardiovascular diseases. However, the biological function of miRNA-23a in hyperglycemia-related cardiomyocyte injury is not fully understood. The present study investigated the effect of miRNA-23a-3p on cell proliferation and apoptosis in a myocardial injury model induced by high glucose. H9c2 cardiomyocytes were exposed to high glucose to establish an in vitro myocardial injury model and then transfected with miRNA-23a-3p mimics. After miRNA-23a-3p transfection, lens-free microscopy was used to dynamically monitor cell numbers and confluence and calculate the cell cycle duration. CCK-8 and EdU incorporation assays were performed to detect cell proliferation. Flow cytometry was used to measured cell apoptosis. Upregulation of miRNA-23a-3p significantly alleviated high glucose-induced cell apoptosis and cell proliferation inhibition (p < 0.01 and p < 0.0001, respectively). The cell cycle of the miRNA-23a-3p mimics group was significantly shorter than that of the negative control group (p < 0.01). The expression of cell cycle–activating and apoptosis inhibition-associated factors Ccna2, Ccne1, and Bcl-2 was downregulated by high glucose and upregulated by miRNA-23a-3p overexpression in high glucose-injured H9c2 cells. miRNA-23a-3p mimics transfection before high glucose treatment had a significantly greater benefit than transfection after high glucose treatment (p < 0.0001), and the rescue effect of miRNA-23a-3p increased as the concentration increased. This study suggests that miRNA-23a-3p exerted a dose- and time-dependent protective effect on high glucose-induced H9c2 cardiomyocyte injury.

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Late‐gestation ventricular myocardial reduction in fetuses of hyperglycemic CD1 mice is associated with increased apoptosis

Cited by 14 publications

References 24 publications

Paracetamol and Cardiac Congenital Malformations in Prediabetic Pregnancy Women

Paracetamol and Cardiac Congenital Malformations in Prediabetic Pregnancy Women

Diverse ability of maternal immune stimulation to reduce birth defects in mice exposed to teratogens: a review

Upregulation of miRNA-23a-3p rescues high glucose-induced cell apoptosis and proliferation inhibition in cardiomyocytes

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