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Molecular Mechanisms Underlying the Fetal Programming of Adult Disease
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Molecular Mechanisms Underlying the Fetal Programming of Adult Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 2108

Special Issue Editors

Dr. Karen Jonscher

E-Mail Website
Guest Editor
University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
Interests: maternal microbiome; fetal programming; innate immune memory; nonalcoholic fatty liver disease
Dr. Marisol Castillo-Castrejon

E-Mail
Guest Editor
University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
Interests: nutritional sciences; environmental exposures; fetal programming; women’s health

Special Issue Information

Dear Colleagues,

Multiple lines of evidence show a striking association between maternal exposures and the development of chronic diseases in adult offspring; however, molecular mechanisms underpinning the disease risk remain poorly understood. Moreover, the role of paternal exposures in programming offspring diseases is understudied. The goals of this Special Issue entitled “Molecular Mechanisms Underlying the Fetal Programming of Adult Disease” are to report current research activities aimed at:

  • Exploring mechanisms, at the molecular and cellular levels, by which maternal or paternal exposures, including diet (excessive or insufficient nutrition), pollutants, drugs, tobacco, and psychological stress/psychopathology, determine health trajectories in the offspring across the lifespan.
  • Elucidating genes, pathways, and functions in the offspring that are epigenetically rewired by maternal or paternal exposures to exacerbate disease risk.
  • Examining effects of maternal or paternal treatment strategies on the microbiome and targetable molecules in the placenta and offspring.

This Special Issue welcomes the submission of reviews and experimental findings in both animal and human models of all adult diseases that report molecular, cellular, and systemic responses of the offspring to maternal or paternal environmental exposures and/or therapeutics at timepoints throughout the lifespan; submissions focused on the role of the placenta in fetal programming are also welcomed.

Dr. Karen Jonscher
Dr. Marisol Castillo-Castrejon
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • fetal programming
  • maternal environmental exposures
  • paternal
  • epigenetics
  • innate immune memory
  • microbiome
  • adult disease risk

Published Papers (2 papers)

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Research

18 pages, 3388 KiB  
Article
Maternal Exercise Prior to and during Gestation Induces Sex-Specific Alterations in the Mouse Placenta
by Meghan L. Ruebel, Sarah J. Borengasser, Ying Zhong, Ping Kang, Jennifer Faske and Kartik Shankar
Int. J. Mol. Sci. 2023, 24(22), 16441; https://doi.org/10.3390/ijms242216441 - 17 Nov 2023
Viewed by 960
Abstract
While exercise (EX) during pregnancy is beneficial for both mother and child, little is known about the mechanisms by which maternal exercise mediates changes in utero. Six-week-old female C57BL/6 mice were divided into two groups: with (exercise, EX; N = 7) or without [...] Read more.
While exercise (EX) during pregnancy is beneficial for both mother and child, little is known about the mechanisms by which maternal exercise mediates changes in utero. Six-week-old female C57BL/6 mice were divided into two groups: with (exercise, EX; N = 7) or without (sedentary, SED; N = 8) access to voluntary running wheels. EX was provided via 24 h access to wheels for 10 weeks prior to conception until late pregnancy (18.5 days post coitum). Sex-stratified placentas and fetal livers were collected. Microarray analysis of SED and EX placentas revealed that EX affected gene transcript expression of 283 and 661 transcripts in male and female placentas, respectively (±1.4-fold, p < 0.05). Gene Set Enrichment and Ingenuity Pathway Analyses of male placentas showed that EX led to inhibition of signaling pathways, biological functions, and down-regulation of transcripts related to lipid and steroid metabolism, while EX in female placentas led to activation of pathways, biological functions, and gene expression related to muscle growth, brain, vascular development, and growth factors. Overall, our results suggest that the effects of maternal EX on the placenta and presumably on the offspring are sexually dimorphic. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying the Fetal Programming of Adult Disease)
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13 pages, 2263 KiB  
Article
Decreased Pyruvate but Not Fatty Acid Driven Mitochondrial Respiration in Skeletal Muscle of Growth Restricted Fetal Sheep
by Weicheng Zhao, Amy C. Kelly, Rosa I. Luna-Ramirez, Christopher A. Bidwell, Miranda J. Anderson and Sean W. Limesand
Int. J. Mol. Sci. 2023, 24(21), 15760; https://doi.org/10.3390/ijms242115760 - 30 Oct 2023
Cited by 1 | Viewed by 818
Abstract
Fetuses with intrauterine growth restriction (FGR) have impaired oxidative and energy metabolism, with persistent consequences on their postnatal development. In this study, we test the hypothesis that FGR skeletal muscle has lower mitochondrial respiration rate and alters the transcriptomic profiles associated with energy [...] Read more.
Fetuses with intrauterine growth restriction (FGR) have impaired oxidative and energy metabolism, with persistent consequences on their postnatal development. In this study, we test the hypothesis that FGR skeletal muscle has lower mitochondrial respiration rate and alters the transcriptomic profiles associated with energy metabolism in an ovine model. At late gestation, mitochondrial oxygen consumption rates (OCRs) and transcriptome profiles were evaluated in the skeletal muscle collected from FGR and control fetuses. The ex vivo mitochondrial OCRs were reduced (p < 0.01) in permeabilized FGR soleus muscle compared to the control muscle but only with pyruvate as the metabolic substrate. Mitochondrial OCRs were similar between the FGR and control groups for palmitoyl-carnitine (fatty acid-driven) or pyruvate plus palmitoyl-carnitine metabolic substrates. A total of 2284 genes were differentially expressed in the semitendinosus muscle from growth restricted fetuses (false discovery rate (FDR) ≤ 0.05). A pathway analysis showed that the upregulated genes (FGR compared to control) were overrepresented for autophagy, HIF-1, AMPK, and FOXO signaling pathways (all with an FDR < 0.05). In addition, the expression of genes modulating pyruvate’s entry into the TCA cycle was downregulated, whereas the genes encoding key fatty acid oxidation enzymes were upregulated in the FGR muscle. These findings show that FGR skeletal muscle had attenuated mitochondrial pyruvate oxidation, possibly associated with the inability of pyruvate to enter into the TCA cycle, and that fatty acid oxidation might compensate for the attenuated energy metabolism. The current study provided phenotypic and molecular evidence for adaptive deficiencies in FGR skeletal muscle. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying the Fetal Programming of Adult Disease)
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