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Cells
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Select Topics in Molecular and Cellular Mechanisms of Mammalian Reproduction
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Select Topics in Molecular and Cellular Mechanisms of Mammalian Reproduction

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Reproductive Cells and Development".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 2123

Special Issue Editors

Dr. Zhengui Zheng

E-Mail Website
Guest Editor
Department of Physiology, Southern Illinois University Carbondale, Carbondale, IL 62901, USA
Interests: sexually dimorphic development of external genitalia; sexually dimorphic limb and brain development and behavior; role of environmental endocrine disrupting chemicals on reproductive organ development
Dr. Brent M. Bany

E-Mail Website
Guest Editor
Department of Physiology, Southern Illinois University Carbondale, Carbondale, IL 62901, USA
Interests: development of the decidua during early pregnancy; mechanism of transdifferentiation of rodent and human endometrial fibroblasts into decidual cells; interactions between the conceptus and components of the endometrium (immune, vascular endothelial, decidual cells) during implantation and placental development
Dr. Liang Ma

E-Mail Website
Guest Editor
Department of Medicine, Division of Dermatology, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA
Interests: the development and function of the female reproductive tract; transcription factors regulating uterine epithelial differentiation and uterine decidualization; genetic mechanism of external genital development; spermatogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

All living organisms must reproduce in some way. In mammals, the reproductive process includes the formation and maturation of the sperm (males) and eggs (females), fertilization, implantation, and embryonic/placental/fetal development, parturition and lactation. The molecular and cellular mechanisms of these processes are largely unknown. The major organs of the reproductive system include external genitalia (penis and vulva) and some internal organs, including the gonads (testes and ovaries), which produce gametes. The cellular and molecular mechanisms underlying these developmental and reproductive organ functions are limited in many areas. Further, genetic factors, hormones and environmental endocrine-disrupting chemicals all have major impacts on reproduction, and human reproductive disorders are very common and widespread. It is essential to study the cellular and molecular mechanisms of not only the reproductive processes of reproductive organs, but also their development. Against this background, this Special Issue aims to provide an overview of advances in reproduction, with a particular focus on cellular and molecular mechanisms underlying reproductive organ development and their reproductive processes required for the successful procreation of mammalian species. Research articles and reviews summarizing the state of the art on special topics in this broad area are welcome. Potential topics include, but are not limited to, mechanisms of reproductive organ formation, sexual differentiation and function.

Furthermore, genetic and/or hormonal control of reproductive organ development, sexual differentiation, and function, fertilization, implantation, placentation, parturition and lactation are also of relevance. This can include, but is not limited to, studies linking molecular mechanisms to reproductive organ-related human disease, and also studies that include whole-genome genetic or epigenomic analyses.

Dr. Zhengui Zheng
Dr. Brent M. Bany
Dr. Liang Ma
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • reproductive organ development
  • sexual differentiation
  • reproductive tract function
  • fertilization
  • implantation
  • placentation
  • parturition
  • lactation

Published Papers (2 papers)

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Research

19 pages, 2196 KiB  
Article
HDAC1-Mediated lncRNA Stimulatory Factor of Follicular Development to Inhibit the Apoptosis of Granulosa Cells and Regulate Sexual Maturity through miR-202-3p-COX1 Axis
by Xiaofeng Zhou, Yingting He, Hongyan Quan, Xiangchun Pan, Yinqi Zhou, Zhe Zhang, Xiaolong Yuan and Jiaqi Li
Cells 2023, 12(23), 2734; https://doi.org/10.3390/cells12232734 - 29 Nov 2023
Cited by 2 | Viewed by 826
Abstract
Abnormal sexual maturity exhibits significant detrimental effects on adult health outcomes, and previous studies have indicated that targeting histone acetylation might serve as a potential therapeutic approach to regulate sexual maturity. However, the mechanisms that account for it remain to be further elucidated. [...] Read more.
Abnormal sexual maturity exhibits significant detrimental effects on adult health outcomes, and previous studies have indicated that targeting histone acetylation might serve as a potential therapeutic approach to regulate sexual maturity. However, the mechanisms that account for it remain to be further elucidated. Using the mouse model, we showed that Trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, downregulated the protein level of Hdac1 in ovaries to promote the apoptosis of granulosa cells (GCs), and thus arrested follicular development and delayed sexual maturity. Using porcine GCs as a cell model, a novel sexual maturity-associated lncRNA, which was named as the stimulatory factor of follicular development (SFFD), transcribed from mitochondrion and mediated by HDAC1, was identified using RNA sequencing. Mechanistically, HDAC1 knockdown significantly reduced the H3K27ac level at the −953/−661 region of SFFD to epigenetically inhibit its transcription. SFFD knockdown released miR-202-3p to reduce the expression of cyclooxygenase 1 (COX1), an essential rate-limited enzyme involved in prostaglandin synthesis. This reduction inhibited the proliferation and secretion of 17β-estradiol (E2) while promoting the apoptosis of GCs. Consequently, follicular development was arrested and sexual maturity was delayed. Taken together, HDAC1 knockdown-mediated SFFD downregulation promoted the apoptosis of GCs through the miR-202-3p-COX1 axis and lead to delayed sexual maturity. Our findings reveal a novel regulatory network modulated by HDAC1, and HDAC1-mediated SFFD may be a promising new therapeutic target to treat delayed sexual maturity. Full article
(This article belongs to the Special Issue Select Topics in Molecular and Cellular Mechanisms of Mammalian Reproduction)
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12 pages, 4389 KiB  
Article
Lysophosphatidic Acid Signalling Regulates Human Sperm Viability via the Phosphoinositide 3-Kinase/AKT Pathway
by Hao-Yu Liao and Cristian O’Flaherty
Cells 2023, 12(17), 2196; https://doi.org/10.3390/cells12172196 - 02 Sep 2023
Viewed by 1016
Abstract
Lysophosphatidic acid (LPA) signalling is essential for maintaining germ cell viability during mouse spermatogenesis; however, its role in human spermatozoa is unknown. We previously demonstrated that peroxiredoxin 6 (PRDX6) calcium-independent phospholipase A2 (iPLA2) releases lysophospholipids such as LPA or arachidonic [...] Read more.
Lysophosphatidic acid (LPA) signalling is essential for maintaining germ cell viability during mouse spermatogenesis; however, its role in human spermatozoa is unknown. We previously demonstrated that peroxiredoxin 6 (PRDX6) calcium-independent phospholipase A2 (iPLA2) releases lysophospholipids such as LPA or arachidonic acid (AA) and that inhibiting PRDX6 iPLA2 activity impairs sperm cell viability. The exogenous addition of LPA bypassed the inhibition of PRDX6 iPLA2 activity and maintained the active phosphoinositide 3-kinase (PI3K)/AKT pathway. Here, we aimed to study PI3K/AKT pathway regulation via LPA signalling and protein kinases in maintaining sperm viability. The localization of LPARs in human spermatozoa was determined using immunocytochemistry, and P-PI3K and P-AKT substrate phosphorylations via immunoblotting. Sperm viability was determined using the hypo-osmotic swelling test. LPAR1, 3, 5 and 6 were located on the sperm plasma membrane. The inhibition of LPAR1-3 with Ki16425 promoted the impairment of sperm viability and decreased the phosphorylation of PI3K AKT substrates. Inhibitors of PKC, receptor-type PTK and PLC impaired sperm viability and the PI3K/AKT pathway. Adding 1-oleoyl-2-acetyl-snglycerol (OAG), a cell-permeable analog of diacylglycerol (DAG), prevented the loss of sperm viability and maintained the phosphorylation of PI3K. In conclusion, human sperm viability is supported by LPAR signalling and regulated by PLC, PKC and RT-PTK by maintaining phosphorylation levels of PI3K and AKT substrates. Full article
(This article belongs to the Special Issue Select Topics in Molecular and Cellular Mechanisms of Mammalian Reproduction)
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