scholarly journals The Role of MicroRNAs in Mammalian Fertility: From Gametogenesis to Embryo Implantation

2020 ◽  
Vol 21 (2) ◽  
pp. 585 ◽  
Author(s):  
Dessie Salilew-Wondim ◽  
Samuel Gebremedhn ◽  
Michael Hoelker ◽  
Ernst Tholen ◽  
Tsige Hailay ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Ovarian Tissue ◽  
Genetic Regulation ◽  
Adult Life ◽  
Subsequent Development ◽  
Early Embryo ◽  
Regulatory Mechanisms ◽  
Developmental Processes ◽  
Transcriptional Regulatory Mechanisms

The genetic codes inscribed during two key developmental processes, namely gametogenesis and embryogenesis, are believed to determine subsequent development and survival of adult life. Once the embryo is formed, its further development mainly depends on its intrinsic characteristics, maternal environment (the endometrial receptivity), and the embryo–maternal interactions established during each phase of development. These developmental processes are under strict genetic regulation that could be manifested temporally and spatially depending on the physiological and developmental status of the cell. MicroRNAs (miRNAs), one of the small non-coding classes of RNAs, approximately 19–22 nucleotides in length, are one of the candidates for post-transcriptional developmental regulators. These tiny non-coding RNAs are expressed in ovarian tissue, granulosa cells, testis, oocytes, follicular fluid, and embryos and are implicated in diverse biological processes such as cell-to-cell communication. Moreover, accumulated evidences have also highlighted that miRNAs can be released into the extracellular environment through different mechanisms facilitating intercellular communication. Therefore, understanding miRNAs mediated regulatory mechanisms during gametogenesis and embryogenesis provides further insights about the molecular mechanisms underlying oocyte/sperm formation, early embryo development, and implantation. Thus, this review highlights the role of miRNAs in mammalian gametogenesis and embryogenesis and summarizes recent findings about miRNA-mediated post-transcriptional regulatory mechanisms occurring during early mammalian development.

The impact of Traditional Chinese Medicine on mitophagy in disease models

2021 ◽  
Vol 27 ◽  
Author(s):  
Li-Ping Yu ◽  
Ting-Ting Shi ◽  
Yan-Qin Li ◽  
Jian-Kang Mu ◽  
Ya-Qin Yang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Molecular Mechanisms ◽  
Human Diseases ◽  
Regulatory Mechanisms ◽  
Disease Models ◽  
Relationship Of ◽  
The Impact ◽  
The Relationship

: Mitophagy plays an important role in maintaining mitochondrial quality and cell homeostasis through the degradation of damaged, aged, and dysfunctional mitochondria and misfolded proteins. Many human diseases, particularly neurodegenerative diseases, are related to disorders of mitochondrial phagocytosis. Exploring the regulatory mechanisms of mitophagy is of great significance for revealing the molecular mechanisms underlying the related diseases. Herein, we summarize the major mechanisms of mitophagy, the relationship of mitophagy with human diseases, and the role of traditional Chinese medicine (TCM) in mitophagy. These discussions enhance our knowledge of mitophagy and its potential therapeutic targets using TCM.

scholarly journals ROLE OF INNATE IMMUNITY FACTORS IN PERIODONTITIS PATHOGENESIS

2016 ◽  
pp. 100-107 ◽  
Author(s):  
L. V. Gankovskaya ◽  
N. M. Khelminskaya ◽  
E. A. Molchanova ◽  
O. A. Svitich
Keyword(s):  
Innate Immunity ◽  
Molecular Mechanisms ◽  
Subsequent Development ◽  
Cell Populations ◽  
Immune Protection ◽  
Local Inflammation ◽  
Tissue Destruction ◽  
Inflammation Reaction ◽  
Pro Inflammatory Cytokines

Chronic generalized periodontitis (CGP) is a disease of periodontium tissues supporting tooth induced by bacteria, that is characterized by the presence of processes of inflammation with destruction ofbone tissue. The knowledge of molecular mechanisms of CGP pathogenesis facilitates creation of the most effective methods of therapy of this disease. Bacterial infection is a primary factor in periodontitis etiology, however is not sufficient for its start and subsequent development. It is known, that bacterial factors induce a local inflammation reaction and activate the system of innate immunity through activation of Toll-like receptors (TLR), located on the surface of resident cells and leukocytes. Activation of these cells results in production of pro-inflammatory cytokines and recruitment of phagocytes and lymphocytes into the inflammation zone. In review we examined the known data regarding factors of immune protection of periodontium including cell populations and cytokines, as well as mechanisms of tissue destruction, that support the tooth. Perspectives of therapy are also discussed.

scholarly journals HIV Tat controls RNA Polymerase II and the epigenetic landscape to transcriptionally reprogram target immune cells

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Jonathan E Reeder ◽  
Youn-Tae Kwak ◽  
Ryan P McNamara ◽  
Christian V Forst ◽  
Iván D'Orso
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Immune Cells ◽  
Rna Structure ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Regulatory Mechanisms ◽  
Messenger Rnas ◽  
Transcriptional Regulatory Mechanisms ◽  
Cellular Transcription

HIV encodes Tat, a small protein that facilitates viral transcription by binding an RNA structure (trans-activating RNA [TAR]) formed on nascent viral pre-messenger RNAs. Besides this well-characterized mechanism, Tat appears to modulate cellular transcription, but the target genes and molecular mechanisms remain poorly understood. We report here that Tat uses unexpected regulatory mechanisms to reprogram target immune cells to promote viral replication and rewire pathways beneficial for the virus. Tat functions through master transcriptional regulators bound at promoters and enhancers, rather than through cellular ‘TAR-like’ motifs, to both activate and repress gene sets sharing common functional annotations. Despite the complexity of transcriptional regulatory mechanisms in the cell, Tat precisely controls RNA polymerase II recruitment and pause release to fine-tune the initiation and elongation steps in target genes. We propose that a virus with a limited coding capacity has optimized its genome by evolving a small but ‘multitasking’ protein to simultaneously control viral and cellular transcription.

scholarly journals The Dual Role of TGFβ in Human Cancer: From Tumor Suppression to Cancer Metastasis

2012 ◽  
Vol 2012 ◽  
pp. 1-28 ◽  
Author(s):  
Jean-Charles Neel ◽  
Laure Humbert ◽  
Jean-Jacques Lebrun
Keyword(s):  
Cell Growth ◽  
Cancer Progression ◽  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Transforming Growth Factor ◽  
Human Cancer ◽  
Adult Life ◽  
Dual Role

The transforming growth factor-beta (TGFβ) superfamily encompasses widespread and evolutionarily conserved polypeptide growth factors that regulate and orchestrate growth and differentiation in all cell types and tissues. While they regulate asymmetric cell division and cell fate determination during early development and embryogenesis, TGFβ family members play a major regulatory role in hormonal and immune responses, cell growth, cell death and cell immortalization, bone formation, tissue remodeling and repair, and erythropoiesis throughout adult life. The biological and physiological functions of TGFβ, the founding member of this family, and its receptors are of central importance to human diseases, particularly cancer. By regulating cell growth, death, and immortalization, TGFβ signaling pathways exert tumor suppressor effects in normal cells and early carcinomas. Thus, it is not surprising that a high number of human tumors arise due to mutations or deletions in the genes coding for the various TGFβ signaling components. As tumors develop and progress, these protective and cytostatic effects of TGFβ are often lost. TGFβ signaling then switches to promote cancer progression, invasion, and tumor metastasis. The molecular mechanisms underlying this dual role of TGFβ in human cancer will be discussed in depth in this paper, and it will highlight the challenge and importance of developing novel therapeutic strategies specifically aimed at blocking the prometastatic arm of the TGFβ signaling pathway without affecting its tumor suppressive effects.

Apoptosis in health and disease

2010 ◽  
pp. 177-188
Author(s):  
Andrew H. Wyllie ◽  
Mark J. Arends
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
Cytotoxic T Cells ◽  
Single Cells ◽  
Critical Role ◽  
Adult Life ◽  
Early Embryo ◽  
Cellular Processes ◽  
Living Tissues

Apoptosis is the process by which single cells die in the midst of living tissues. It is responsible for most—perhaps all—of the cell-death events that occur during the formation of the early embryo and the sculpting and moulding of organs. Apoptotic cell death continues to play a critical role in the maintenance of cell numbers in those tissues in which cell turnover persists into adult life, such as the epithelium of the gastrointestinal tract, the bone marrow, and lymphoid system including both B- and T-cell lineages. Apoptosis is the usual mode of death in the targets of natural killer (NK) cells and cytotoxic T-cells, and in involution and atrophy induced by hormonal and other stimuli. It also appears in the reaction of many tissues to injury, including mild degrees of ischaemia, exposure to ionizing and ultraviolet radiation, or treatment with cancer chemotherapeutic drugs. Excessive or too little apoptosis play a significant part in the pathogenesis of autoimmunity, infectious disease, AIDS, stroke, myocardial disease, and cancer. When cancers regress, apoptosis is part of the mechanism involved. Here the cellular processes and molecular mechanisms of apoptosis are set out, together with a conspectus of its involvement in many diseases....

scholarly journals Divergence in alternative polyadenylation contributes to gene regulatory differences between humans and chimpanzees

2020 ◽  
Author(s):  
Briana Mittleman ◽  
Sebastian Pott ◽  
Shane Warland ◽  
Kenneth Barr ◽  
Claudia Cuevas ◽  
...  
Keyword(s):  
Protein Expression ◽  
Species Differences ◽  
Genetic Regulation ◽  
Alternative Polyadenylation ◽  
Transcript Level ◽  
Protein Translation ◽  
Regulatory Mechanisms ◽  
Genomic Studies ◽  
Gene Regulatory ◽  
Transcriptional Regulatory Mechanisms

AbstractComparative functional genomic studies have shown that differences in gene expression between species can often be explained by corresponding inter-species differences in genetic and epigenetic regulatory mechanisms. In the quest to understand gene regulatory evolution in primates, the role of co-transcriptional regulatory mechanisms, such as alternative polyadenylation (APA), have so far received little attention. To begin addressing this gap, we studied APA in lymphoblastoid cell lines from six humans and six chimpanzees, and estimated usage for 44,432 polyadenylation sites (PAS) in 9,518 genes in both species. While APA is largely conserved in humans and chimpanzees, we identified 1,705 genes with significantly different PAS usage (FDR of 0.05) between the two species. We found that genes with divergent APA patterns are enriched among differentially expressed genes, as well as among genes that show differences in protein translation between species. In particular, differences in APA between humans and chimpanzees can explain a subset of observed inter-species protein expression differences that do not display corresponding differences at the transcript level. Finally, we focused on genes that have a dominant PAS, namely a PAS that is used more often than all others. Dominant PAS are highly conserved, and inter-species differences in dominant PAS are particularly enriched for genes that also show expression differences between the species. This study establishes APA as another key mechanism underlying the genetic regulation of transcript and protein expression levels in primates.

scholarly journals The Role of Non-Coding RNA in Congenital Heart Diseases

2019 ◽  
Vol 6 (2) ◽  
pp. 15 ◽  
Author(s):  
Angel Dueñas ◽  
Almudena Expósito ◽  
Amelia Aranega ◽  
Diego Franco
Keyword(s):  
Congenital Heart ◽  
Heart Diseases ◽  
Regulatory Mechanisms ◽  
Congenital Heart Diseases ◽  
Cardiovascular Development ◽  
Transcriptional Regulatory ◽  
Non Coding Rnas ◽  
Transcriptional Regulatory Mechanisms ◽  
The Impact

Cardiovascular development is a complex developmental process starting with the formation of an early straight heart tube, followed by a rightward looping and the configuration of atrial and ventricular chambers. The subsequent step allows the separation of these cardiac chambers leading to the formation of a four-chambered organ. Impairment in any of these developmental processes invariably leads to cardiac defects. Importantly, our understanding of the developmental defects causing cardiac congenital heart diseases has largely increased over the last decades. The advent of the molecular era allowed to bridge morphogenetic with genetic defects and therefore our current understanding of the transcriptional regulation of cardiac morphogenesis has enormously increased. Moreover, the impact of environmental agents to genetic cascades has been demonstrated as well as of novel genomic mechanisms modulating gene regulation such as post-transcriptional regulatory mechanisms. Among post-transcriptional regulatory mechanisms, non-coding RNAs, including therein microRNAs and lncRNAs, are emerging to play pivotal roles. In this review, we summarize current knowledge on the functional role of non-coding RNAs in distinct congenital heart diseases, with particular emphasis on microRNAs and long non-coding RNAs.

GASOTRANSMITTERS IN THE REGULATION OF THE FUNCTIONS OF THE INTRAORGANIC BLOOD VESSELS OF THE UTERUS

2020 ◽  
pp. 98-111
Author(s):  
В. М. Черток ◽  
И. А. Храмова ◽  
А. Е. Коцюба
Keyword(s):  
Blood Vessels ◽  
Molecular Mechanisms ◽  
Capillary Permeability ◽  
Smooth Muscles ◽  
General System ◽  
Regulatory Mechanisms ◽  
Main Element ◽  
Adequate Blood Supply ◽  
The One

Несмотря на то, что внутриорганное кровеносное русло является основным звеном для адекватного кровоснабжения органных структур, в матке ее строение, функции и механизмы регуляции во многом не изучены. В обзоре представлены данные литературы и собственные материалы по локализации и распределению газотрансмиттеров во внутриорганных сосудах матки. Рассматриваются клеточные и молекулярные механизмы участия NO, СО и HS в регуляции функций этих сосудов. Приведенные материалы, с одной стороны, подчеркивают значимость данных сигнальных молекул в регуляции сократимости гладких мышц сосудов, проницаемости капилляров, с другой - указывают на необходимость дальнейших исследований роли газотрансмиттеров в общей системе регуляции гемодинамики матки. Despite the fact that the intraorganic circulatory bed is the main element providing adequate blood supply to organ structures, its structure, functions and regulatory mechanisms in the uterus are largely unknown. The review presents the literature data and own materials on the localization and distribution of gasotransmitters in the intraorganic vessels of the uterus. The cellular and molecular mechanisms of the participation of NO, CO and H2S in the regulation of the function of these vessels are rewieved. On the one hand, these materials emphasize the importance of these signaling molecules in the regulation of contractility of the smooth muscles of the blood vessels and capillary permeability, on the other hand, point out the need for further studies of the role of gasotransmitters in the general system of uterine hemodynamic regulation.

scholarly journals Role of IL-10-Producing Natural Killer Cells in the Regulatory Mechanisms of Inflammation during Systemic Infection

Biomolecules ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 4
Author(s):  
Israel Martinez-Espinosa ◽  
José A. Serrato ◽  
Blanca Ortiz-Quintero
Keyword(s):  
Nk Cells ◽  
Natural Killer ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Systemic Infection ◽  
Regulatory Mechanisms ◽  
Infection Model ◽  
Immune Mediated ◽  
Model Understanding

Natural killer (NK) cells have the dual ability to produce pro-inflammatory (IFNγ) and anti-inflammatory (IL-10) cytokines during systemic infection, which points to their crucial role both as inflammatory effectors for infection clearance and as regulators to counterbalance inflammation to limit immune-mediated damage to the host. In particular, immunosuppressive IL-10 secretion by NK cells has been described to occur in systemic, but not local, infections as a recent immunoregulatory mechanism of inflammation that may be detrimental or beneficial, depending on the timing of release, type of disease, or the infection model. Understanding the factors that drive the production of IL-10 by NK cells and their impact during dualistic inflammatory states, such as sepsis and other non-controlled inflammatory diseases, is relevant for achieving effective therapeutic advancements. In this review, the evidence regarding the immunoregulatory role of IL-10-producing NK cells in systemic infection is summarized and discussed in detail, and the potential molecular mechanisms that drive IL-10 production by NK cells are considered.

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