scholarly journals LncRNAs Regulatory Networks in Cellular Senescence

2019 ◽  
Vol 20 (11) ◽  
pp. 2615 ◽  
Author(s):  
Pavan Kumar Puvvula
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Regulatory Networks ◽  
Translation Regulation ◽  
Reading Frame ◽  
Downstream Signaling ◽  
Cellular Processes ◽  
Fate Decision ◽  
Functional Mechanisms

Long noncoding RNAs (lncRNAs) are a class of transcripts longer than 200 nucleotides with no open reading frame. They play a key role in the regulation of cellular processes such as genome integrity, chromatin organization, gene expression, translation regulation, and signal transduction. Recent studies indicated that lncRNAs are not only dysregulated in different types of diseases but also function as direct effectors or mediators for many pathological symptoms. This review focuses on the current findings of the lncRNAs and their dysregulated signaling pathways in senescence. Different functional mechanisms of lncRNAs and their downstream signaling pathways are integrated to provide a bird’s-eye view of lncRNA networks in senescence. This review not only highlights the role of lncRNAs in cell fate decision but also discusses how several feedback loops are interconnected to execute persistent senescence response. Finally, the significance of lncRNAs in senescence-associated diseases and their therapeutic and diagnostic potentials are highlighted.

scholarly journals The Role of Autophagy and lncRNAs in the Maintenance of Cancer Stem Cells

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1239
Author(s):  
Leila Jahangiri ◽  
Tala Ishola ◽  
Perla Pucci ◽  
Ricky M. Trigg ◽  
Joao Pereira ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Progression ◽  
Regulatory Networks ◽  
Epithelial To Mesenchymal Transition ◽  
Tumour Microenvironment ◽  
Repair Capacity ◽  
Mesenchymal Transition ◽  
Cellular Processes

Cancer stem cells (CSCs) possess properties such as self-renewal, resistance to apoptotic cues, quiescence, and DNA-damage repair capacity. Moreover, CSCs strongly influence the tumour microenvironment (TME) and may account for cancer progression, recurrence, and relapse. CSCs represent a distinct subpopulation in tumours and the detection, characterisation, and understanding of the regulatory landscape and cellular processes that govern their maintenance may pave the way to improving prognosis, selective targeted therapy, and therapy outcomes. In this review, we have discussed the characteristics of CSCs identified in various cancer types and the role of autophagy and long noncoding RNAs (lncRNAs) in maintaining the homeostasis of CSCs. Further, we have discussed methods to detect CSCs and strategies for treatment and relapse, taking into account the requirement to inhibit CSC growth and survival within the complex backdrop of cellular processes, microenvironmental interactions, and regulatory networks associated with cancer. Finally, we critique the computationally reinforced triangle of factors inclusive of CSC properties, the process of autophagy, and lncRNA and their associated networks with respect to hypoxia, epithelial-to-mesenchymal transition (EMT), and signalling pathways.

S1-1 Role of intrinsic and extrinsic determinants in cell fate decision during neural development

1996 ◽  
Vol 25 ◽  
pp. S2
Author(s):  
Hideyuki Okano ◽  
Kazunobu Sawamoto ◽  
Masataka Okabe ◽  
Takao Imai ◽  
Shin-Ichi Sakakibara ◽  
...  
Keyword(s):  
Cell Fate ◽  
Neural Development ◽  
Cell Fate Decision ◽  
Fate Decision

scholarly journals Chromatin Dynamics in Intestinal Epithelial Homeostasis: A Paradigm of Cell Fate Determination versus Cell Plasticity

2020 ◽  
Vol 16 (6) ◽  
pp. 1062-1080
Author(s):  
Jérémie Rispal ◽  
Fabrice Escaffit ◽  
Didier Trouche
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Chromatin Modification ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Cell Plasticity ◽  
Chromatin Dynamics ◽  
Irritable Bowel ◽  
The Many

AbstractThe rapid renewal of intestinal epithelium is mediated by a pool of stem cells, located at the bottom of crypts, giving rise to highly proliferative progenitor cells, which in turn differentiate during their migration along the villus. The equilibrium between renewal and differentiation is critical for establishment and maintenance of tissue homeostasis, and is regulated by signaling pathways (Wnt, Notch, Bmp…) and specific transcription factors (TCF4, CDX2…). Such regulation controls intestinal cell identities by modulating the cellular transcriptome. Recently, chromatin modification and dynamics have been identified as major actors linking signaling pathways and transcriptional regulation in the control of intestinal homeostasis. In this review, we synthesize the many facets of chromatin dynamics involved in controlling intestinal cell fate, such as stemness maintenance, progenitor identity, lineage choice and commitment, and terminal differentiation. In addition, we present recent data underlying the fundamental role of chromatin dynamics in intestinal cell plasticity. Indeed, this plasticity, which includes dedifferentiation processes or the response to environmental cues (like microbiota’s presence or food ingestion), is central for the organ’s physiology. Finally, we discuss the role of chromatin dynamics in the appearance and treatment of diseases caused by deficiencies in the aforementioned mechanisms, such as gastrointestinal cancer, inflammatory bowel disease or irritable bowel syndrome.

scholarly journals The role of RHOA signaling in trophectoderm cell-fate decision in cattle

2020 ◽  
Vol 528 (4) ◽  
pp. 713-718
Author(s):  
Nanami Kohri ◽  
Hiroki Akizawa ◽  
Sakie Iisaka ◽  
Hanako Bai ◽  
Masashi Takahashi ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Fate Decision ◽  
Fate Decision ◽  
Rhoa Signaling

scholarly journals Retinogenesis of the Human Fetal Retina: An Apical Polarity Perspective

Genes ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 987 ◽  
Author(s):  
Peter M.J. Quinn ◽  
Jan Wijnholds
Keyword(s):  
Stem Cell ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Cell Polarity ◽  
Apical Cell ◽  
Embryonic Stem ◽  
Induced Pluripotent Stem Cell ◽  
Downstream Signaling ◽  
Fetal Retina ◽  
Crumbs Complex

The Crumbs complex has prominent roles in the control of apical cell polarity, in the coupling of cell density sensing to downstream cell signaling pathways, and in regulating junctional structures and cell adhesion. The Crumbs complex acts as a conductor orchestrating multiple downstream signaling pathways in epithelial and neuronal tissue development. These pathways lead to the regulation of cell size, cell fate, cell self-renewal, proliferation, differentiation, migration, mitosis, and apoptosis. In retinogenesis, these are all pivotal processes with important roles for the Crumbs complex to maintain proper spatiotemporal cell processes. Loss of Crumbs function in the retina results in loss of the stratified appearance resulting in retinal degeneration and loss of visual function. In this review, we begin by discussing the physiology of vision. We continue by outlining the processes of retinogenesis and how well this is recapitulated between the human fetal retina and human embryonic stem cell (ESC) or induced pluripotent stem cell (iPSC)-derived retinal organoids. Additionally, we discuss the functionality of in utero and preterm human fetal retina and the current level of functionality as detected in human stem cell-derived organoids. We discuss the roles of apical-basal cell polarity in retinogenesis with a focus on Leber congenital amaurosis which leads to blindness shortly after birth. Finally, we discuss Crumbs homolog (CRB)-based gene augmentation.

scholarly journals Protein Kinases and Their Inhibitors in Pluripotent Stem Cell Fate Regulation

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jungwoon Lee ◽  
Young-Jun Park ◽  
Haiyoung Jung
Keyword(s):  
Stem Cells ◽  
Signaling Pathways ◽  
Protein Kinases ◽  
Cell Fate ◽  
Pluripotent Stem Cells ◽  
Intracellular Signaling ◽  
Regulatory Networks ◽  
Kinase Signaling ◽  
Self Renewal ◽  
Lineage Differentiation

Protein kinases modulate the reversible postmodifications of substrate proteins to their phosphorylated forms as an essential process in regulating intracellular signaling transduction cascades. Moreover, phosphorylation has recently been shown to tightly control the regulatory network of kinases responsible for the induction and maintenance of pluripotency, defined as the particular ability to differentiate pluripotent stem cells (PSCs) into every cell type in the adult body. In particular, emerging evidence indicates that the balance between the self-renewal and differentiation of PSCs is regulated by the small molecules that modulate kinase signaling pathways. Furthermore, new reprogramming technologies have been developed using kinase modulators, which have provided novel insight of the mechanisms underlying the kinase regulatory networks involved in the generation of induced pluripotent stem cells (iPSCs). In this review, we highlight the recent progress made in defining the roles of protein kinase signaling pathways and their small molecule modulators in regulating the pluripotent states, self-renewal, reprogramming process, and lineage differentiation of PSCs.

scholarly journals Stochastic antagonism between two proteins governs a bacterial cell fate switch

Science ◽  
2019 ◽  
Vol 366 (6461) ◽  
pp. 116-120 ◽  
Author(s):  
Nathan D. Lord ◽  
Thomas M. Norman ◽  
Ruoshi Yuan ◽  
Somenath Bakshi ◽  
Richard Losick ◽  
...  
Keyword(s):  
Cell Fate ◽  
Regulatory Networks ◽  
Cell Types ◽  
Feedback Loops ◽  
Cell Fate Determination ◽  
Cell Fate Decision ◽  
A Cell ◽  
Fate Decision ◽  
Antagonistic Interactions

Cell fate decision circuits must be variable enough for genetically identical cells to adopt a multitude of fates, yet ensure that these states are distinct, stably maintained, and coordinated with neighboring cells. A long-standing view is that this is achieved by regulatory networks involving self-stabilizing feedback loops that convert small differences into long-lived cell types. We combined regulatory mutants and in vivo reconstitution with theory for stochastic processes to show that the marquee features of a cell fate switch in Bacillus subtilis—discrete states, multigenerational inheritance, and timing of commitments—can instead be explained by simple stochastic competition between two constitutively produced proteins that form an inactive complex. Such antagonistic interactions are commonplace in cells and could provide powerful mechanisms for cell fate determination more broadly.

scholarly journals Anaphylactic shock depends on endothelial Gq/G11

2009 ◽  
Vol 206 (2) ◽  
pp. 411-420 ◽  
Author(s):  
Hanna Korhonen ◽  
Beate Fisslthaler ◽  
Alexandra Moers ◽  
Angela Wirth ◽  
Daniel Habermehl ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Anaphylactic Shock ◽  
Platelet Activating Factor ◽  
Severe Allergic Reaction ◽  
Downstream Signaling ◽  
Systemic Anaphylaxis ◽  
Multiple Organs ◽  
Nitric Oxide Formation ◽  
G Protein Coupled

Anaphylactic shock is a severe allergic reaction involving multiple organs including the bronchial and cardiovascular system. Most anaphylactic mediators, like platelet-activating factor (PAF), histamine, and others, act through G protein–coupled receptors, which are linked to the heterotrimeric G proteins Gq/G11, G12/G13, and Gi. The role of downstream signaling pathways activated by anaphylactic mediators in defined organs during anaphylactic reactions is largely unknown. Using genetic mouse models that allow for the conditional abrogation of Gq/G11- and G12/G13-mediated signaling pathways by inducible Cre/loxP-mediated mutagenesis in endothelial cells (ECs), we show that Gq/G11-mediated signaling in ECs is required for the opening of the endothelial barrier and the stimulation of nitric oxide formation by various inflammatory mediators as well as by local anaphylaxis. The systemic effects of anaphylactic mediators like histamine and PAF, but not of bacterial lipopolysaccharide (LPS), are blunted in mice with endothelial Gαq/Gα11 deficiency. Mice with endothelium-specific Gαq/Gα11 deficiency, but not with Gα12/Gα13 deficiency, are protected against the fatal consequences of passive and active systemic anaphylaxis. This identifies endothelial Gq/G11-mediated signaling as a critical mediator of fatal systemic anaphylaxis and, hence, as a potential new target to prevent or treat anaphylactic reactions.

Sign in / Sign up

Export Citation Format

Share Document