What Is The Function Of Smooth Muscle Cells – NLRP3 inflammasome activation increases IL-1β levels and reduces GLUT4 transcription in skeletal muscle during insulin resistance

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What Is The Function Of Smooth Muscle Cells

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Exploring The Role Of Hypoxia Inducible Factors In Vascular Smooth Muscle Cells Under Panvascular Pathologies

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By Immanuel D. Green Immanuel D. Green Scilit Preprints.org Google Scholar 1, 2, Renjing Liu Renjing Liu Scilit Preprints.org Google Scholar 3 and Justin J. L. Wang Justin J. L. Wang Scilit Preprints.org Google Scholar 1, 2 , *

Disease Relevant Transcriptional Signatures Identified In Individual Smooth Muscle Cells From Healthy Mouse Vessels

Received: 19 August 2021 / Revised: 15 September 2021 / Accepted: 18 September 2021 / Published: 23 September 2021

Vascular smooth muscle cells (VSMCs) show extraordinary phenotypic plasticity. This allows them to differentiate or differentiate, depending on environmental cues. The ability to “switch” between a quiescent contractile phenotype to a highly proliferative synthetic state renders VSMCs as primary mediators of neural repair and regeneration. When their plasticity is pathological, it can lead to cardiovascular diseases such as atherosclerosis and retinosis. Coinciding with significant technological and conceptual innovations in RNA biology, there is a growing focus on the role of alternative splicing in the regulation of VSMC gene expression. Here, we review how alternative splicing and its regulatory factors are involved in generating protein diversity and altering gene expression levels in VSMC plasticity. In addition, we explore how recent advances in the development of differentiation-modulating therapies can be applied to VSMC-related pathologies.

The ability of mature cells to differentiate is a rare phenomenon in normal physiology. Once a cell is committed to a particular fate or identity, there is a very limited capacity to revert to that developmental state. This process ensures proper somatic cell production, development and function. However, vascular smooth muscle cells (VSMCs) are an exception. They show extraordinary phenotypic plasticity that enables them to differentiate or differentiate based on environmental cues. A prime example of this phenomenon occurs after injury to blood vessels, where differentiated VSMCs respond by differentiating, replicating, and migrating to the site of injury to initiate repair. Similarly, angiogenesis, the formation of new blood vessels, is characterized by highly plastic VSMCs that interact with endothelial cells to generate new vascular networks. As such, the ability to “switch” between a quiescent contractile phenotype to a highly proliferative synthetic state renders VSMCs as primary mediators of neural repair and regeneration [ 1 , 2 , 3 , 4 , 5 ].

Differentiated VSMCs have a characteristic contractile phenotype under physiological conditions. Including the tunica media, these VSMCs control local hemodynamics through coordinated contraction. In arteries and in culture, differentiated VSMCs are enriched with pro-contractile proteins, such as smooth muscle alpha-actin 2 (ACTA2) and transgellin (TAGLN), and Ca

A: Structure And Function Of The Muscular System

Ion channels and signaling factors [1, 6]. They express low levels of proliferative and extracellular matrix (ECM) proteins, and are quiescent and largely non-migratory (Figure 1). The contraction state is accompanied by an isolated or synthetic phenotype. Differentiated VSMCs undergo differentiation in response to a flood of stimulatory factors, resulting in damage to the vasculature. These include widely altered local hemodynamics, biomechanical stress, growth factors, cytokines, inflammatory cell mediators, ECM, lipids and reactive oxygen species [ 7 , 8 , 9 ].

VSMC phenotypic plasticity is critical after mechanical injury of the artery, particularly during angioplasty and/or stenting. This results in a new time thickening, forming a new layer near the media (Figure 1) [3, 10, 11, 12]. In these conditions, VSMCs form a large part of the thickened neointima in the affected vessels, which severely narrows the lumen [ 3 , 4 , 5 ]. Neointimal thickening after physical injury involves the initial proliferation and migration of VSMCs, and is subsequently dominated by a select few (and in some cases, an individual cell) that undergoes clonal expansion to form the majority of the neointima [3 , 4, 5].

VSMC phenotypic switching involves multiple processes, from overt morphological and functional changes, to more subtle changes in molecular signaling [ 1 , 2 , 13 , 14 , 15 , 16 ]. These processes are regulated by a series of gene expression control mechanisms. Great strides have been made to understand how transcription factors and epigenetics regulate phenotypic plasticity by altering gene expression. Most of these studies have focused on histone modifications and DNA methylation, and have been extensively reviewed [ 15 , 17 ]. Consistent with significant technological and conceptual innovations in RNA biology, there is a growing focus on the co-transcriptional processes that regulate gene expression in VSMCs. In particular, alternative splicing (AS) of mRNAs and its regulatory factors have been investigated in various physiological and pathological VSMC conditions [ 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ]. Collectively, these studies have revealed an expanding role of AS and splicing factors in promoting protein diversity and regulating gene expression in VSMC biology. In this review, we highlight key findings from such work and discuss the implications of AS in healthy and pathological VSMC states. Furthermore, we are critically evaluating potential ways of modulating AS in VSMCs for therapeutic benefit.

During replication from DNA in eukaryotes, nosic pre-mRNAs arise first in their sequence with protein-coding exons and non-coding introns. To generate mature mRNA transcripts for subsequent translation into protein, non-coding introns must be spliced ​​out by intramolecular splicing. It produces mature mRNAs that contain only exogenous sequences, ready for translation. When mature mRNAs have exons occurring in the same order as their precursor mRNA, this form of splicing is constitutive. Since the splicing of introns is an energy-intensive process, the evolution of introns and their conservation in eukaryotic biology continues to increase in research, discussion, and debate. It has previously been argued that introns impose a “burden” on an organism [ 26 , 27 , 28 ]. It appears that eukaryotic cells spend considerable time and energy maintaining introns in the genome, only to remove them during transcription. As detailed in the last section of this review, it is clear that introns are essential for promoting protein diversity through AS, which facilitates tissue-specific functions in eukaryotes [ 29 , 30 , 31 , 32 ]. Some introns also contain regulatory elements that regulate gene expression, and others can serve as precursors to non-coding RNAs that play a role in a myriad of biological processes [ 33 , 34 , 35 , 36 , 37 ].

Coronary Artery Spasm: The Interplay Between Endothelial Dysfunction And Vascular Smooth Muscle Cell Hyperreactivity

Alternative splicing of mRNA is characterized by differential inclusion or splicing of exons and introns in transcripts. In contrast to constitutive splicing, AS is responsible for the production of multiple mature mRNA isoforms from a single precursor mRNA. This allows the production of multiple proteins from a single gene, meaning that genetic information can be stored and preserved in a more economical fashion. Therefore, AS is recognized as an efficient way to create and maintain biological complexity [ 38 ]. Deep transcriptomic and proteomic analyzes have shown that approximately 95% of human genes are subject to AS, and protein diversity is one of the main sources [ 38 , 39 ]. As such, AS plays a central role in regulating cell function, proliferation, survival and differentiation [11].

There are five main types of AS that cause a range of functional consequences, including changes in mRNA stability, localization and translation (Figure 2). This, in conjunction with changes in mRNA base sequence, can contribute to proteomic diversity or regulate gene expression levels [ 29 , 38 , 40 ]. Many cases of AS can result in truncated mRNA transcription, for example exon exclusion, and alternative 5′ and 3′ splice site selection (Figure 2). Such events, along with mutation-specific exon splicing, are capable of significantly increasing the pool of proteins produced or altering mRNA metabolism. In contrast, intron retention (IR) produces longer transcripts because the internal sequences are preserved in the mature mRNA.

Although initially dismissed as degenerative, IR has now been established as a key mechanism of gene expression control in many cell types, particularly in neuronal and hematopoietic lineages and more recently in VSMCs [ 21 , 41, 42, 43, 44, 45, 46., 47, 48]. IR can result in post-transcriptional gene repression, as many introns contain premature termination codons that facilitate cytoplasmic uncoupling intermediates [ 47 , 49 ]. There can also be erosion

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