Vascular Smooth Muscle Cells Mechanosensitive Regulators and Vascular Remodeling

Liu, Shangmin; Lin, Zhanyi

doi:10.1159/000519845

Cited by 38 publications

(20 citation statements)

References 282 publications

(322 reference statements)

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“…Amongst the biochemical changes occurring in this common metabolic disorder, matrix protein glycation, as well as matrix protein deposition, potentially affects all cellular elements of the vascular wall. As many molecules residing in the extracellular matrix (ECM) are now accepted to participate in active signaling pathways in vascular cells ( Davis et al, 2001 ; Davis et al, 2002 ; Martinez-Lemus et al, 2003 ; Malinin et al, 2012 ; Finney et al, 2017 ; Liu and Lin, 2021 ) it is likely that matrix protein modification impacts normal vessel function.…”

Section: Introductionmentioning

confidence: 99%

Modification of Fibronectin by Non-Enzymatic Glycation Impairs K+ Channel Function in Rat Cerebral Artery Smooth Muscle Cells

Yang¹,

Nourian²,

Li³

et al. 2022

Front. Physiol.

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Fibronectin (FN) enhances K+ channel activity by integrin-mediated mechanisms. As vascular smooth muscle (VSM) K+ channels mediate vasodilation, we hypothesized that modification of fibronectin, via advanced non-enzymatic glycation, would alter signaling of this extracellular matrix protein through these channels. Bovine FN (1 mg/ml) was glycated (gFN) for 5 days using methylglyoxal (50 mM), and albumin was similarly glycated as a non-matrix protein control. VSM cells were isolated from rat cerebral arteries for measurement of macroscopic K+ channel activity using whole cell patch clamp methodology. Pharmacological inhibitors, iberiotoxin (0.1 μM) and 4-aminopyridine (0.1 mM), were used to identify contributions of large-conductance, Ca2+-activated, K+ channels and voltage-gated K+ channels, respectively. Compared with baseline, native FN enhanced whole cell K+ current in a concentration-dependent manner, whereas gFN inhibited basal current. Furthermore, native albumin did not enhance basal K+ current, but the glycated form (gAlb) caused inhibition. gFN was shown to impair both the Kv and BKCa components of total macroscopic K+ current. Anti-integrin α5 and β1 antibodies attenuated the effects of both FN and gFN on macroscopic K+ current at +70 mV. Consistent with an action on BKCa activity, FN increased, whereas gFN decreased the frequency of spontaneous transient outward current (STOCs). In contrast, gAlb inhibited whole cell K+ current predominantly through Kv, showing little effect on STOCs. A function-blocking, anti-RAGE antibody partially reversed the inhibitory effects of gFN, suggesting involvement of this receptor. Further, gFN caused production of reactive oxygen species (ROS) by isolated VSMCs as revealed by the fluorescent indicator, DHE. Evoked ROS production was attenuated by the RAGE blocking antibody. Collectively, these studies identify ion channel-related mechanisms (integrin and ROS-mediated) by which protein glycation may modify VSMC function.

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Section: Introductionmentioning

confidence: 99%

Modification of Fibronectin by Non-Enzymatic Glycation Impairs K+ Channel Function in Rat Cerebral Artery Smooth Muscle Cells

Yang¹,

Nourian²,

Li³

et al. 2022

Front. Physiol.

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“…Histone modifications are shown to be involved in vascular homeostasis (regulated by the KLF2 gene) [ 105 ], the interaction between endothelial cells and vessel wall reactive oxygen species [ 106 ], vascular remodeling in response to laminar stress flow [ 107 ], and vascular endothelial response to hypoxia [ 17 , 108 ].…”

Section: Discussion and Future Challengesmentioning

confidence: 99%

The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

Butnariu

Gorduza

Florea

et al. 2022

IJMS

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Lower extremity artery disease (LEAD), caused by atherosclerotic obstruction of the arteries of the lower limb extremities, has exhibited an increase in mortality and morbidity worldwide. The phenotypic variability of LEAD is correlated with its complex, multifactorial etiology. In addition to traditional risk factors, it has been shown that the interaction between genetic factors (epistasis) or between genes and the environment potentially have an independent role in the development and progression of LEAD. In recent years, progress has been made in identifying genetic variants associated with LEAD, by Genome-Wide Association Studies (GWAS), Whole Exome Sequencing (WES) studies, and epigenetic profiling. The aim of this review is to present the current knowledge about the genetic factors involved in the etiopathogenic mechanisms of LEAD, as well as possible directions for future research. We analyzed data from the literature, starting with candidate gene-based association studies, and then continuing with extensive association studies, such as GWAS and WES. The results of these studies showed that the genetic architecture of LEAD is extremely heterogeneous. In the future, the identification of new genetic factors will allow for the development of targeted molecular therapies, and the use of polygenic risk scores (PRS) to identify individuals at an increased risk of LEAD will allow for early prophylactic measures and personalized therapy to improve their prognosis.

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“…The aortic wall mainly includes the inner layer, middle layer, and outer layer. Vascular smooth muscle cells (VSMCs), elastic fibers, and collagen fibers constitute the middle layer of the aortic wall [ 35 , 36 , 37 ].…”

Section: Overview Of Admentioning

confidence: 99%

Emerging Role of Non-Coding RNAs in Aortic Dissection

Ding

Liu

et al. 2022

Biomolecules

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Aortic dissection (AD) is a fatal cardiovascular acute disease with high incidence and mortality, and it seriously threatens patients’ lives and health. The pathogenesis of AD mainly includes vascular inflammation, extracellular matrix degradation, and phenotypic conversion as well as apoptosis of vascular smooth muscle cells (VSMCs); however, its detailed mechanisms are still not fully elucidated. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are an emerging class of RNA molecules without protein-coding ability, and they play crucial roles in the progression of many diseases, including AD. A growing number of studies have shown that the dysregulation of ncRNAs contributes to the occurrence and development of AD by modulating the expression of specific target genes or the activity of related proteins. In addition, some ncRNAs exhibit great potential as promising biomarkers and therapeutic targets in AD treatment. In this review, we systematically summarize the recent findings on the underlying mechanism of ncRNA involved in AD regulation and highlight their clinical application as biomarkers and therapeutic targets in AD treatment. The information reviewed here will be of great benefit to the development of ncRNA-based therapeutic strategies for AD patients.

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Vascular Smooth Muscle Cells Mechanosensitive Regulators and Vascular Remodeling

Cited by 38 publications

References 282 publications

Modification of Fibronectin by Non-Enzymatic Glycation Impairs K+ Channel Function in Rat Cerebral Artery Smooth Muscle Cells

Modification of Fibronectin by Non-Enzymatic Glycation Impairs K+ Channel Function in Rat Cerebral Artery Smooth Muscle Cells

The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

Emerging Role of Non-Coding RNAs in Aortic Dissection

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