TRPV1 inhibits smooth muscle cell phenotype switching in a mouse model of abdominal aortic aneurysm

Wang, Shuo; Jia, Chenhong

doi:10.1080/19336950.2020.1730020

Cited by 10 publications

(13 citation statements)

References 37 publications

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“…The transient receptor potential vanilloid (TRPV) family is expressed abundantly in cerebral artery VSMCs and has been shown to be an important mediator of vascular tone ( Guibert et al, 2011 ). The overexpression of TRPV1 has been found to inhibit Ang II induced VSMC migration and phenotype transitions from a contractile to secretory state ( Wang and Jia, 2020 ). Another study found that activated TRPV1 inhibited VSMC proliferation, migration, and ROS production by upregulating the expression of PPARα ( Zhou et al, 2021 ).…”

Section: Therapeutic Opportunitiesmentioning

confidence: 99%

Vascular smooth muscle cell dysfunction in neurodegeneration

Hayes

Pinto²,

Sparks³

et al. 2022

Front. Neurosci.

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Vascular smooth muscle cells (VSMCs) are the key moderators of cerebrovascular dynamics in response to the brain’s oxygen and nutrient demands. Crucially, VSMCs may provide a sensitive biomarker for neurodegenerative pathologies where vasculature is compromised. An increasing body of research suggests that VSMCs have remarkable plasticity and their pathophysiology may play a key role in the complex process of neurodegeneration. Furthermore, extrinsic risk factors, including environmental conditions and traumatic events can impact vascular function through changes in VSMC morphology. VSMC dysfunction can be characterised at the molecular level both preclinically, and clinically ex vivo. However the identification of VSMC dysfunction in living individuals is important to understand changes in vascular function at the onset and progression of neurological disorders such as dementia, Alzheimer’s disease, and Parkinson’s disease. A promising technique to identify changes in the state of cerebral smooth muscle is cerebrovascular reactivity (CVR) which reflects the intrinsic dynamic response of blood vessels in the brain to vasoactive stimuli in order to modulate regional cerebral blood flow (CBF). In this work, we review the role of VSMCs in the most common neurodegenerative disorders and identify physiological systems that may contribute to VSMC dysfunction. The evidence collected here identifies VSMC dysfunction as a strong candidate for novel therapeutics to combat the development and progression of neurodegeneration, and highlights the need for more research on the role of VSMCs and cerebrovascular dynamics in healthy and diseased states.

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Section: Therapeutic Opportunitiesmentioning

confidence: 99%

Vascular smooth muscle cell dysfunction in neurodegeneration

Hayes

Pinto²,

Sparks³

et al. 2022

Front. Neurosci.

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“…AA is characterized by permanent dilation of the arteries to 1.5 times their normal size, making them prone to rupture or dissection ( Malecki et al, 2020 ). AA is a chronic degenerative disease involving the breakdown and loss of the structural extracellular matrix (ECM) of the aortic wall, leading to progressive thinning, weakness and eventual rupture of the vessel wall ( Wang and Jia, 2020 ; Dahal et al, 2022 ). Chronic inflammatory infiltration, degradation of collagen and elastin, and other pathological changes are also involved ( Wang and Jia, 2020 ; Dahal et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

“…AA is a chronic degenerative disease involving the breakdown and loss of the structural extracellular matrix (ECM) of the aortic wall, leading to progressive thinning, weakness and eventual rupture of the vessel wall ( Wang and Jia, 2020 ; Dahal et al, 2022 ). Chronic inflammatory infiltration, degradation of collagen and elastin, and other pathological changes are also involved ( Wang and Jia, 2020 ; Dahal et al, 2022 ). AA is a life-threatening condition, with approximately 150,000–200,000 deaths reported worldwide annually, leading to a significant socioeconomic burden and causing great suffering to the families of patients ( Golledge, 2019 ; Wen et al, 2020 ; Ibrahim et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Cromolyn prevents cerebral vasospasm and dementia by targeting WDR43

Wang

Kong

Lin

2023

Front. Aging Neurosci.

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BackgroundCerebral vasospasm (CV) can cause inflammation and damage to neuronal cells in the elderly, leading to dementia.PurposeThis study aimed to investigate the genetic mechanisms underlying dementia caused by CV in the elderly, identify preventive and therapeutic drugs, and evaluate their efficacy in treating neurodegenerative diseases.MethodsGenes associated with subarachnoid hemorrhage and CV were acquired and screened for differentially expressed miRNAs (DEmiRNAs) associated with aneurysm rupture. A regulatory network of DEmiRNAs and mRNAs was constructed, and virtual screening was performed to evaluate possible binding patterns between Food and Drug Administration (FDA)-approved drugs and core proteins. Molecular dynamics simulations were performed on the optimal docked complexes. Optimally docked drugs were evaluated for efficacy in the treatment of neurodegenerative diseases through cellular experiments.ResultsThe study found upregulated genes (including WDR43 and THBS1) and one downregulated gene associated with aneurysm rupture. Differences in the expression of these genes indicate greater disease risk. DEmiRNAs associated with ruptured aortic aneurysm were identified, of which two could bind to THBS1 and WDR43. Cromolyn and lanoxin formed the best docking complexes with WDR43 and THBS1, respectively. Cellular experiments showed that cromolyn improved BV2 cell viability and enhanced Aβ42 uptake, suggesting its potential as a therapeutic agent for inflammation-related disorders.ConclusionThe findings suggest that WDR43 and THBS1 are potential targets for preventing and treating CV-induced dementia in the elderly. Cromolyn may have therapeutic value in the treatment of Alzheimer’s disease and dementia.

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“…Inflammation is one of the leading causes of cardiovascular death, as clinical 3 treatments are limited [1][2][3]. Vascular smooth muscle cells (VSMCs) are the main components of the vascular wall and play an important role in maintaining the vascular structure.…”

Section: Introductionmentioning

confidence: 99%

RelB represses miR-193a-5p expression to promote the phenotypic transformation of vascular smooth muscle cells in aortic aneurysm

Han

Liu²,

Tian³

et al. 2023

Preprint

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Aortic aneurysm (AA) is a potentially fatal disease with the possibility of rupture, causing high mortality rates with no effective drugs for the treatment of AA. The mechanism of AA, as well as its therapeutic potential to inhibit aneurysm expansion, has been minimally explored. Small non-coding RNA (miRNAs and miRs) is emerging as a new fundamental regulator of gene expression. This study aimed to explore the role and mechanism of miR-193a-5p in abdominal aortic aneurysms (AAA). In AAA vascular tissue and Angiotensin II (Ang II)-treated vascular smooth muscle cells (VSMCs), the expression of miR-193a-5 was determined using real-time quantitative PCR (RT-qPCR). Western blotting was used to detect the effects of miR-193a-5p on PCNA, CCND1, CCNE1, and CXCR4. To detect the effect of miR-193a-5p on the proliferation and migration of VSMCs, CCK-8, and EdU immunostaining, flow cytometry, wound healing, and Transwell Chamber analysis were performed. In vitro results suggest that overexpression of miR-193a-5p inhibited the proliferation and migration of VSMCs, and its inhibition aggravated their proliferation and migration.

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TRPV1 inhibits smooth muscle cell phenotype switching in a mouse model of abdominal aortic aneurysm

Cited by 10 publications

References 37 publications

Vascular smooth muscle cell dysfunction in neurodegeneration

Vascular smooth muscle cell dysfunction in neurodegeneration

Cromolyn prevents cerebral vasospasm and dementia by targeting WDR43

RelB represses miR-193a-5p expression to promote the phenotypic transformation of vascular smooth muscle cells in aortic aneurysm

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