Mechanosensing and Mechanosignal Transduction in Atherosclerosis

Rahaman, Suneha G.; Mahanty, Manisha; Mukherjee, Pritha; Dutta, Bidisha; Rahaman, Shaik O.

doi:10.1007/s11883-023-01139-6

Cited by 5 publications

(8 citation statements)

References 68 publications

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“…Given TRPV4's previously identified pro-inflammatory role, these findings suggest TRPV4 may downregulate anti-inflammatory miR-146a, promoting inflammation in response to rigid biomaterial implantation which is linked to increased tissue stiffness (20)(21)(22)(23)(24)29). Macrophages are the predominant cell type in the initiation, maintenance, and resolution of inflammation (1)(2)(3)(4)(5)(6)(7). Therefore, we next sought to investigate if the absence of TRPV4 also promoted the expression of miR-146a in macrophages.…”

Section: Mir-146a Expression Is Upregulated In the Absence Of Trpv4 I...mentioning

confidence: 99%

“…Persistent inflammation plays a crucial role in the development of inflammation-driven diseases such as atherosclerosis, foreign body response, and fibrosis (1)(2)(3)(4)(5)(6)(7). Macrophages, pivotal in regulating inflammation and tissue repair, possess the capability to detect and eliminate foreign invaders and apoptotic cells due to their phagocytic nature.…”

Section: Introductionmentioning

confidence: 99%

“…Macrophages, pivotal in regulating inflammation and tissue repair, possess the capability to detect and eliminate foreign invaders and apoptotic cells due to their phagocytic nature. The adaptability of macrophages supports inflammation management, tissue repair, and regeneration, with their dysregulation potentially leading to numerous pathological states (1)(2)(3)(4)(5)(6)(7). The effectiveness of macrophage-driven inflammation hinges on the coordinated expression of key proteins and microRNAs (miRs) involved in their activation, polarization, and phagocytosis, necessitating tight regulation of these factors at transcriptional and post-transcriptional levels through a network of transcription factors (TFs), co-regulators, and epigenetic modifications (1)(2)(3)(4)(5)(6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

“…The adaptability of macrophages supports inflammation management, tissue repair, and regeneration, with their dysregulation potentially leading to numerous pathological states (1)(2)(3)(4)(5)(6)(7). The effectiveness of macrophage-driven inflammation hinges on the coordinated expression of key proteins and microRNAs (miRs) involved in their activation, polarization, and phagocytosis, necessitating tight regulation of these factors at transcriptional and post-transcriptional levels through a network of transcription factors (TFs), co-regulators, and epigenetic modifications (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Key TFs such as PU.1, IRF8, STAT1, NFκB, AP1, and PPAR have been extensively studied for their roles in macrophage function (4)(5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms underlying TRPV4-mediated regulation of miR-146a expression

Dutta,

Mahanty,

Kesavalu

et al. 2024

Preprint

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Persistent inflammation is a major contributor in the development of various inflammatory diseases like atherosclerosis. Our study investigates how transient receptor potential vanilloid 4 (TRPV4), a mechanosensitive ion channel, interacts with microRNA-146a (miR-146a), within the context of inflammation and atherosclerosis. Micro-RNAs play a critical role in controlling gene expression, and miR-146a is notable for its anti-inflammatory actions. TRPV4 is activated by diverse soluble and mechanical stimuli, and often associated with inflammatory responses in various diseases. Here, we find that TRPV4 negatively regulates miR-146a expression in macrophages, especially following stimulation by lipopolysaccharides or alterations in matrix stiffness. We show that in atherosclerosis, a condition characterized by matrix stiffening, TRPV4 decreases miR-146a expression in aortic tissue macrophages. We find that TRPV4’s impact on miR-146a is independent of activation of NFκB, Stat1, P38, and AKT, but is rather mediated through a mechanism involving histone deacetylation instead of DNA methylation at the miR-146a promoter site. Furthermore, we show that N-terminal residues 1 to 130 in TRPV4 is essential in suppression of miR-146a expression in LPS-stimulated macrophages. Altogether, this study identifies a regulatory mechanism of miR-146a expression by TRPV4 which may open new potential therapeutic strategies for managing inflammatory diseases.

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Section: Mir-146a Expression Is Upregulated In the Absence Of Trpv4 I...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms underlying TRPV4-mediated regulation of miR-146a expression

Dutta,

Mahanty,

Kesavalu

et al. 2024

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…Moreover, the remodeling process generates physical forces that can influence tumor cell behavior [24] . For example, the increased stiffness of the ECM due to CAF-mediated remodeling can promote tumor cell invasion [61] and migration [62] .…”

Section: Direct Extrusion Through Ecm Remodeling Mediated By Cafs (St...mentioning

confidence: 99%

Mechanical force-mediated interactions between cancer cells and fibroblasts and their role in the progression of hepatocellular carcinoma

Peng,

Ding,

Zhang

et al. 2024

J Cancer Metastasis Treat

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Mechanical forces play a key role in the initiation and progression of cancer. Intercellular interactions between fibroblasts and cancer cells contribute a large portion of the mechanical forces in tumor tissue. Hence, further investigation of the mechanical force-mediated intercellular interactions between cancer cells and fibroblasts is urgently needed, given the slow progress in the management of various solid cancers. In our previous study, we observed obvious mechanical force-mediated interactions between hepatocellular carcinoma (HCC) cells and fibroblasts through integrins and ECM proteins by using our coculture model and discovered that these interactions play important roles in 3D structure formation and tumor growth, suggesting their potential application in HCC treatment. In this review, we summarize the recent research progress in this field in hopes of providing insight into the development of potential anticancer strategies, with a special focus on HCC.

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Applications, challenges, and prospects of induced pluripotent stem cells for vascular disease

Biswas,

Park

2024

Molecules and Cells

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Mechanosensing and Mechanosignal Transduction in Atherosclerosis

Cited by 5 publications

References 68 publications

Mechanisms underlying TRPV4-mediated regulation of miR-146a expression

Mechanisms underlying TRPV4-mediated regulation of miR-146a expression

Mechanical force-mediated interactions between cancer cells and fibroblasts and their role in the progression of hepatocellular carcinoma

Applications, challenges, and prospects of induced pluripotent stem cells for vascular disease

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