On the Roles of the Transient Receptor Potential Canonical 3 (TRPC3) Channel in Endothelium and Macrophages: Implications in Atherosclerosis

Vázquez, Guillermo; Solanki, Sumeet; Dube, Prabhatachandra; Smedlund, Kathryn; Ampem, Prince Tuffour

doi:10.1007/978-3-319-26974-0_9

Cited by 10 publications

(7 citation statements)

References 66 publications

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“…TRPCs have been proved to be involved in the pathogenesis of cardiovascular diseases, such as essential hypertension, cardiac hypertrophy, intima hyperplasia and endothelial dysfunction, and atherosclerosis [ 37 ]. TRPC3 has been documented to be implicated in atherosclerosis through regulating endothelium and macrophages [ 38 ]. A previous study demonstrated that TRPC3 had a dual beneficial effect on lesion progression by reducing cellularity at early stages and necrosis in the advanced plaques in apoe −/− mouse model [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

miR-26a inhibits atherosclerosis progression by targeting TRPC3

Feng

Wang

2018

Cell Biosci

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BackgroundAtherosclerosis, a chronic multi-factorial vascular disease, has become a predominant cause of a variety of cardiovascular disorders. miR-26a was previously reported to be involved in atherosclerosis progression. However, the underlying mechanism of miR-26a in atherosclerosis remains to be further explained.MethodsHigh-fat diet (HFD)-fed apolipoprotein E (apoE)−/− mice and oxidized low-density lipoprotein (ox-LDL)-stimulated human aortic endothelial cells (HAECs) were established as in vivo and in vitro models of atherosclerosis. RT-qPCR and western blot analysis were performed to measure the expression of miR-26a and transient receptor potential canonical 3 (TRPC3), respectively. Binding between miR-26a and TRPC3 was predicted with bioinformatics software and verified using a dual luciferase reporter assay. The effects of miR-26a on the lipid accumulation, atherosclerotic lesion, and inflammatory response in HFD-fed apoE−/− mice were investigated by a colorimetric enzymatic assay system, hematoxylin–eosin and oil-Red-O staining, and ELISA, respectively. Additionally, the effects of miR-26a or combined with TRPC3 on cell viability, apoptosis and the nuclear factor-kappa B (NF-κB) pathway in ox-LDL-stimulated HAECs were evaluated by MTT assay, TUNEL assay, and western blot, respectively.ResultsmiR-26a was downregulated in HFD-fed apoE−/− mice and ox-LDL-stimulated HAECs. miR-26a overexpression inhibited the pathogenesis of atherosclerosis by attenuating hyperlipidemia, atherosclerotic lesion and suppressing inflammatory response in HFD-fed apoE−/− mice. Moreover, miR-26a overexpression suppressed inflammatory response and the NF-κB pathway, promoted cell viability and inhibited apoptosis in ox-LDL-stimulated HAECs. Additionally, TRPC3 was demonstrated to be a direct target of miR-26a. Enforced expression of TRPC3 reversed the effects of miR-26a on cell viability, apoptosis, and the NF-κB pathway in ox-LDL-treated HAECs.ConclusionsmiR-26a alleviated the development of atherosclerosis by regulating TRPC3, providing a potential target for atherosclerosis treatment.

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Section: Discussionmentioning

confidence: 99%

miR-26a inhibits atherosclerosis progression by targeting TRPC3

Feng

Wang

2018

Cell Biosci

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“…Moreover, TRPC3 shows its impact on endothelial dysfunction and is responsible for causing apoptosis of macrophages related to the pathogenesis of atherosclerosis. The relevance of TRPC3 with atherosclerosis has also been verified by in vivo studies [ 60 ], where the process is associated with endoplasmic reticulum stress that is considered the primary mechanism of cell apoptosis in atherosclerotic plaques [ 61 ]. It is well known that endothelial barrier function dysfunction is regarded as a leading cause of atherosclerotic plaque formation.…”

Section: Pathological Roles Of Store-operated Channels In Cardiovascu...mentioning

confidence: 99%

Role of store-operated Ca2+ entry in cardiovascular disease

Lu¹,

Zhang²,

Su³

et al. 2022

Cell Commun Signal

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Store-operated channels (SOCs) are highly selective Ca2+ channels that mediate Ca2+ influx in non-excitable and excitable (i.e., skeletal and cardiac muscle) cells. These channels are triggered by Ca2+ depletion of the endoplasmic reticulum and sarcoplasmic reticulum, independently of inositol 1,4,5-trisphosphate (InsP3), which is involved in cell growth, differentiation, and gene transcription. When the Ca2+ store is depleted, stromal interaction molecule1 (STIM1) as Ca2+ sensor redistributes into discrete puncta near the plasma membrane and activates the protein Ca2+ release activated Ca2+ channel protein 1 (Orai1). Accumulating evidence suggests that SOC is associated with several physiological roles in endothelial dysfunction and vascular smooth muscle proliferation that contribute to the progression of cardiovascular disease. This review mainly elaborates on the contribution of SOC in the vasculature (endothelial cells and vascular smooth muscle cells). We will further retrospect the literature implicating a critical role for these proteins in cardiovascular disease. Graphical Abstract

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“…Inactivating FLNA in mice models also led to impaired macrophage signaling and function, accompanied by reduced atherosclerosis [ 100 ]. Transient receptor potential canonical 3 (TRPC3) in macrophages has been linked with various mechanisms in atherosclerosis disease progression [ 104 ]. In novel studies, mice with a macrophage-specific deficiency of transient receptor potential canonical 3 (TRPC3) displayed reduced stress-induced apoptosis, necrosis, and calcification in advanced atherosclerotic plaque [ 105 , 106 , 107 ].…”

Section: Macrophages and Atherosclerosismentioning

confidence: 99%

Dirty Jobs: Macrophages at the Heart of Cardiovascular Disease

et al. 2022

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Cardiovascular disease (CVD) is one of the greatest public health concerns and is the leading cause of morbidity and mortality in the United States and worldwide. CVD is a broad yet complex term referring to numerous heart and vascular conditions, all with varying pathologies. Macrophages are one of the key factors in the development of these conditions. Macrophages play diverse roles in the maintenance of cardiovascular homeostasis, and an imbalance of these mechanisms contributes to the development of CVD. In the current review, we provide an in-depth analysis of the diversity of macrophages, their roles in maintaining tissue homeostasis within the heart and vasculature, and the mechanisms through which imbalances in homeostasis may lead to CVD. Through this review, we aim to highlight the potential importance of macrophages in the identification of preventative, diagnostic, and therapeutic strategies for patients with CVD.

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On the Roles of the Transient Receptor Potential Canonical 3 (TRPC3) Channel in Endothelium and Macrophages: Implications in Atherosclerosis

Cited by 10 publications

References 66 publications

miR-26a inhibits atherosclerosis progression by targeting TRPC3

miR-26a inhibits atherosclerosis progression by targeting TRPC3

Role of store-operated Ca2+ entry in cardiovascular disease

Dirty Jobs: Macrophages at the Heart of Cardiovascular Disease

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