Association of transient receptor potential canonical type 3 (TRPC3) channel transcripts with proinflammatory cytokines

Thilo, Florian; Scholze, Alexandra; Liu, Dao Yan; Zidek, Walter; Tepel, Martín

doi:10.1016/j.abb.2007.12.006

Cited by 35 publications

(20 citation statements)

References 19 publications

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“…Nonselective Ca 2+ permeant TRPC channels (more specifically, TRPC3) have been implicated in many cardiorenal diseases, such as cardiac hypertrophy [36][37][38][39]42 and hypertension. [28][29][30][31][33][34][35] Some studies showed a certain correlation with kidney disease. 27,32,50 However, no study to our knowledge has investigated the role of fibroblast TRPC3 in renal disease, such as fibrosis, and whether its inhibition could prevent the development of renal dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…25,26 TRPC3 is upregulated in kidney and monocytes from patients with hypertension and correlates with proinflammatory cytokines. [27][28][29][30][31] Increased TRPC3 channel protein expression is found in human monocytes from patients with CKD, 32 and association of TRPC3 with hypertension is increasingly being reported. [33][34][35] TRPC3 also promotes cardiac hypertrophy through calcineurin and NF of activated T cells [36][37][38][39] and mediates a proarrhythmic Ca 2+ entry in cardiac myocytes.…”

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confidence: 99%

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Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis

Saliba¹,

Karam²,

Smayra

et al. 2015

Journal of the American Society of Nephrology

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Transient receptor potential canonical (TRPC) Ca 2+ -permeant channels, especially TRPC3, are increasingly implicated in cardiorenal diseases. We studied the possible role of fibroblast TRPC3 in the development of renal fibrosis. In vitro, a macromolecular complex formed by TRPC1/TRPC3/TRPC6 existed in isolated cultured rat renal fibroblasts. However, specific blockade of TRPC3 with the pharmacologic inhibitor pyr3 was sufficient to inhibit both angiotensin II-and 1-oleoyl-2-acetyl-sn-glycerol-induced Ca 2+ entry in these cells, which was detected by fura-2 Ca 2+ imaging. TRPC3 blockade or Ca 2+ removal inhibited fibroblast proliferation and myofibroblast differentiation by suppressing the phosphorylation of extracellular signalregulated kinase (ERK1/2). In addition, pyr3 inhibited fibrosis and inflammation-associated markers in a noncytotoxic manner. Furthermore, TRPC3 knockdown by siRNA confirmed these pharmacologic findings. In adult male Wistar rats or wild-type mice subjected to unilateral ureteral obstruction, TRPC3 expression increased in the fibroblasts of obstructed kidneys and was associated with increased Ca 2+ entry, ERK1/2 phosphorylation, and fibroblast proliferation. Both TRPC3 blockade in rats and TRPC3 knockout in mice inhibited ERK1/2 phosphorylation and fibroblast activation as well as myofibroblast differentiation and extracellular matrix remodeling in obstructed kidneys, thus ameliorating tubulointerstitial damage and renal fibrosis. In conclusion, TRPC3 channels are present in renal fibroblasts and control fibroblast proliferation, differentiation, and activation through Ca 2+ -mediated ERK signaling. TRPC3 channels might constitute important therapeutic targets for improving renal remodeling in kidney disease.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis

Saliba¹,

Karam²,

Smayra

et al. 2015

Journal of the American Society of Nephrology

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“…In addition, TRPC channels have been reported to be associated with the production of proinflammatory cytokines and inflammation. 27,28 A very recent study has demonstrated that TLR4 activation of TRPC6-dependent Ca 2+ signaling mediates endotoxin-induced lung vascular permeability and inflammation. 27 Strikingly, except NOD2-mediated Ca 2+ signaling directly contributing to cytoskeleton rearrangement and podocyte apoptosis, our preliminary results indicate that knockdown of TRPC6 can also attenuate NOD2-induced production of proinflammatory mediators in podocytes (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Novel Role of NOD2 in Mediating Ca ²⁺ Signaling

Han

Wang

et al. 2013

Hypertension

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“…The recruitment of circulating peripheral monocytes, their activation and their differentiation into tissue macrophages play an important role in the early stages of atherosclerotic lesion formation [59]. Thilo et al [60] observed an approximately 8-fold increase of TRPC3 transcripts in monocytes from patients with essential hypertension compared to normotensive control subjects, demonstrating a significant correlation between TRPC3 transcripts and systolic blood pressure, expression of IL-1beta, and TNF-alpha. In addition, increased TRPC3 and TRPC5 expression in monocytes of patients with essential hypertension, a subsequent storeoperated Ca 2+ influx, and increased 1-oleoyl-2-acetyl-snglycerol-induced cation influx in monocytes of patients with essential hypertension were observed [61].…”

Section: Trp Channel Subtype C Dysfunction Promotes the Development Omentioning

confidence: 99%

Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension

Liu

Xiong

Zhu

2014

Sci. China Life Sci.

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Intracellular Ca 2+ homeostasis is essential for vascular function and blood pressure regulation. Because of their unique roles in regulating intracellular Ca 2+ concentration and vascular function, a novel class of non-selective cation channels, called transient receptor potential (TRP) channels, have emerged at the frontier of hypertension research. Based on their role in vasculature function regulation, TRP channels can be divided into two functional subtypes: one that participates in vasoconstriction and one that participates in vasodilatation. A functional imbalance of these two subtypes of TRP channels may disturb intracellular calcium ([Ca 2+ ]i) homeostasis, and the consequent vascular dysfunction may contribute to the development of hypertension. The potential of these TRP channels as novel pharmacological targets for the treatment of human hypertension is of great interest. TRP channels, Ca 2+ homeostasis, vascular function, hypertension Citation:Liu DY, Xiong SQ, Zhu ZM. Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension. Sci China Life Sci, 2014, 57: 818 -825,

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Association of transient receptor potential canonical type 3 (TRPC3) channel transcripts with proinflammatory cytokines

Cited by 35 publications

References 19 publications

Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis

Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis

Novel Role of NOD2 in Mediating Ca ²⁺ Signaling

Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension

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Association of transient receptor potential canonical type 3 (TRPC3) channel transcripts with proinflammatory cytokines

Cited by 35 publications

References 19 publications

Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis

Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis

Novel Role of NOD2 in Mediating Ca 2+ Signaling

Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension

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Product

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Novel Role of NOD2 in Mediating Ca ²⁺ Signaling