Increased store-operated and 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx in monocytes is mediated by transient receptor potential canonical channels in human essential hypertension

Liu, Dao Yan; Thilo, Florian; Scholze, Alexandra; Wittstock, Antje; Zhao, Zhi Gang; Harteneck, Christian; Zidek, Walter; Zhu, Zhihao; Tepel, Martín

doi:10.1097/hjh.0b013e32803cae2b

Cited by 50 publications

(37 citation statements)

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“…These studies using animal models of primary hypertension or peripheral blood cells from humans reported an increased expression of TRPC3 channel transcripts, increased TRPC3 channel proteins, and increased TRPC3 activation in hypertension. [3][4][5][6][7] TRPC3 channels are nonselective cation channels mediating calcium influx. The acute calcium influx through TRPC3 channels is a key signaling mechanism that stimulates the calcium-dependent release of several endothelium-derived vasoconstrictive agents including endothelin, urotensin, or epoxyeicosatrienoic acids.…”

Section: Discussionmentioning

confidence: 99%

“…Previously published immunoblottings from our group already confirmed that these antibodies can be used to identify TRPC3 or TRPC6 channels in human tissue. 5,6 The streptavidin AP kit (K5005; Dako, Glostrup, Denmark) was used for detection and alkaline phosphatase was developed using Fast Red as the chromogen. After counterstaining with hematoxylin, the slides were dehydrated and mounted.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…Dietrich et al 4 reported that TRPC6-deficient mice with consecutively increased TRPC3 channel expression developed higher blood pressure. Liu et al 5,6 and Thilo et al 7 reported increased TRPC3 protein expression and increased TRPC3 transcripts in peripheral blood monocytes from patients with essential hypertension compared to normotensive control subjects. The expression of TRPC3 in human vascular endothelium has not been associated with malignant hypertension yet.…”

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Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

et al. 2009

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An increased expression of transient receptor potential canonical type 3 (TRPC3) cation channels has been proposed as one of the factors contributing to the pathogenesis of hypertension. To test that hypothesis we compared the expression of TRPC3 and TRPC6 as an endogenous control in human vascular endothelium of preglomerular arterioles in kidney biopsies from six patients with malignant hypertension and from four patients with diarrhea-associated hemolytic-uremic syndrome. Patients with malignant hypertension showed significantly higher systolic blood pressure and more prominent expression of TRPC3 in vascular endothelium of preglomerular arterioles compared to patients with hemolytic-uremic syndrome. The expression of TRPC6 was not different between the two groups. The study supports the hypothesis that the increased expression of TRPC3 is associated with malignant hypertension in humans. Malignant hypertension is a hypertensive emergency with severe elevation of blood pressure, a Keith-Wagener-Barker grade III or IV hypertensive retinopathy, and acute impairment of renal function in most cases. In white subjects, essential hypertension accounts for approximately 30% of malignant hypertension, whereas in blacks essential hypertension is the predominant cause, accounting for approximately 82% of all cases. The characteristic pathological change of malignant hypertension represents endothelial injury. Its pathophysiology involves mechanical stress on the vessel wall, a proliferative endarteriitis in small arteries and arterioles, and fibrinoid necrosis with fine subendothelial droplets and hyalin thrombi formation.

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Section: Discussionmentioning

confidence: 99%

Section: Immunohistochemistrymentioning

confidence: 99%

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Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

et al. 2009

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“…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]. Liu et al [1] compared the expression level and function of TRPCs between essential hypertensive patients and normotensive control subjects.…”

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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“…10,11 Cells were grown on 96-well plates and fixed by 3.7% formaldehyde. Measurements were performed in quadruplicate and averaged.…”

Section: Quantitative In-cell Western Assay Of Trpc5mentioning

confidence: 99%

Erythropoietin Increases Expression and Function of Transient Receptor Potential Canonical 5 Channels

Liu

Thilo

et al. 2011

Hypertension

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Abstract-Hypertension is a common complication in hemodialysis patients during erythropoietin (EPO) treatment. The underlying mechanisms of EPO-induced hypertension still remain to be determined. Key Words: transient receptor potential channel Ⅲ erythropoietin Ⅲ hypertension E levated arterial blood pressure is a common adverse effect of erythropoietin (EPO) administration in patients and animal models with chronic kidney disease. [1][2][3][4] Several observations indicate that EPO-induced hypertension is not only mediated by changes in erythrocyte mass but also by direct adverse effects of EPO. The underlying mechanisms of EPO-induced rise in blood pressure still remain to be determined. 4,5 Considerable evidence has been accumulated for impaired cellular calcium homeostasis in EPO-associated hypertension. EPO significantly increases cytosolic free calcium concentration and expands sarcoplasmic calcium stores in platelets from essential hypertensive or EPO-associated hypertension patients and cultured vascular smooth muscle cells from rats. 6 -8 Transient receptor potential canonical (TRPC) channels are calcium-permeable nonselective cation channels that had been identified in many cell types, including endothelial cells and peripheral blood cells. 9 We previously showed significantly increased expression of functional TRPC5 channel protein in patients with essential hypertension and in spontaneously hypertensive rats. 10 -12 In the present study, we hypothesized that EPO increases the expression and function of the TRPC5 gene, finally contributing to the pathogenesis of hypertension. To test this hypothesis, we examined the effects of EPO on TRPC5 channel expression and function in cultured human endothelial cells and peripheral blood cells. Experimental Procedures Cell CultureHuman umbilical vein endothelial cell-derived EA.hy926 cells (American Type Culture Collection) were maintained at 37°C and 5% CO 2 in DMEM containing 10% FCS, 100 U/mL of penicillin, and 100 g/mL of streptomycin (BIOCHROM AG, Berlin, Germany). After detachment with 0.25% trypsin, cells were seeded in plates as appropriate, that is, 6-well plates for RNA and protein isolation, 12-well plates for patch clamp experiments, and 96-well

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Increased store-operated and 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx in monocytes is mediated by transient receptor potential canonical channels in human essential hypertension

Cited by 50 publications

References 45 publications

Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

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

Erythropoietin Increases Expression and Function of Transient Receptor Potential Canonical 5 Channels

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