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Li L.,Chongqing Medical University | Chen J.,Chongqing Medical University | Ni Y.,Chongqing Medical University | Feng X.,Chongqing Medical University | And 8 more authors.
Pflugers Archiv European Journal of Physiology

Nonalcoholic fatty liver is characterized by the fatty deformation and lipid deposition of hepatic parenchymal cells that are associated with cardiometabolic diseases. In this study, we report the effect of capsaicin on its receptor, transient receptor potential vanilloid 1 (TRPV1) cation channel, in preventing fatty liver formation. Functional TRPV1 has been detected in hepatocytes and liver tissues. TRPV1 activation by capsaicin reduced lipid accumulation and triglyceride level in the liver from wild-type (WT) mice. However, these effects were absent in the liver from TRPV1-/- mice. Chronic dietary capsaicin increased the hepatic uncoupling protein 2 (UCP2) expression in WT but not in TRPV1-/- mice (P<0.01). We conclude that TRPV1 long-time activation might prevent high-fat diet-induced fatty liver in mice through upregulation of hepatic UCP2. Dietary capsaicin may represent a promising intervention in populations at high risk for fatty liver. © Springer-Verlag 2012. Source

Nilius B.,Laboratory Ion Channel Research | Carbone E.,University of Turin
Pflugers Archiv European Journal of Physiology

T-type Ca2+ channels have gained, 15 years after cloning, an immense interest as novel players in very unexpected cell functions, and its many relations to diseases have been discovered. This special issue provides a state-of-the-art overview on novel functional properties of T-type Ca 2+ channels, unexpected cellular functions, and most importantly will also summarizes and review the involvement of this "tiny, transient" type of Ca2+ channels in several diseases. It is tried to bridge the gap between molecular biophysical properties of T-type Ca2+ channels and diseases providing finally a translational view on this amazing ion channel. © 2014 Springer-Verlag. Source

Li L.,Chongqing Institute of Hypertension | Wang F.,Chongqing Institute of Hypertension | Wei X.,Chongqing Institute of Hypertension | Liang Y.,Chongqing Institute of Hypertension | And 11 more authors.

High salt (HS) intake contributes to the development of hypertension. Epithelial sodium channels play crucial roles in regulating renal sodium reabsorption and blood pressure. The renal transient receptor potential vanilloid 1 (TRPV1) cation channel can be activated by its agonist capsaicin. However, it is unknown whether dietary factors can act on urinary sodium excretion and renal epithelial sodium channel (ENaC) function. Here, we report that TRPV1 activation by dietary capsaicin increased urinary sodium excretion through reducing sodium reabsorption in wild-type (WT) mice on a HS diet but not in TRPV1 mice. The effect of capsaicin on urinary sodium excretion was involved in inhibiting αENaC and its related with-no-lysine kinase 1/serum-and glucocorticoid-inducible protein kinase 1 pathway in renal cortical collecting ducts of WT mice. Dietary capsaicin further reduced the increased αENaC activity in WT mice attributed to the HS diet. In contrast, this capsaicin effect was absent in TRPV1 mice. Immunoprecipitation study indicated αENaC specifically coexpressed and functionally interact with TRPV1 in renal cortical collecting ducts of WT mice. Additionally, ENaC activity and expression were suppressed by capsaicin-mediated TRPV1 activation in cultured M1-cortical collecting duct cells. Long-term dietary capsaicin prevented the development of high blood pressure in WT mice on a HS diet. It concludes that TRPV1 activation in the cortical collecting ducts by capsaicin increases urinary sodium excretion and avoids HS diet-induced hypertension through antagonizing αENaC-mediated urinary sodium reabsorption. Dietary capsaicin may represent a promising lifestyle intervention in populations exposed to a high dietary salt intake. © 2014 American Heart Association, Inc. Source

Kim H.K.,Inje University | Youm J.B.,Inje University | Jeong S.H.,Inje University | Lee S.R.,Inje University | And 11 more authors.
Pflugers Archiv European Journal of Physiology

Echinochrome A (Ech A), a marine bio-product isolated from sea urchin eggs, is known to have cardioprotective effects through its strong antioxidant and ATP-sparing capabilities. However, the effects of Ech A on cardiac excitation–contraction (E-C) are not known. In this study, we investigated the effects of Ech A on cardiac contractility and Ca2+ handling in the rat heart. In ex vivo Langendorff hearts, Ech A (3 μM) decreased left ventricular developing pressure to 77.7 ± 6.5 % of basal level. In isolated ventricular myocytes, Ech A reduced the fractional cell shortening from 3.4 % at baseline to 2.1 %. Ech A increased both diastolic and peak systolic intracellular Ca2+ ([Ca2+]i). However, the ratio of peak [Ca]i to resting [Ca]i was significantly decreased. Ech A did not affect the L-type Ca2+ current. Inhibiting the Na+/Ca2+ exchanger with either NiCl2 or SEA400 did not affect the Ech A-dependent changes in Ca2+ handling. Our data demonstrate that treatment with Ech A results in a significant reduction in the phosphorylation of phospholamban at both serine 16 and threonine 17 leading to a significant inhibition of SR Ca2+-ATPase 2A (SERCA2A) and subsequent reduced Ca2+ uptake into the intracellular Ca2+ store. Taken together, our data show that Ech A negatively regulates cardiac contractility by inhibiting SERCA2A activity, which leads to a reduction in internal Ca2+ stores. © 2014, Springer-Verlag Berlin Heidelberg. Source

Everaerts W.,Laboratory Ion Channel Research | Everaerts W.,Catholic University of Leuven | Nilius B.,Laboratory Ion Channel Research | Owsianik G.,Laboratory Ion Channel Research
Progress in Biophysics and Molecular Biology

The Transient Receptor Potential Vanilloid 4 channel, TRPV4, is a Ca 2+ and Mg 2+ permeable non-selective cation channel involved in many different cellular functions. It is activated by a variety of physical and chemical stimuli, including heat, mechano-stimuli, endogenous substances such as arachidonic acid and its cytochrome P450-derived metabolites (epoxyeicosatrienoic acids), endocannabinoids (anandamide and 2-arachidonoylglycerol), as well as synthetic α-phorbol derivatives. Recently, TRPV4 has been characterized as an important player modulating osteoclast differentiation in bone remodelling and as a urothelial mechanosensor that controls normal voiding. Several TRPV4 gain-of-function mutations are shown to cause autosomal-dominant bone dysplasias such as brachyolmia and Koszlowski disease. In this review we comprehensively describe the structural, biophysical and (patho)physiological properties of the TRPV4 channel and we summarize the current knowledge about the role of TRPV4 in the pathogenesis of several diseases. © 2009 Elsevier Ltd. Source

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