scholarly journals Role of Transient Receptor Potential Canonical Channels in Heart Physiology and Pathophysiology

2020 ◽  
Vol 7 ◽  
Author(s):  
Hairuo Wen ◽  
Judith K. Gwathmey ◽  
Lai-Hua Xie
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Canonical ◽  
Transient Receptor ◽  
Heart Physiology

scholarly journals Examining the role of transient receptor potential canonical 5 (TRPC5) in osteoarthritis

2020 ◽  
Vol 2 (4) ◽  
pp. 100119
Author(s):  
João de Sousa Valente ◽  
Khadija M. Alawi ◽  
Patrik Keringer ◽  
Sabah Bharde ◽  
Faseeha Ayaz ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Canonical ◽  
Transient Receptor

scholarly journals Role of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Qian Wang ◽  
Xuefei Tian ◽  
Yuyang Wang ◽  
Yan Wang ◽  
Jialin Li ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Actin Cytoskeleton ◽  
Diabetic Kidney Disease ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Diabetic Kidney ◽  
Transient Receptor Potential Canonical ◽  
Transient Receptor ◽  
Cytoskeleton Rearrangement

Podocyte injury is an important pathogenesis step causing proteinuric kidney diseases such as diabetic kidney disease (DKD). Actin cytoskeleton rearrangement in podocyte induced by multiple pathogenic factors is believed to be the key process resulting in glomerular injury. Many studies have recently shown that transient receptor potential canonical channel 6 (TRPC6) in podocyte plays a critical role in the development and progression of proteinuric kidney disease by regulating its actin cytoskeleton rearrangement. This review is aimed at summarizing the role of TRPC6 on DKD by regulating the podocyte actin cytoskeleton rearrangement, thereby help further broaden our views and understanding on the mechanism of DKD and provide a theoretic basis for exploring new therapeutic targets for DKD patients.

Angiotensin II-stimulated Ca2+ entry mechanisms in afferent arterioles: role of transient receptor potential canonical channels and reverse Na+/Ca2+ exchange

2008 ◽  
Vol 294 (1) ◽  
pp. F212-F219 ◽  
Author(s):  
Susan K. Fellner ◽  
William J. Arendshorst
Keyword(s):  
Angiotensin Ii ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Flufenamic Acid ◽  
Polystyrene Bead ◽  
Ang Ii ◽  
Transient Receptor Potential Canonical ◽  
Afferent Arterioles ◽  
Transient Receptor

In afferent arterioles, the signaling events that lead to an increase in cytosolic Ca2+ concentration ([Ca2+]i) and initiation of vascular contraction are increasingly being delineated. We have recently studied angiotensin II (ANG II)-mediated effects on sarcoplasmic reticulum (SR) mobilization of Ca2+ and the role of superoxide and cyclic adenosine diphosphoribose in these processes. In the current study we investigated the participation of transient receptor potential canonical channels (TRPC) and a Na+/Ca2+ exchanger (NCX) in Ca2+ entry mechanisms. Afferent arterioles, isolated with the magnetized polystyrene bead method, were loaded with fura-2 to measure [Ca2+]i ratiometrically. We observed that the Ca2+-dependent chloride channel blocker niflumic acid (10 and 50 μ M) affects neither the peak nor plateau [Ca2+]i response to ANG II. Arterioles were pretreated with ryanodine (100 μM) and TMB-8 to block SR mobilization via the ryanodine receptor and inositol trisphosphate receptor, respectively. The peak [Ca2+]i response to ANG II was reduced by 40%. Addition of 2-aminoethoxydiphenyl borane to block TRPC-mediated Ca2+ entry inhibited the peak [Ca2+]i ANG II response by 80% and the plateau by 74%. Flufenamic acid (FFA; 50 μM), which stimulates TRPC6, caused a sustained increase of [Ca2+]i of 146 nM. This response was unaffected by diltiazem or nifedipine. KB-R7943 (at the low concentration of 10 μM) inhibits reverse (but not forward) mode NCX. KB-R7943 decreased the peak [Ca2+]i response to ANG II by 48% and to FFA by 38%. We conclude that TRPC6 and reverse-mode NCX may be important Ca2+ entry pathways in afferent arterioles.

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