scholarly journals Transient Receptor Potential Vanilloid 1 Regulates Mitochondrial Membrane Potential and Myocardial Reperfusion Injury

2016 ◽  
Vol 5 (9) ◽  
Author(s):  
Carl M. Hurt ◽  
Yao Lu ◽  
Creed M. Stary ◽  
Honit Piplani ◽  
Bryce A. Small ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Reperfusion Injury ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Transient Receptor Potential Vanilloid ◽  
Transient Receptor

scholarly journals TREK-1 channels regulate pressure sensitivity and calcium signaling in trabecular meshwork cells

2018 ◽  
Vol 150 (12) ◽  
pp. 1660-1675 ◽  
Author(s):  
Oleg Yarishkin ◽  
Tam T.T. Phuong ◽  
Colin A. Bretz ◽  
Kenneth W. Olsen ◽  
Jackson M. Baumann ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Trabecular Meshwork ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Gene Profiling ◽  
Resting Membrane Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Pressure Sensitivity ◽  
Trabecular Meshwork Cells ◽  
Transient Receptor

Mechanotransduction by the trabecular meshwork (TM) is an essential component of intraocular pressure regulation in the vertebrate eye. This process is compromised in glaucoma but is poorly understood. In this study, we identify transient receptor potential vanilloid isoform 4 (TRPV4) and TWIK-related potassium channel-1 (TREK-1) as key molecular determinants of TM membrane potential, pressure sensitivity, calcium homeostasis, and transcellular permeability. We show that resting membrane potential in human TM cells is unaffected by “classical” inhibitors of voltage-activated, calcium-activated, and inwardly rectifying potassium channels but is depolarized by blockers of tandem-pore K+ channels. Using gene profiling, we reveal the presence of TREK-1, TASK-1, TWIK-2, and THIK transcripts in TM cells. Pressure stimuli, arachidonic acid, and TREK-1 activators hyperpolarize these cells, effects that are antagonized by quinine, amlodipine, spadin, and short-hairpin RNA–mediated knockdown of TREK-1 but not TASK-1. Activation and inhibition of TREK-1 modulates [Ca2+]TM and lowers the impedance of cell monolayers. Together, these results suggest that tensile homeostasis in the TM may be regulated by balanced, pressure-dependent activation of TRPV4 and TREK-1 mechanotransducers.

scholarly journals Dynamic coupling between TRPV4 and Ca2+-activated SK1/3 and IK1 K+ channels plays a critical role in regulating the K+-secretory BK channel in kidney collecting duct cells

2017 ◽  
Vol 312 (6) ◽  
pp. F1081-F1089 ◽  
Author(s):  
Yue Li ◽  
Hongxiang Hu ◽  
Jin-Bin Tian ◽  
Michael X. Zhu ◽  
Roger G. O’Neil
Keyword(s):  
Membrane Potential ◽  
Transient Receptor Potential ◽  
Collecting Duct ◽  
Critical Role ◽  
Receptor Potential ◽  
Bk Channel ◽  
Transient Receptor Potential Vanilloid ◽  
Cortical Collecting Duct ◽  
Intracellular Ca ◽  
Transient Receptor

The large-conductance Ca2+-activated K+ channel, BK (KCNMA1), is expressed along the connecting tubule (CNT) and cortical collecting duct (CCD) where it underlies flow- and Ca2+-dependent K+ secretion. Its activity is partially under the control of the mechanosensitive transient receptor potential vanilloid type 4 (TRPV4) Ca2+-permeable channel. Recently, we identified three small-/intermediate-conductance Ca2+-activated K+ channels, SK1 (KCNN1), SK3 (KCNN3), and IK1 (KCNN4), with notably high Ca2+-binding affinities, that are expressed in CNT/CCD and may be regulated by TRPV4-mediated Ca2+ influx. The K+-secreting CCD mCCDcl1 cells, which express these channels, were used to determine whether SK1/3 and IK1 are activated on TRPV4 stimulation and whether they contribute to Ca2+ influx and activation of BK. Activation of TRPV4 (GSK1016790A) modestly depolarized the membrane potential and robustly increased intracellular Ca2+, [Ca2+]i. Inhibition of both SK1/3 and IK1 by application of apamin and 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34), respectively, further depolarized the membrane potential and markedly suppressed the TRPV4-mediated rise in [Ca2+]i. Application of BK inhibitor iberiotoxin after activation of TRPV4 without apamin/TRAM-34 also reduced [Ca2+]i and further intensified membrane depolarization, demonstrating BK involvement. However, the BK-dependent effects on [Ca2+]i and membrane potential were largely abolished by pretreatment with apamin and TRAM-34, identical to that observed by separately suppressing TRPV4-mediated Ca2+ influx, demonstrating that SK1/3-IK1 channels potently contribute to TRPV4-mediated BK activation. Our data indicate a direct correlation between TRPV4-mediated Ca2+ signal and BK activation but where early activation of SK1/3 and IK1 channels are critical to sufficiently enhanced Ca2+ entry and [Ca2+]i levels required for activation of BK.

A Review on Potential Involvement of TRPV1 Channels in Ischemia–Reperfusion Injury

2017 ◽  
Vol 23 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Amteshwar Singh Jaggi
Keyword(s):  
Reperfusion Injury ◽  
Inflammatory Cytokines ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Channel Activation ◽  
Trpv1 Channels ◽  
Transient Receptor

Besides functioning as thermosensors, transient receptor potential vanilloid 1 (TRPV1) channels play a pivotal role in ischemia–reperfusion injury. Transient receptor potential vanilloid 1 channel activation attenuates ischemia–reperfusion-induced injury in various organs including the heart, lungs, kidneys, and the brain. Transient receptor potential vanilloid 1 channels are expressed on the sensory neurons innervating the myocardium, ventricles of the heart, epicardial surface of the heart, endothelial cells, and the vascular smooth muscle cells. During ischemic conditions, activation of TRPV1 channels on the perivascular nerves stimulates the release of calcitonin gene-related peptide and substance P to produce cardioprotection. Furthermore, TRPV1 channel activation reduces the generation of free radicals and inflammatory cytokines, inhibits neutrophil infiltration, and enhances the production of anti-inflammatory cytokines to reduce ischemia–reperfusion-induced tissue injury. The present review describes the potential involvement of TRPV1 channels and the signaling cascade in attenuating ischemia–reperfusion injury in various organs.

scholarly journals Regulation of [Ca2+]i Oscillations and Mitochondrial Activity by Various Calcium Transporters in Mouse Oocytes

2020 ◽  
Author(s):  
Feng Wang ◽  
Ang Li ◽  
Tie-Gang Meng ◽  
Li-Juan Wang ◽  
Yi Hou ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Membrane Potential ◽  
Calcium Channel ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Transient Receptor Potential ◽  
Critical Role ◽  
Receptor Potential ◽  
Mitochondrial Activity ◽  
Oocyte Activation

Abstract Oocyte activation inefficiency is one of the reasons for female infertility and Ca 2+ functions play a critical role in the regulation of oocyte activation. We used various inhibitors of Ca 2+ channels and pumps located on the plasma membrane, the endoplasmic reticulum or both, including sarcoplasmic/endoplasmic reticulum Ca 2+ ATPases (SERCAs, the main Ca 2+ pumps which decrease the intracellular Ca 2+ level by reaccumulating Ca 2+ into the sarcoplasmic reticulum), transient receptor potential (TRP) ion channel subfamily member 7 (TRPM7, a Ca 2+ /Mg 2+ -permeable non-selective cation channel), T-type Ca 2+ channels and calcium channel Orai1, to investigate their roles in[Ca 2+ ] i oscillation patterns and mitochondrial membrane potential during oocyte activation by real-time recording. Our results show that SERCAs, TRPM7 and T-type Ca 2+ channels are important for initiation and maintenance of [Ca 2+ ] i oscillations, which is required for mitochondrial membrane potential changes during oocyte activation, as well as for subsequent pronuclear formation and transition to embryo development, while the function of calcium channel Orai1 is not confirmed. Increasing the knowledge of these transporters may provide a theoretical basis for improving oocyte activation in human assisted reproduction clinics.

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