TRPM4, a Ca2+-activated nonselective cation channel in mouse sino-atrial node cells

Demion, Marie; Bois, Patrick; Launay, Pierre; Guinamard, Romain

doi:10.1016/j.cardiores.2006.11.023

Cited by 154 publications

(153 citation statements)

References 29 publications

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“…Thus, excess PIP3, but not excess PIP2, appeared to reverse the attenuated VRAC current in PIP3-or PIP2-depleted cells. We conclude that PIP3 is more directly linked to the activation of VRAC current their effects on PIP3-regulated transporters and channels (4,8), further studies are necessary to clarify to what extent PI3K activation can increase the PIP3 level in intact cardiac cells. As with the relationship between cell swelling and PI3K-related signaling pathways, several reports have shown that mechanical stretch of membrane and cell swelling cause activation of PI3K (16), and the activated PI3K has been suggested to trigger some downstream signaling cascades leading to the activation of VRAC current (5,7,26,33).…”

Section: Resultsmentioning

confidence: 90%

“…These results are in agreement with the previous studies, in which the effect of these inhibitors on VRAC current was examined in rabbit ventricular cells (5,26), cultured smooth muscle cells (33) and hepatoma cells (11,12 (8), and PIP3 dic8 (Echelon Biosciences) (4) were added to the pipette solution. PIP2 and PIP3 were directly dissolved in the control pipette solution at a concentration of 10 μM (4,8). PIP2-Ab and PIP3-Ab were used at a 1 : 50 dilution.…”

Section: Methodsmentioning

confidence: 99%

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Regulation of volume-regulated outwardly rectifying anion channels by phosphatidylinositol 3,4,5-trisphosphate in mouse ventricular cells

2008

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Volume-regulated outwardly rectifying anion channel (VRAC) plays an important role in cellvolume regulation in many types of cells. Little is known about the regulation of VRAC by phosphatidylinositides (PIs), which include phosphatidylinositol 3,4,5-trisphosphate (PIP3) and phosphatidylinositol 4,5-bisphosphate (PIP2). We examined the effect of PIs on the VRAC current activated in hypotonic solution in mouse ventricular cells. VRAC current was inhibited strongly by intracellular application of LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor) or anti-PIP3 antibody (PIP3-Ab), and less strongly by anti-PIP2 antibody (PIP2-Ab). LY294002 inhibited regulatory volume decrease in hypotonically swollen cells, which was in parallel with the VRAC inhibition. Intracellular PIP3 or PIP2 influenced neither the basal background current in isotonic solution nor the VRAC current in hypotonic solution. However, PIP3, but not PIP2, restored the VRAC current suppressed by LY294002 or PIP2-Ab. These results suggest that the activation of VRAC current requires the presence of intracellular PIP3, that PI3K-mediated increase in PIP3 level is sufficient to fully activate VRAC current, and that PIP3 alone without osmotic stimulation cannot induce VRAC current. We propose that VRAC in mouse ventricular cells is regulated by PIP3 and/or its down stream signaling pathways.

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Section: Resultsmentioning

confidence: 90%

Section: Methodsmentioning

confidence: 99%

Regulation of volume-regulated outwardly rectifying anion channels by phosphatidylinositol 3,4,5-trisphosphate in mouse ventricular cells

2008

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“…blood flow, the generation of heart rhythm, and the immune response (33)(34)(35)(36)(37)(38)(39). TRPM4-mediated currents are up-regulated in cardiomyocytes from spontaneous hypertensive rats (40), and gain-of-function mutations in TRPM4 have been associated with familial heart disease (41,42).…”

Section: Discussionmentioning

confidence: 99%

On Potential Interactions between Non-selective Cation Channel TRPM4 and Sulfonylurea Receptor SUR1

Sala-Rabanal

Wang

Nichols

2012

Journal of Biological Chemistry

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Background: SUR1, the regulatory subunit of K ATP channels, was hypothesized to associate with TRPM4 to form novel channels, implicated in cell death following neurovascular trauma. Results: The properties of heterologously expressed TRPM4 channels are not modified by SUR1. Conclusion:The coupling between SUR1 and TRPM4 is unlikely. Significance: The roles of TRPM4 and K ATP channels in the pathogenesis of brain edema and hemorrhage should be reassessed.

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“…A typical trace of an ECG shows the "P-wave", the "P-Q interval" (isoelectric line), the "QRS complex", the "T-wave" and the "U-wave". [60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75] in the SAN). This "SAN overdrive suppression" on the other elements of the conductive network explains its leading role in driving the pacemaker.…”

Section: Development Of the Human Cardiac Conduction Systemmentioning

confidence: 99%

“…Recently, different transient receptor potential (TRPM) channels have also been described as having a role in this physiological process. TRPM4, a non-selective, calcium-activated cation channel was characterized in the rodent SAN [69] . This sodium and potassium inward current is positively regulated by [Ca 2+ ] i and negatively regulated by ATP.…”

Section: Wwwchinapharcom Weisbrod D Et Almentioning

confidence: 99%

Mechanisms underlying the cardiac pacemaker: the role of SK4 calcium-activated potassium channels

et al. 2016

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The proper expression and function of the cardiac pacemaker is a critical feature of heart physiology. The sinoatrial node (SAN) in human right atrium generates an electrical stimulation approximately 70 times per minute, which propagates from a conductive network to the myocardium leading to chamber contractions during the systoles. Although the SAN and other nodal conductive structures were identified more than a century ago, the mechanisms involved in the generation of cardiac automaticity remain highly debated. In this short review, we survey the current data related to the development of the human cardiac conduction system and the various mechanisms that have been proposed to underlie the pacemaker activity. We also present the human embryonic stem cellderived cardiomyocyte system, which is used as a model for studying the pacemaker. Finally, we describe our latest characterization of the previously unrecognized role of the SK4 Ca 2+ -activated K + channel conductance in pacemaker cells. By exquisitely balancing the inward currents during the diastolic depolarization, the SK4 channels appear to play a crucial role in human cardiac automaticity.

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TRPM4, a Ca2+-activated nonselective cation channel in mouse sino-atrial node cells

Abstract: TRPM4 is functionally expressed in SAN cells and may be a key player in the generation and/or perturbation of heart rhythm.

Cited by 154 publications

References 29 publications

Regulation of volume-regulated outwardly rectifying anion channels by phosphatidylinositol 3,4,5-trisphosphate in mouse ventricular cells

Regulation of volume-regulated outwardly rectifying anion channels by phosphatidylinositol 3,4,5-trisphosphate in mouse ventricular cells

On Potential Interactions between Non-selective Cation Channel TRPM4 and Sulfonylurea Receptor SUR1

Mechanisms underlying the cardiac pacemaker: the role of SK4 calcium-activated potassium channels

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