Modulation of BK channel activities by calcium-sensing receptor in rat bronchopulmonary sensory neurons

Vysotskaya, Zhanna; Moss, Charles R.; Gilbert, Carolyn A.; Gabriel, Sabry A.; Gu, Qihai

doi:10.1016/j.resp.2014.08.014

Cited by 7 publications

(9 citation statements)

References 42 publications

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“…Our results further show that pretreatment with PAR 2 -AP also significantly increases APD 50 and the number of evoked action potentials without significantly altering the resting membrane potential, a similar effect as displayed by paxilline. It is noteworthy that PAR 2 -AP pretreatment shows exclusively a suppressive effect on BK current, which is different from the dual effects of calciumsensing receptor activation on BK channel activities reported in our recent study: a potentiation in cells exhibiting low baseline BK activity and an inhibition in cells with high baseline BK activity [25]. In the latter study, our results further demonstrate that BK and TRPV1 channels are coexpressed in the majority (∼75%) of bronchopulmonary sensory neurons, while TRPV1-expressing neurons exclusively exhibit BK sensitivity.…”

Section: Discussioncontrasting

confidence: 99%

“…Sensory neurons innervating airways and lungs were identified by retrograde labeling using the fluorescent tracer 1,1 -dioctadecyl-3,3,3 ,3 -tetramethylindocarbocyanine perchlorate (DiI), as described in our recent studies [25].…”

Section: Retrograde Labeling Of Vagal Bronchopulmonary Sensory Neuronsmentioning

confidence: 99%

“…Rat nodose and jugular ganglia were extracted, desheathed, and subject to tissue culture process, as described previously [25]. The isolated neurons were plated onto poly-l-lysine-coated glass coverslips, incubated overnight and used within 48 h.…”

Section: Isolation Of Nodose and Jugular Ganglion Neuronsmentioning

confidence: 99%

“…They are expressed in many excitable cells and play significant physiological roles such as regulation of smooth muscle tone, modulation of neurotransmitter release and neuronal spike frequency adaptation [2,19] that BK channels contribute to membrane repolarization and rapid afterhyperpolarization, and could lead to reduced repetitive firing [16,26,27]. The functional expression of BK channels in vagal bronchopulmonary sensory neurons has been reported recently [25]. Our present study was carried out to investigate the potential regulation of BK channel activities by PAR 2 activation in these afferent neurons.…”

Section: Introductionmentioning

confidence: 99%

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Protease-activated receptor-2 inhibits BK channel activity in bronchopulmonary sensory neurons

Moss

Gilbert

Gabriel

et al. 2015

Neuroscience Letters

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Section: Discussioncontrasting

confidence: 99%

Section: Retrograde Labeling Of Vagal Bronchopulmonary Sensory Neuronsmentioning

confidence: 99%

Section: Isolation Of Nodose and Jugular Ganglion Neuronsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protease-activated receptor-2 inhibits BK channel activity in bronchopulmonary sensory neurons

Moss

Gilbert

Gabriel

et al. 2015

Neuroscience Letters

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“…3, B and C). Given the relationship between calcium-sensing receptors and KCNMA1 channels (Vysotskaya et al, 2014), we explored the possibility that KCNMA1 channels might be responsible for the reductions in [Ca 21 ] i that preceded elevations. Therefore, we incubated podocyte-like cells with the KCNMA1 channel inhibitor iberiotoxin (100 nM), as well as the less specific voltage-gated potassium channel blocker TEA (5 mM), prior to the addition of (Fig.…”

Section: Responses To Extracellular Calcium: Hipsmentioning

confidence: 99%

Induced Pluripotent Stem Cell–Derived Podocyte-Like Cells as Models for Assessing Mechanisms Underlying Heritable Disease Phenotype: Initial Studies Using Two Alport Syndrome Patient Lines Indicate Impaired Potassium Channel Activity

Haynes

Selby

Vandekolk

et al. 2018

J Pharmacol Exp Ther

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Renal podocyte survival depends upon the dynamic regulation of a complex cell architecture that links the glomerular basement membrane to integrins, ion channels, and receptors. Alport syndrome is a heritable chronic kidney disease where mutations in 3,4, or 5 collagen genes promote podocyte death. In rodent models of renal failure, activation of the calcium-sensing receptor (CaSR) can protect podocytes from stress-related death. In this study, we assessed CaSR function in podocyte-like cells derived from induced-pluripotent stem cells from two patients with Alport Syndrome (AS1& AS2) and a renal disease free individual [normal human mesangial cell (NHMC)], as well as a human immortalized podocyte-like (HIP) cell line. Extracellular calcium elicited concentration-dependent elevations of intracellular calcium in all podocyte-like cells. NHMC and HIP, but not AS1 or AS2 podocyte-like cells, also showed acute reductions in intracellular calcium prior to elevation. In NHMC podocyte-like cells this acute reduction was blocked by the large-conductance potassium channel (KCNMA1) inhibitors iberiotoxin (10 nM) and tetraethylammonium (5 mM), as well as the focal adhesion kinase inhibitor PF562271 (N-methyl-N-(3-((2-(2-oxo-2,3-dihydro-1H-indol-5-ylamino)-5-trifluoromethyl-pyrimidin-4-ylamino)-methyl)-pyridin-2-yl)-methanesulfonamide, 10 nM). Quantitative polymerase chain reaction (qPCR) and immunolabeling showed the presence of transcript and protein in all podocyte-like cells tested. Cultivation of AS1 podocytes on decellularized plates of NHMC podocyte-like cells partially restored acute reductions in intracellular calcium in response to extracellular calcium. We conclude that the AS patient-derived podocyte-like cells used in this study showed dysfunctional integrin signaling and potassium channel function, which may contribute to podocyte death seen in Alport syndrome.

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Extracellular Calcium Has Multiple Targets to Control Cell Proliferation

Capiod

2016

Advances in Experimental Medicine and Biology

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Calcium channels and the two G-protein coupled receptors sensing extracellular calcium, calcium-sensing receptor (CaSR) and GPRC6a, are the two main means by which extracellular calcium can signal to cells and regulate many cellular processes including cell proliferation, migration and invasion of tumoral cells. Many intracellular signaling pathways are sensitive to cytosolic calcium rises and conversely intracellular signaling pathways can modulate calcium channel expression and activity. Calcium channels are undoubtedly involved in the former while the CaSR and GPRC6a are most likely to interfere with the latter. As for neurotransmitters, calcium ions use plasma membrane channels and GPCR to trigger cytosolic free calcium concentration rises and intracellular signaling and regulatory pathways activation. Calcium sensing GPCR, CaSR and GPRC6a, allow a supplemental degree of control and as for metabotropic receptors, they not only modulate calcium channel expression but they may also control calcium-dependent K+ channels. The multiplicity of intracellular signaling pathways involved, their sensitivity to local and global intracellular calcium increase and to CaSR and GPRC6a stimulation, the presence of membrane signalplex, all this confers the cells the plasticity they need to convert the effects of extracellular calcium into complex physiological responses and therefore determine their fate.

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Modulation of BK channel activities by calcium-sensing receptor in rat bronchopulmonary sensory neurons

Cited by 7 publications

References 42 publications

Protease-activated receptor-2 inhibits BK channel activity in bronchopulmonary sensory neurons

Protease-activated receptor-2 inhibits BK channel activity in bronchopulmonary sensory neurons

Induced Pluripotent Stem Cell–Derived Podocyte-Like Cells as Models for Assessing Mechanisms Underlying Heritable Disease Phenotype: Initial Studies Using Two Alport Syndrome Patient Lines Indicate Impaired Potassium Channel Activity

Extracellular Calcium Has Multiple Targets to Control Cell Proliferation

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