Role of Trpc channels, Stim1 and Orai1 in PGF(2 alpha)-induced calcium signaling in NRK fibroblasts

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Synchronized Ca2+ signaling by intercellular propagation of Ca2+ action potentials in NRK fibroblasts

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Synchronized calcium spiking resulting from spontaneous calcium action potentials in monolayers of NRK fibroblasts

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Membrane depolarization in NRK fibroblasts by bradykinin is mediated by a calcium-dependent chloride conductance

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Fast calcium wave propagation mediated by electrically conducted excitation and boosted by CICR.

Contains fulltext : 70278.pdf (publisher's version ) (Closed access) Contains fulltext : 70278.pdf (preprint version ) (Open Access)We have investigated synchronization and propagation of calcium oscillations, mediated by gap junctional excitation transmission. For that purpose we used an experimentally based model of normal rat kidney (NRK) cells, electrically coupled in a one-dimensional configuration (linear strand). Fibroblasts such as NRK cells can form an excitable syncytium and generate spontaneous inositol 1,4,5-trisphosphate (IP(3))-mediated intracellular calcium waves, which may spread over a monolayer culture in a coordinated fashion. An intracellular calcium oscillation in a pacemaker cell causes a membrane depolarization from within that cell via calcium-activated chloride channels, leading to an L-type calcium channel-based action potential (AP) in that cell. This AP is then transmitted to the electrically connected neighbor cell, and the calcium inflow during that transmitted AP triggers a calcium wave in that neighbor cell by opening of IP(3) receptor channels, causing calcium-induced calcium release (CICR). In this way the calcium wave of the pacemaker cell is rapidly propagated by the electrically transmitted AP. Propagation of APs in a strand of cells depends on the number of terminal pacemaker cells, the L-type calcium conductance of the cells, and the electrical coupling between the cells. Our results show that the coupling between IP(3)-mediated calcium oscillations and AP firing provides a robust mechanism for fast propagation of activity across a network of cells, which is representative for many other cell types such as gastrointestinal cells, urethral cells, and pacemaker cells in the heart.14 p

Determination of gap junctional intercellular communication by capacitance measurements

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Inositol 1,4,5-triphosphate releases Ca2+ from vacuolar membrane vesicles of Saccharomyces cerevisiae

AbstractInositol 1,4,5-trisphosphate (IP3) induces a release of Ca2+ from vacuolar membrane vesicles of Saccharomyces cerevisiae. The amount released is dependent on IP3 concentration (concentration for half maximal effect, Kmapparent = 0.4 μM). Myo-inositol, and inositol 1,4-bisphosphate up to 50 μM have no effect on Ca2+ levels in the vesicles. The IP3 -induced Ca2+ release is blocked by dantrolene and 8-(N,N-diethylamino)-octyl 3,4,5-trimethoxybenzoate-HCl (TMB-8), which are known to block Ca2+ release from Ca2+ stores in animal cells. IP3-induced release of Ca2+ also occurs when Ca2+ is accumulated by means of an artificial pH gradient, indicating that the effect of IP3 is not due to an effect on the vacuolar H+-ATPase. The IP3-induced Ca2+ release is not accompanied by a change in the pH gradient, which indicates that it is not due to a reversal of the Ca2+/nH+ antiport or to a decrease in ΔpH by IP3. The present results suggest that IP3 may act as a second messenger in the mobilization of Ca2+ in yeast cells. As in plant cells, the vacuolar membrane of yeast seems to contain a Ca2+ channel, which can be opened by IP3. In this respect the vacuole could function as an IP3-regulated intracellular Ca2+ store, equivalent to the endoplasmic- and sarcoplasmic reticulum in animal cells, and play a role in Ca2+-dependent signal transduction in yeast cells

Bioenergetics of the formyl-methanofuran dehydrogenase and heterodisulfide reductase reactions in Methanothermobacter thermautotrophicus

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