Isoform-specific induction of nuclear free calcium oscillations by platelet-derived growth factor

Diliberto, Pamela A.; Krishna, Sumita; Kwon, Seongwook; Herman, Brian

doi:10.1016/s0021-9258(18)47200-6

Cited by 17 publications

(1 citation statement)

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“…Calcium oscillations have been observed in fibroblasts in response to various stimuli [24][25][26]. Additionally, a relationship between substrate mechanical sensing and Ca 2þ oscillations has been studied, as presented non-comprehensively in table 1. In addition to its dependence on substrate stiffness, periodic Ca 2þ oscillations have been seen to correlate with contractile events in fibroblasts and myofibroblasts [31].…”

Section: Introductionmentioning

confidence: 99%

Mechanics regulates ATP-stimulated collective calcium response in fibroblast cells

Lembong

Sabass

Sun

et al. 2015

J. R. Soc. Interface.

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Cells constantly sense their chemical and mechanical environments. We study the effect of mechanics on the ATP-induced collective calcium response of fibroblast cells in experiments that mimic various tissue environments. We find that closely packed two-dimensional cell cultures on a soft polyacrylamide gel (Young's modulus E = 690 Pa) contain more cells exhibiting calcium oscillations than cultures on a rigid substrate (E = 36 000 Pa). Calcium responses of cells on soft substrates show a slower decay of calcium level relative to those on rigid substrates. Actin enhancement and disruption experiments for the cell cultures allow us to conclude that actin filaments determine the collective Ca(2+) oscillatory behaviour in the culture. Inhibition of gap junctions results in a decrease of the oscillation period and reduced correlation of calcium responses, which suggests additional complexity of signalling upon cell-cell contact. Moreover, the frequency of calcium oscillations is independent of the rigidity of the substrate but depends on ATP concentration. We compare our results with those from similar experiments on individual cells. Overall, our observations show that collective chemical signalling in cell cultures via calcium depends critically on the mechanical environment.

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Section: Introductionmentioning

confidence: 99%

Mechanics regulates ATP-stimulated collective calcium response in fibroblast cells

Lembong

Sabass

Sun

et al. 2015

J. R. Soc. Interface.

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Nuclear membrane receptors and channels: Potential therapeutical targets for drug action

et al. 1997

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The recent use of confocal microscopy showed for the first time that the nucleus plays an important role in excitation‐contraction and secretion coupling of several excitable and nonexcitable cells. It was also suggested that, like the sarcolemma membrane, the nuclear membrane indeed possesses channels as well as receptors which could play a major role in modulating Ca2+ influx and cytosolic Ca2+ buffering capacity of the nucleus. In this study, the mechanism(s) of Ca2+ entry through the sarcolemma and the nuclear membrane during spontaneous contraction of heart cells and during sustained stimulation of ET‐1 and Ang‐II receptors were examined in cardiomyocytes as well as in human vascular smooth muscle and endothelial cells. During spontaneous contraction of heart cells, the cytosolic Ca2+ increase was immediately followed by a transient increase of nuclear Ca2+, both of which were blocked by the L‐type Ca2+ channel blocker apamine at a concentration of 100 nM. Sustained stimulation of bradykinin, Ang‐II, or ET‐1 receptors induced a sustained increase of intracellular Ca2+ which was mainly nuclear. Using the cell attached patch clamp configuration, the potent voltage‐dependent steady‐state R‐type Ca2+ channel blocker PN200‐110 (in the presence of the specific L‐type Ca2+‐blocker nifedipine) decreased the PAF‐induced increase of the probability of opening the sarcolemmal steady‐state resting voltage‐dependent R‐type Ca2+ channel. The use of an Ang‐II fluorescent probe and sarcolemmal perforated technique showed that Ang II receptors are also located at the nuclear membrane level. These results demonstrate that like the sarcolemmal membrane, the nuclear membrane possesses receptors as well as channels that could be a target for cytosolic free hormones, and thus also constituting a new target for drug action. Drug Dev. Res. 42:211–222, 1997. © 1997 Wiley‐Liss, Inc.

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Calcium signalling and cell proliferation

1995

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The orderly sequence of events that constitutes the cell cycle is carefully regulated. A part of this regulation depends upon the ubiquitous calcium signalling system. Many growth factors utilize the messenger inositol trisphosphate (InsP3) to set up prolonged calcium signals, often organized in an oscillatory pattern. These repetitive calcium spikes require both the entry of external calcium and its release from internal stores. One function of this calcium signal is to activate the immediate early genes responsible for inducing resting cells (G0) to re-enter the cell cycle. It may also promote the initiation of DNA synthesis at the G1/S transition. Finally, calcium contributes to the completion of the cell cycle by stimulating events at mitosis. The role of calcium in cell proliferation is highlighted by the increasing number of anticancer therapies and immunosuppressant drugs directed towards this calcium signalling pathway.

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Isoform-specific induction of nuclear free calcium oscillations by platelet-derived growth factor

Cited by 17 publications

References 50 publications

Mechanics regulates ATP-stimulated collective calcium response in fibroblast cells

Mechanics regulates ATP-stimulated collective calcium response in fibroblast cells

Nuclear membrane receptors and channels: Potential therapeutical targets for drug action

Calcium signalling and cell proliferation

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