Capacitative Calcium Entry

The effect of inositol 1,3,4,5-tetrakisphosphate on inositol trisphosphate-induced Ca2+ mobilization in freshly isolated and cultured mouse lacrimal acinar cells

“…These functional differences were supported by evident structural changes seen under the electron microscope. A similar sort of phenomenon is an intriguing possibility that would account for what we describe here, and indeed, Putney [30] has discussed the possibility that Ca# + pool integrity could be different in freshly isolated versus cultured lacrimal acinar cells (see also [31,32]). …”

Chronic Lithium Treatment Attenuates Intracellular Calcium Mobilization

“…The decay phase reflects the restitution of Ca 2 þ towards baseline levels through homeostatic control mechanisms including plasma membrane and ER Ca 2 þ ATPase pumps (Brini and Carafoli, 2000) and Na þ /Ca 2 þ exchangers (Blaustein and Lederer, 1999 To test whether the above lithium-induced changes were dependent on the duration of exposure, BLCLs from a subset of subjects (eight patients, two healthy) were treated for 24 h or 7 days with 0.75 mM lithium or vehicle, and LPAstimulated Ca 2 þ responses determined. As shown in Figure 4a Lithium attenuates calcium mobilization MJ Wasserman et al store depletion induced by TG (Putney et al, 2001 Figure 4d), it was in fact reduced in chronic lithium-treated BLCLs compared with the vehicle-treated condition (F ¼ 5.17; df ¼ 1,13; p ¼ 0.04).…”

“…Intracellular Ca 2 þ signaling and homeostasis are maintained by an intricate array of processes acting in concert (Berridge et al, 2000;Putney et al, 2001) including, for example, inositol trisphosphate (IP 3 )-and ryanodinestimulated release of Ca 2 þ from endoplasmic reticulum (ER) storage pools (Berridge, 1995;Barritt, 1999;Putney and Ribeiro, 2000), voltage-and ligand-gated ion channel mediated Ca 2 þ influx (Ghosh and Greenberg, 1995), storeoperated Ca 2 þ entry (SOCE) (Putney et al, 2001), plasma membrane and sarcoplasmic/ER Ca 2 þ -ATPase pumps (PMCAs and SERCAs) (Brini and Carafoli, 2000), and mitochondrial Ca 2 þ uptake, storage, and release (Brini and Carafoli, 2000;Fall and Keizer, 2001). Disturbances of intracellular Ca 2 þ signaling can critically affect cellular function due to calcium's essential role in vital cellular processes including gene expression (Ghosh and Greenberg, 1995), neurogenesis and plasticity (Mattson, 2000), and cell death (Szalai et al, 1999).…”

Atherosclerosis and calcium signalling in endothelial cells

“…Furthermore, release of Ca 2 + from stores appears to stimulates influx of Ca 2 + across the plasma membrane, a process termed capacitative calcium entry (CCE) (Putney et al, 2001). The mechanism of action of CCE is unclear and a variety of explanations have been suggested, including: direct regulation of Ca 2 + channels in the plasma membrane by Ca 2 + concentration in the cytosol; release-sensitive production of a diffusible "calcium influx factor"; activation of Ca 2 + channels by kinases (such as tyrosine kinase and myosin light chain kinase), produced as a result of Ca 2 +-calmodulin complexes in the cytosol; conformational coupling between the IP 3 sensitive channel in the ER and Ca 2 + channels in the plasma membrane (Watanabe et al, 1998;Tran et al, 2000;Putney et al, 2001). CCE appears to be inhibited by cyclic guanosine monophosphate (cGMP) and G-kinase, which are produced as downstream effects of NO and Ca 2 + signalling.…”

“…IP3 binds to sites on the ER membrane, opening cation channels and thus allowing stored Ca 2 + to be released into the cytosol ('Iran et al, 2000). Depletion of the internal stores appears to stimulate influx of Ca 2 + into the cell via plasma membrane ion channels (a process known as capacitative Ca 2 + entry) (Putney et al, 2001), and can also accelerate the rate of release of Ca 2 + from the ER into the cytosol (Ca 2 +-induced Ca 2 + release) (Wood and Gillespie, 1998). Wall shear stress appears to contribute to Ca 2 + signalling by activating plasma membrane Ca 2 + channels, thus allowing further influx (Kwan et al, 2003).…”