Calcium pools, calcium entry, and cell growth. Issue 2 (April 1996)

• Record Type: Journal Article
• Authors: Gill, Donald L.; Waldron, Richard T.; Rys-Sikora, Krystyna E.; Ufret-Vincenty, Carmen A.; Graber, Matthew N.; Favre, Cécile J.; Alfonso, Amparo
• Is Part Of: Bioscience reports. Volume 16:Issue 2(1996)
• Page Start: 139
• Page End: 157
• Publication Date: 1996-04
• Subjects: Calcium -- serca pump -- endoplasmic reticulum -- cell growth; Molecular biology -- Periodicals; Cytology -- Periodicals; 572.8
• DOI: 10.1007/BF01206203
• Languages: English
• ISSNs: 0144-8463

Abstract

Abstract : The Ca 2+ pump and Ca 2+ release functions of intracellular Ca 2+ pools have been well characterized. However, the nature and identity of Ca 2+ pools as well as the physiological implications of Ca 2+ levels within them, have remained elusive. Ca 2+ pools appear to be contained within the endoplasmic reticulum (ER); however, ER is a heterogeneous and widely distributed organelle, with numerous other functions than Ca 2+ regulation. Studies described here center on trying to determine more about subcellular distribution of Ca 2+ pools, the levels of Ca 2+ within Ca 2+ pools, and how these intraluminal Ca 2+ levels may be physiologically related to ER function. Experiments utilizing in situ high resolution subcellular morphological analysis of ER loaded with ratiometric fluroescent Ca 2+ dyes, indicate a wide distribution of inositol 1, 4, 5-trisphosphate (InsP3 )-sensitive Ca 2+ pools within cells, and large changes in the levels of Ca 2+ within pools following InsP3 -mediated Ca 2+ release. Such changes in Ca 2+ may be of great significance to the translation, translocation, and folding of proteins in ER, in particular with respect to the function of the now numerously described luminal Ca 2+ -sensitive chaperonin proteins. Studies have also focussed on the physiological role of pool Ca 2+ changes with respect to cell growth. Emptying of pools using Ca 2+ pump blockers can result in cells entering a stable quiescent G0 -like growth state. After treatment with the irreversible pump blocker, thapsigargin, cells remain in this state until they are stimulated with essential fatty acids whereupon new pump protein is synthesized, functional Ca 2+ pools return, and cells reenter the cell cycle. During the Ca 2+ pool-depleted growth-arrested state, cells express a Ca 2+ influx channel that is distinct from the store-operated Ca 2+ influx channels activated after short-term depletion of Ca 2+ pools. Overall, these studies indicate that significant changes in intraluminal ER Ca 2+ do occur and that such changes appear linked to alteration of essential ER functions as well as to the cell cycle-state and the growth of cells.