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Intracellular Ca(2+) release mechanisms: multiple pathways having multiple functions within the same cell type?

C P da Silva1, A H Guse

  • 1University of Hamburg, University Clinic Hamburg-Eppendorf, Institute for Medical Biochemistry and Molecular Biology, Division of Cellular Signal Transduction, Grindelallee 117, D-20146, Hamburg, Germany.

Biochimica Et Biophysica Acta
|December 8, 2000
PubMed
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Calcium signaling is vital in eukaryotic cells, utilizing three key messengers: InsP3, cADPR, and NAADP. This study explores why these calcium-mobilizing ligands are conserved together in certain cell types.

Area of Science:

  • Cellular Biology
  • Molecular Signaling
  • Biochemistry

Background:

  • Cytosolic and nuclear calcium (Ca2+) concentration elevation is a fundamental signal transduction mechanism in eukaryotic cells.
  • Three Ca2+-mobilizing second messengers, D-myo-inositol 1,4,5-trisphosphate (InsP3), cyclic adenosine diphosphoribose (cADPR), and nicotinic acid adenine dinucleotide phosphate (NAADP+), are conserved across diverse organisms.
  • In specific cell types like sea urchin eggs, mouse pancreatic acinar cells, and human Jurkat T-lymphocytes, all three messengers are implicated in Ca2+ signal generation.

Purpose of the Study:

  • To investigate the evolutionary conservation of three distinct Ca2+-mobilizing second messengers within the same cell types.
  • To explore theoretical reasons for the co-conservation of InsP3, cADPR, and NAADP, including redundancy, subcellular localization, and temporal control of Ca2+ signaling.

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  • To compare these theoretical considerations with existing knowledge of the three messengers in sea urchin eggs, mouse pancreatic acinar cells, and human Jurkat T-lymphocytes.

    • Main Methods:

    • Theoretical analysis of potential roles for conserved Ca2+ signaling pathways.
    • Comparative review of existing literature on InsP3, cADPR, and NAADP function in specific cell models.
    • Examination of Ca2+ signal generation mechanisms in sea urchin eggs, mouse pancreatic acinar cells, and human Jurkat T-lymphocytes.

    Main Results:

    • The study posits three theoretical explanations for the co-conservation of InsP3, cADPR, and NAADP.
    • These include the potential for redundant signaling pathways to ensure signal integrity.
    • The need for spatially restricted Ca2+ signals and precise temporal control over cellular responses are also considered.

    Conclusions:

    • The co-existence of InsP3, cADPR, and NAADP in certain cell types suggests sophisticated regulatory roles beyond simple redundancy.
    • These messengers may enable fine-tuning of cellular responses through localized and temporally distinct calcium elevations.
    • Further research is needed to fully elucidate the integrated functions of these three key calcium-mobilizing ligands in complex cellular signaling.