ArticleThe Journal of physiology2004
Mitochondrial calcium sequestration and protein kinase C cooperate in the regulation of cortical F-actin disassembly and secretion in bovine chromaffin cells.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 2019Article
- Hydrogen sulphide facilitates exocytosis by regulating the handling of intracellular calcium by chromaffin cells.Pflugers Archiv : European journal of physiology · 2018Article
- Article
- Tight mitochondrial control of calcium and exocytotic signals in chromaffin cells at embryonic life.Pflugers Archiv : European journal of physiology · 2015Article
- Article
- Novel features on the regulation by mitochondria of calcium and secretion transients in chromaffin cells challenged with acetylcholine at 37°C.Physiological reports · 2013Article
- The cortical acto-Myosin network: from diffusion barrier to functional gateway in the transport of neurosecretory vesicles to the plasma membrane.Frontiers in endocrinology · 2013Review
- Protein kinase C-delta deficiency perturbs bone homeostasis by selective uncoupling of cathepsin K secretion and ruffled border formation in osteoclasts.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012Article
- CD151 restricts the α6 integrin diffusion mode.Journal of cell science · 2012Article
- Permissive role of sphingosine on calcium-dependent endocytosis in chromaffin cells.Pflugers Archiv : European journal of physiology · 2010Article
- Cortical F-actin, the exocytic mode, and neuropeptide release in mouse chromaffin cells is regulated by myristoylated alanine-rich C-kinase substrate and myosin II.Molecular biology of the cell · 2009Article
- F-actin and myosin II accelerate catecholamine release from chromaffin granules.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Myosin II activation and actin reorganization regulate the mode of quantal exocytosis in mouse adrenal chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria play an important role in the homeostasis of intracellular Ca(2+) and regulate its availability for exocytosis. Inhibitors of mitochondria Ca(2+) uptake such as protonophore CCCP potentiate the secretory response to a depolarizing pulse of K(+). Exposure of cells to agents that directly (cytochalasin D, latrunculin B) or indirectly (PMA) disrupt cortical F-actin networks also potentiate the secretory response to high K(+). The effects of cytochalasin D and CCCP on secretion were additive whereas those of PMA and CCCP were not; this suggests different mechanisms for cytochalasin D and CCCP and a similar mechanism for PMA and CCCP. Mitochondria were the site of action of CCCP, because the potentiation of secretion by CCCP was observed even after depletion of Ca(2+) from the endoplasmic reticulum. CCCP induced a small increase in the cytosolic Ca(2+) concentration ([Ca(2+)](c)) that was not modified by the protein kinase C (PKC) inhibitor chelerythrine. Both CCCP and PMA induced cortical F-actin disassembly, an effect abolished by chelerythrine. In addition, rotenone and oligomycin A, two other mitochondrial inhibitors, also evoked cortical F-actin disassembly and potentiated secretion; again, these effects were blocked by chelerythrine. CCCP also enhanced the phosphorylation of PKC and myristoylated alanine-rich C kinase substance (MARCKS), and these were also inhibited by chelerythrine. The results suggest that the rapid sequestration of Ca(2+) by mitochondria would protect the cell from an enhanced PKC activation and cortical F-actin disassembly, thereby limiting the magnitude of the secretory response.
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