Mitochondrial oversight of cellular Ca2+ signaling

Current Opinion in Neurobiology

Volumn 8, Issue 3, 1998, Pages 398-404

  Babcock, Donner F ^a   Hille, Bertil ^a  

^a UNIVERSITY OF WASHINGTON   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM; CARBONYL CYANIDE 4 (TRIFLUOROMETHOXY)PHENYLHYDRAZONE; CARBONYL CYANIDE CHLOROPHENYLHYDRAZONE;

BRAIN MITOCHONDRION; CALCIUM CELL LEVEL; CALCIUM TRANSPORT; NONHUMAN; PRIORITY JOURNAL; REVIEW; SIGNAL TRANSDUCTION;

EID: 0032102068     PISSN: 09594388     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0959-4388(98)80067-6     Document Type: Article

References (62)

1. Lehninger AL, Carafoli E, Rossi CS. Energy-linked ion movements in mitochondrial systems. Adv Enzymol. 29:1967;259-320.
2. Carafoli E. The calcium cycle of mitochondria. FEBS Lett. 104:1979;1-5.
3. Gunter TE, Pfeiffer DR. Mechanisms by which mitochondria transport calcium. Am J Physiol. 258:1990;C755-C786.
4. Gunter TE, Gunter KK, Sheu S-S, Gavin CE. Mitochondrial calcium transport: physiological and pathological relevance. Am J Physiol. 267:1994;C313-C339.
5. Zoratti M, Szabò I. The mitochondrial permeability transition. Biochim Biophys Acta. 1241:1995;139-176.
6. Thayer SA, Miller RJ. Regulation of the intracellular free calcium concentration in single rat dorsal root ganglion neurones in vitro. J Physiol. 425:1990;85-116.
7. Werth JL, Thayer SA. Mitochondria buffer physiological calcium loads in cultured rat dorsal root ganglion neurons. J Neurosci. 14:1994;346-356.
8. i. J Neurosci. 14:1994;4007-4024.
9. 2+ uniporter by external adenine nucleotides: the uniporter behaves like a gated channel which is regulated by nucleotides and divalent cations. Biochemistry. 36:1997;7071-7080.
10. Jung DW, Baysal K, Brierly GP. The sodium-calcium antiport of heart mitochondrial is not electroneutral. J Biol Chem. 270:1995;672-678.
11. 2+ exchange. Trends Pharmacol Sci. 14:1993;408-413.
12. 2+ probe during ester loading and subsequent extrusion of residual dye from the cytosol. Similar prolonged incubations were claimed to enhance localization of rhod-2 to myocyte (Trollinger et al., 1997 [42]), hepatocyte (Hajnóczky et al., 1995 [32]) and glial (Simpson and Russell, 1996 [41]) mitochondria. Whether these protocols are applicable to other cells remains to be determined.
13. Griffiths EJ, Wei S-K, Haigney MCP, Ocampo CJ, Stern MD, Silverman HS. Inhibition of mitochondrial calcium efflux by clonazepam in intact single rat cardiomyocytes and effects on NADH production. Cell Calcium. 21:1997;321-329.
14. Nicholls DG, Scott ID. The regulation of brain mitochondrial calcium-ion transport. The role of ATP in the discrimination between kinetic and membrane-potential-dependent calcium-ion efflux mechanisms. Biochem J. 186:1980;833-839.
15. 2+ exchanger is electroneutral is inconsistent with Jung et al., 1995 [10].
16. Nicolli A, Basso E, Petronilli V, Wenger RM, Bernardi P. Interactions of cyclophilin with the mitochondrial inner membrane and regulation of the permeability transition pore, a cyclosporin A-sensitive channel. J Biol Chem. 271:1996;2185-2192.
17. 2+ signaling. High resolution imaging (see Golovina and Blaustein, 1997 [36], Simpson and Russell, 1996 [41] and Simpson et al., 1997 [46]) will be required to test this proposal. The CsA-sensitive responses of neurons to excitotoxic glutamate exposure (White and Reynolds, 1997 [22]) might be particularly interesting to examine.
18. Beutner G, Rück A, Riede B, Welte W, Brdiczka D. Complexes between kinases, mitochondrial porin and adenylate translocator in rat brain resemble the permeability transition pore. FEBS Lett. 396:1996;189-195.
19. O'Gorman E, Beutner G, Dolder M, Koretsky AP, Brdiczka D, Walliman T. The role of creatine kinase in inhibition of mitochondrial permeability transition. FEBS Lett. 414:1997;253-257.
20. 2+ exchange buffer glutamate-induced calcium loads in cultured cortical neurones. J Neurosci. 15:1995;1318-1328.
21. White RJ, Reynolds IJ. Mitochondrial depolarization in glutamate-stimulated neurones: and early signal specific to excitotoxin exposure. J Neurosci. 16:1996;5688-5697.
22. 2+ following intense glutamate stimulation of cultured rat forebrain neurones. J Physiol. 498:1997;31-47.
23. 2+ homeostasis. J Neurochem. 66:1996;403-411.
24. 2+-loads by mitochondria in cultured rat hippocampal neurons. J Neurophysiol. 76:1996;1611-1621.
25. 2+ release in mouse DRG neurones. Mol Neurosci. 18:1997;3929-3932.
26. 2+ homeostasis in cultured rat dorsal root ganglion neurons. Eur J Pharmacol. 340:1997;295-300.
27. 2+ removal in smooth muscle cells. Pflügers Arch. 431:1996;473-482.
28. 2+ clearance from a rat adrenal chromaffin cells. Neuron. 16:1996;219-228.
29. 2+ signaling is best viewed as an interactive network in which mitochondria participate actively.
30. Hehl S, Golard A, Hille B. Involvement of mitochondria in intracellular calcium sequestration by rat gonadotropes. Cell Calcium. 20:1996;515-524.
31. 2+-dependent changes in the mitochondrial energetics in single dissociated mouse sensory neurons. Biochem J. 283:1992;41-50.
32. Hajnóczky G, Robb-Gaspers LD, Seitz MB, Thomas AP. Decoding of cytosolic calcium oscillations in the mitochondria. Cell. 82:1995;415-424.
33. m rise required to increase NAD(P)H production was estimated by Griffiths et al., 1997 [13].
34. 2+ concentration in living single rat cardiac myocytes. Am J Physiol. 261:1991;H1123-H1134.
35. 2+ measurement in the mitochondria and the cytosol by confocal microscopy. Cell Calcium. 20:1996;53-61.
36. m.
37. 3-sensitive channels that are sensed by neighboring mitochondria. Science. 262:1993;744-747.
38. +, angiotensin II and vasopressin. Biochem J. 322:1997;785-792.
39. 2+ import normally prevents inactivation of the entry channel (see also Budd and Nicholls, 1996 [23]). However, other explanations are possible.
40. 2+ concentration in single cultured rat brain astrocytes. J Physiol. 497:1996;299-308.
41. 2+ waves in cultured oligodendrocytes. J Biol Chem. 271:1996;33493-33501.
42. 2+ transients during the contractile cycle in adult rabbit cardiac myocytes. Biochem Biophys Res Commun. 236:1997;742-838.
43. 2+ content, thapsigargin a larger (10-20-fold) more sustained increase. Experiments with okadaic acid suggested that receptor-mediated alterations in cellular protein phosphorylation status are conveyed directly or indirectly to mitochondria.
44. 2+ accumulated during tetanic stimulus, consistent with findings in chromaffin cells (Babcock et al., 1997 [29]) and neurons from other source (6-8,20-26]. It is proposed that the related phenomena of augmentation and facilitation of synaptic transmission may have a similar basis.
45. Jouaville LS, Ichas F, Hohlmuhamedov EL, Camacho P, Lechleiter JF. Synchronization of calcium waves by mitochondrial substrates in Xenopus laevis oocytes. Nature. 377:1995;438-441.
46. 2+ (Ichas et al., 1997 [17]), and that mitochondria may be a source of messengers for other signaling processes (Zeigler et al., 1997 [47], Maechler et al., 1997 [48]).
47. + glycohydrolase as ADP-ribosyl cyclase. Biochem J. 326:1997;401-405.
48. + are two messenger candidates whose production may be related to opening of the permeability transition pore (Zeigler et al., 1997 [47]).
49. Ankarcrona M, Dypbukt JM, Bonfoco E, Zhivotovsky B, Orrenius S, Lipton SA, Nicotera P. Glutamate-induced neuronal death: a succession of necrosis or apoptosis depending on mitochondrial function. Neuron. 15:1995;961-973.
50. Beal MF. Mitochondria, free radicals, and neurodegeneration. Curr Opin Neurobiol. 6:1996;661-666.
51. Nieminen A-L, Byrne AM, Herman B, Lemasters JJ. Mitochondrial permeability transition in hepatocytes induced by t-BuOOH: NAD(P)H and reactive oxygen species. Am J Physiol. 272:1997;C1286-C1294.
52. Zamzami N, Hirsch T, Dallporta B, Petit PZ, Kroemer G. Mitochondrial implication in accidental and programmed cell death: apoptosis and necrosis. J Bioenerg Biomembr. 29:1997;185-193.
53. m during Fas-induced apoptosis. Recombinant caspase 1 caused isolated mitochondria to swell, but by a mechanism that was resistant to the permeability transition inhibitors CsA and bongkrekic acid and not suppressed by overexpression of Bcl-2. Nevertheless, they propose that caspase-induced swelling results from opening of the transition pore (see Van der Heiden et al., 1997 [54] for a possible alternate explanation).
54. m.
55. Kluck RM, Bossy-Wetzel E, Green DR, Newmeyer DD. The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis. Science. 275:1997;1132-11336.
56. Yang J, Liu X, Bhalla K, Kim CN, Ibrado AM, Cai J, Peng T-I, Jones DP, Wang X. Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked. Science. 275:1997;1129-1132.
57. Murphy AN, Bredesen DE, Cortopassi Wang E, Fiskum G. Bcl-2 potentiates the maximal calcium uptake capacity of neural cell mitochondria. Proc Natl Acad Sci USA. 93:1996;9893-9898.
58. Antonsson B, Conti F, Ciavatta A, Montessuit S, Lewis S, Martinou I, Bernasconi L, Bernard A, Mermod JJ, Mazzei G, et al. Inhibition of Bax channel-forming activity by Bcl-2. Science. 277:1997;370-372.
59. L forms anion channel in synthetic lipid membranes. Nature. 385:1997;353-357.
60. Schendel SL, Xie Z, Montal MO, Matsuyama S, Montal M, Reed JC. Channel formation by antiapoptotic protein Bcl-2. Proc Natl Acad Sci USA. 94:1997;5113-5118.
61. Schlesinger PH, Gross A, Yin X-M, Yamamoto K, Saito M, Waksman G, Korsmeyer SJ. Comparison of the ion channel characteristics of proapoptotic BAX and antiapoptotic BCL-2. Proc Natl Acad Sci USA. 94:1997;11357-11362.
62. L fusion constructs co-localized with mitochondria, but Bax fusion protein was diffusely distributed. During staurosporine-induced apoptosis, Bax redistributed from cytosol to mitochondria within 90 min, consistent with the concept that at least a portion of its apoptotic action is exerted at or upon mitochondria.