Genetic ablation of caveolin-1 modifies Ca2+ spark coupling in murine arterial smooth muscle cells.

Szczegóły
Abstrakt

Tytuł:: Genetic ablation of caveolin-1 modifies Ca2+ spark coupling in murine arterial smooth muscle cells.
Autorzy:: Cheng X; Department of Physiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Jaggar JH
Źródło:: American journal of physiology. Heart and circulatory physiology [Am J Physiol Heart Circ Physiol] 2006 Jun; Vol. 290 (6), pp. H2309-19. Date of Electronic Publication: 2006 Jan 20.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: Bethesda, Md. : American Physiological Society,
MeSH Terms:: Calcium Signaling/*genetics
Calcium Signaling/*physiology
Caveolin 1/*genetics
Caveolin 1/*physiology
Muscle, Smooth, Vascular/*physiology
Myocytes, Smooth Muscle/*physiology
Animals ; Barium/pharmacology ; Cadmium/pharmacology ; Calcium Signaling/drug effects ; Electrophysiology ; Enzyme Inhibitors/pharmacology ; Fluorescent Dyes ; Fura-2 ; Indoles/pharmacology ; Mice ; Mice, Knockout ; Microscopy, Confocal ; Microscopy, Electron ; Muscle, Smooth, Vascular/ultrastructure ; Myocytes, Smooth Muscle/ultrastructure ; Nitroarginine/pharmacology ; Patch-Clamp Techniques ; Ryanodine Receptor Calcium Release Channel/physiology
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Grant Information:: R01 HL067061 United States HL NHLBI NIH HHS; R01 HL077678 United States HL NHLBI NIH HHS
Substance Nomenclature:: 0 (Caveolin 1)
0 (Enzyme Inhibitors)
0 (Fluorescent Dyes)
0 (Indoles)
0 (Ryanodine Receptor Calcium Release Channel)
00BH33GNGH (Cadmium)
2149-70-4 (Nitroarginine)
24GP945V5T (Barium)
3T9U9Z96L7 (paxilline)
TSN3DL106G (Fura-2)
Entry Date(s):: Date Created: 20060124 Date Completed: 20060622 Latest Revision: 20200930
Update Code:: 20240104
PubMed Central ID:: PMC1698957
DOI:: 10.1152/ajpheart.01226.2005
PMID:: 16428350
: Czasopismo naukowe

L-type, voltage-dependent calcium (Ca(2+)) channels, ryanodine-sensitive Ca(2+) release (RyR) channels, and large-conductance Ca(2+)-activated potassium (K(Ca)) channels comprise a functional unit that regulates smooth muscle contractility. Here, we investigated whether genetic ablation of caveolin-1 (cav-1), a caveolae protein, alters Ca(2+) spark to K(Ca) channel coupling and Ca(2+) spark regulation by voltage-dependent Ca(2+) channels in murine cerebral artery smooth muscle cells. Caveolae were abundant in the sarcolemma of control (cav-1(+/+)) cells but were not observed in cav-1-deficient (cav-1(-/-)) cells. Ca(2+) spark and transient K(Ca) current frequency were approximately twofold higher in cav-1(-/-) than in cav-1(+/+) cells. Although voltage-dependent Ca(2+) current density was similar in cav-1(+/+) and cav-1(-/-) cells, diltiazem and Cd(2+), voltage-dependent Ca(2+) channel blockers, reduced transient K(Ca) current frequency to approximately 55% of control in cav-1(+/+) cells but did not alter transient K(Ca) current frequency in cav-1(-/-) cells. Furthermore, although K(Ca) channel density was elevated in cav-1(-/-) cells, transient K(Ca) current amplitude was similar to that in cav-1(+/+) cells. Higher Ca(2+) spark frequency in cav-1(-/-) cells was not due to elevated intracellular Ca(2+) concentration, sarcoplasmic reticulum Ca(2+) load, or nitric oxide synthase activity. Similarly, Ca(2+) spark amplitude and spread, the percentage of Ca(2+) sparks that activated a transient K(Ca) current, the amplitude relationship between sparks and transient K(Ca) currents, and K(Ca) channel conductance and apparent Ca(2+) sensitivity were similar in cav-1(+/+) and cav-1(-/-) cells. In summary, cav-1 ablation elevates Ca(2+) spark and transient K(Ca) current frequency, attenuates the coupling relationship between voltage-dependent Ca(2+) channels and RyR channels that generate Ca(2+) sparks, and elevates K(Ca) channel density but does not alter transient K(Ca) current activation by Ca(2+) sparks. These findings indicate that cav-1 is required for physiological Ca(2+) spark and transient K(Ca) current regulation in cerebral artery smooth muscle cells.

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