Methyl-β-cyclodextrin Prevents Ca2+-Induced Ca2+ Release in Smooth Muscle Cells of Mouse Urinary Bladder

Abstract

Abstract. We examined the effects of methyl-β-cyclodextrin (MβCD) on Ca

Caveolin-1 Assembles Type 1 Inositol 1,4,5-Trisphosphate Receptors and Canonical Transient Receptor Potential 3 Channels into a Functional Signaling Complex in Arterial Smooth Muscle Cells

“…M␤CD reduced smooth muscle cell membrane capacitance and this was reversed by subsequent cholesterol treatment. Reduced cell capacitance has also been reported in arterial smooth muscle cells lacking cav-1, and in M␤CD-treated uterine and urinary bladder smooth muscle cells (13,32,33). These studies and ours indicate that acute and chronic loss of caveolae reduces smooth muscle cell surface area.…”

Ca2+ entry following P2X receptor activation induces IP3 receptor‐mediated Ca2+ release in myocytes from small renal arteries

“…In smooth muscles, elevation of [Ca 2+ ]i is caused either by cell membrane depolarization (electromechanical coupling; Somlyo and Somlyo, 1968) leading to opening of VGCCs, which are manifested by the generation of action potentials or allow Ca 2+ to 'leak' into the cell giving rise to 'sparklets' (Amberg et al, 2007), or by activation of metabotropic receptors (pharmacomechanical coupling; Somlyo and Somlyo, 1968) usually linked to Gq/11-GTP/PLC/IP3/IP3R-mediated Ca 2+ release, or by a combination of these mechanisms Davis and Hill, 1999). The initial Ca 2+ mobilization may be augmented by RyR-mediated Ca 2+ release recruited via a CICR mechanism (Bolton and Gordienko, 1998;Bayguinov et al, 2000;White and McGeown, 2002;Kotlikoff, 2003;Zhang et al, 2003;Hotta et al, 2007;Gordienko et al, 2008). The contribution of these mechanisms to intracellular Ca 2+ mobilization may vary in different SMC types, depending on the type and strength of stimuli, SMC excitability and spatial organisation of intracellular Ca 2+ release units (Walsh, 1994;Bolton and Gordienko, 1998;Bolton et al, 1999;Davis and Hill, 1999;Bayguinov et al, 2000;Gordienko et al, 2001Gordienko et al, , 2008Janiak et al, 2001;Gordienko and Bolton, 2002;White and McGeown, 2002;Kotlikoff, 2003;Wier and Morgan, 2003;Zhang et al, 2003;Lamont and Wier, 2004;McCarron et al, 2006;Amberg et al, 2007;Hotta et al, 2007;Wier et al, 2009).…”

“…The initial Ca 2+ mobilization may be augmented by RyR-mediated Ca 2+ release recruited via a CICR mechanism (Bolton and Gordienko, 1998;Bayguinov et al, 2000;White and McGeown, 2002;Kotlikoff, 2003;Zhang et al, 2003;Hotta et al, 2007;Gordienko et al, 2008). The contribution of these mechanisms to intracellular Ca 2+ mobilization may vary in different SMC types, depending on the type and strength of stimuli, SMC excitability and spatial organisation of intracellular Ca 2+ release units (Walsh, 1994;Bolton and Gordienko, 1998;Bolton et al, 1999;Davis and Hill, 1999;Bayguinov et al, 2000;Gordienko et al, 2001Gordienko et al, , 2008Janiak et al, 2001;Gordienko and Bolton, 2002;White and McGeown, 2002;Kotlikoff, 2003;Wier and Morgan, 2003;Zhang et al, 2003;Lamont and Wier, 2004;McCarron et al, 2006;Amberg et al, 2007;Hotta et al, 2007;Wier et al, 2009).We hypothesized that in vascular myocytes Ca 2+ entry following activation of ionotropic P2X receptors may induce IP3R-mediated Ca 2+ release. Our hypothesis was based on the following findings reported in visceral and vascular myocytes: (i) a localized increase in [Ca 2+ ]i induced by local flash release of Ca 2+ from a 'caged' precursor may trigger IP3R-mediated Ca 2+ release (Ji et al, 2006); (ii) Ca 2+ entry via VGCCs facilitates IP3R-mediated Ca 2+ release following stimulation of metabotropic receptors (Gordienko et al, 2008); (iii) the stoichiometric ratio of RyRs to IP3Rs in SMCs is 1:9-10, suggesting the existence of a Ca 2+ -storage compartment devoid of RyRs but equipped with IP3Rs (Wibo and Godfraind, 1994); (iv) caffeine/ryanodinereleasable and IP3-releasable calcium stores in the SR of vascular myocytes are at least partially distinct with about 56% of the SR being solely IP3-sensitive (Blauste...…”

Caveolin-1 Facilitates the Direct Coupling between Large Conductance Ca2+-activated K+ (BKCa) and Cav1.2 Ca2+ Channels and Their Clustering to Regulate Membrane Excitability in Vascular Myocytes

“…The BK Ca protein contains a binding motif to caveolin-1 and is often co-localized in caveolae (10,11). Several reports indicate that caveolae are involved in Ca 2ϩ hotspot and spark generation (12,13). Caveolin-1 knockout (KO) mice congenitally lack caveolae and exhibit many types of cardiovascular abnormalities (9,14,15).…”