Xestospongin C is an equally potent inhibitor of the inositol 1,4,5-trisphosphate receptor and the endoplasmic-reticulum Ca2+pumps

Smet, Patrick De; Parys, Jan B.; Callewaert, Geert; Weidema, A. Freek; Hill, Evelyn; Smedt, Humbert De; Erneux, Christophé; Sorrentino, Vincenzo; Missiaen, Ludwig

doi:10.1054/ceca.1999.0047

Cited by 120 publications

(86 citation statements)

References 26 publications

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“…Such observations do not encourage a further consideration of ryanodine receptors as the leak mechanism in VSMCs. We have no data on the roles of IP 3 receptors in the leak mechanism, but IP 3 receptor inhibitors (2-aminoethoxydiphenylborate and xestospongin C) either enhanced or had no effect on passive Ca 2ϩ leak from stores of the A7r5 VSMC line (8,21), arguing against IP 3 receptors playing a role.…”

Section: Discussionmentioning

confidence: 86%

Translocon closure to Ca²⁺ leak in proliferating vascular smooth muscle cells

Amer

Li²,

O’Regan³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Discussionmentioning

confidence: 86%

Translocon closure to Ca²⁺ leak in proliferating vascular smooth muscle cells

Amer

Li²,

O’Regan³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, these experiments did not yield clear answers on the involvement of IP 3 Rs, as both 2-aminoethoxydiphenyl borate and xestospongin C by themselves evoked Ca 2ϩ release in a significant proportion of cells (data not shown). Several unspecific effects of these compounds have been described earlier (22)(23)(24)(25). Alternatively, menthol may activate a Ca 2ϩ -release pathway different from the well characterized IP 3 and ryanodine receptors.…”

Section: Discussionmentioning

confidence: 96%

TRPM8-independent Menthol-induced Ca2+ Release from Endoplasmic Reticulum and Golgi

Mahieu

Owsianik

Verbert

et al. 2007

Journal of Biological Chemistry

120

105

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Menthol, a secondary alcohol produced by the peppermint herb, Mentha piperita, is widely used in the food and pharmaceutical industries as a cooling/soothing compound and odorant. It induces Ca 2؉ influx in a subset of sensory neurons from dorsal root and trigeminal ganglia, due to activation of TRPM8, a Ca 2؉ -permeable, cold-activated member of the TRP superfamily of cation channels. Menthol also induces Ca 2؉ release from intracellular stores in several TRPM8-expressing cell types, which has led to the suggestion that TRPM8 can function as an intracellular Ca 2؉ -release channel. Here we show that menthol induces Ca 2؉ release from intracellular stores in four widely used cell lines (HEK293, lymph node carcinoma of the prostate (LNCaP), Chinese hamster ovary (CHO), and COS), and provide several lines of evidence indicating that this release pathway is TRPM8-independent: 1) menthol-induced Ca 2؉ release was potentiated at higher temperatures, which contrasts to the cold activation of TRPM8; 2) overexpression of TRPM8 did not enhance the menthol-induced Ca 2؉ release; 3) menthol-induced Ca 2؉ release was mimicked by geraniol and linalool, which are structurally related to menthol, but not by the more potent TRPM8 agonists icilin or eucalyptol; and 4) TRPM8 expression in HEK293 cells was undetectable at the protein and mRNA levels. Moreover, using a novel TRPM8-specific antibody we demonstrate that both heterologously expressed TRPM8 (in HEK293 cells) and endogenous TRPM8 (in LNCaP cells) are mainly localized in the plasma membrane, which contrast to previous localization studies using commercial anti-TRPM8 antibodies. Finally, aequorin-based measurements demonstrate that the TRPM8-independent menthol-induced Ca 2؉ release originates from both endoplasmic reticulum and Golgi compartments.Menthol is a naturally occurring compound responsible for the minty flavor and smell of the mint plant (Mentha piperita). Whereas the first descriptions of the use of menthol as a cooling/soothing compound and odorant date back to ϳ2000 years ago, menthol is still extensively used as an additive in a wide variety of products ranging from ointments and candies to cigarettes. The soothing, refreshing and invigorating feature of the oil made from the peppermint herb is useful in massage for muscle fatigue. It is also used in the treatment of asthma, colic, exhaustion, fever, flatulence, headache, nausea, scabies, sinusitis, and vertigo (1). Currently the best described molecular target of menthol is TRPM8, 2 a member of the melastatin branch of the TRP superfamily of cation channels. TRPM8 was initially identified in a screening procedure aimed at identifying mRNAs that are up-regulated in prostate cancer (2). Subsequently, TRPM8 expression was also demonstrated to be strongly up-regulated in several other primary tumor types including breast, colon, lung, and skin (2). The following studies identified TRPM8 in a subset of dorsal root and trigeminal neurons (3), and found it to function as a plasma membrane Ca 2ϩ -permeable cation ...

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“…Regardless, we investigated the possibility that PI(3,5)P 2 could also activate IP 3 Rs by blocking them with xestospongin C. In the presence of xestospongin C, the majority of the Ca 2ϩ response to PI(3,5)P 2 was intact. Although selective for IP 3 R, xestospongin C also inhibits SERCA; thus, it may be that SR stores were partially depleted by the inhibitor (13). If so, xestospongin C would be expected to decrease the PI(3,5)P 2 response.…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca²⁺in arterial smooth muscle cells and elicits vasocontraction

Silswal

Parelkar

Wacker

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Silswal N, Parelkar NK, Wacker MJ, Brotto M, Andresen J. Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca 2ϩ in arterial smooth muscle cells and elicits vasocontraction. Am J Physiol Heart Circ Physiol 300: H2016 -H2026, 2011. First published March 18, 2011 doi:10.1152 doi:10. /ajpheart.01011.2010 (51,59). In humans, a deleterious allele of FIG4 is a risk factor for amyotrophic and primary lateral sclerosis, and mutations in MTMR genes are associated with myopathies and Charcot-Marie-Tooth diseases (10, 70). Thus, PI(3,5)P 2 appears important in several diseases, although much remains to be learned regarding its function in eukaryotes.Interestingly, PI(3,5)P 2 binds to and activates ryanodine receptors (RyRs), thereby increasing intracellular Ca 2ϩ by emptying SR stores (59, 71). In arterial smooth muscle, SR Ca 2ϩ contributes to the development and maintenance of vascular tone (52, 73), but the role of PI(3,5)P 2 in arterial vascular Ca 2ϩ signaling remains undefined. We hypothesized that PI(3,5)P 2 would mobilize SR Ca 2ϩ stores, causing vasocontraction. Therefore, we examined the effects of PI(3,5)P 2 in vitro in isolated mouse aortic smooth muscle cells using ratiometric Ca 2ϩ imaging and in isolated arteries using myography. Our results demonstrated that PI(3,5)P 2 caused contraction of aortic rings by activating RyRs to release SR Ca 2ϩ followed by the opening of voltage-dependent Ca 2ϩ channels (VDCCs). If extracellular Ca 2ϩ entry was prevented, either by blockade of VDCC, by removal of extracellular Ca 2ϩ , or by the inclusion of LaCl 3 , PI(3,5)P 2 still generated transient contractions. Prior depletion of SR Ca 2ϩ stores, however, prevented PI(3,5)P 2 from having any effect. Thus, the activation of RyRs by PI(3,5)P 2 was sufficient to release SR Ca 2ϩ and cause small contractions, whereas VDCCs were required to achieve full increases in intracellular Ca 2ϩ and sustained aortic contractions. METHODS Animals and reagents.Male C57BL/6J mice were purchased from The Jackson Laboratory (Bar Harbor, ME) at 12 wk of age. Mice were killed by CO 2 inhalation. The Animal Care and Use Committee of the University of Missouri-Kansas City approved all protocols. All reagents were purchased from Sigma (St. Louis, MO) unless otherwise noted. PI lipids, including PI(3,5)P 2, PI(3)P, and PI(5)P (Echelon Biosciences, Salt Lake City, UT), were prepared by dissolving them in chloroform, methanol, and water at a ratio of 1:2:0.8 as per the manufacturer's instructions, and just before addition to the bath, they were mixed with histone (Echelon Biosciences) solution at a ratio of 1:0.8. Histone carrier protein, which is required for the intracellular delivery of PIs (46), stock solution was prepared by dissolving the protein in double-distilled H 2O to a concentration of 1 mM. Solvents never exceeded 0.1% (vol/vol), and vehicle controls included the solvents and histone carrier protein but not the PI lipid.

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Xestospongin C is an equally potent inhibitor of the inositol 1,4,5-trisphosphate receptor and the endoplasmic-reticulum Ca2+pumps

Cited by 120 publications

References 26 publications

Translocon closure to Ca²⁺ leak in proliferating vascular smooth muscle cells

Translocon closure to Ca²⁺ leak in proliferating vascular smooth muscle cells

TRPM8-independent Menthol-induced Ca2+ Release from Endoplasmic Reticulum and Golgi

Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca²⁺in arterial smooth muscle cells and elicits vasocontraction

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Xestospongin C is an equally potent inhibitor of the inositol 1,4,5-trisphosphate receptor and the endoplasmic-reticulum Ca2+pumps

Cited by 120 publications

References 26 publications

Translocon closure to Ca2+ leak in proliferating vascular smooth muscle cells

Translocon closure to Ca2+ leak in proliferating vascular smooth muscle cells

TRPM8-independent Menthol-induced Ca2+ Release from Endoplasmic Reticulum and Golgi

Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca2+in arterial smooth muscle cells and elicits vasocontraction

Contact Info

Product

Resources

About

Translocon closure to Ca²⁺ leak in proliferating vascular smooth muscle cells

Translocon closure to Ca²⁺ leak in proliferating vascular smooth muscle cells

Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca²⁺in arterial smooth muscle cells and elicits vasocontraction