SK&amp;F 96365 (1-{β-[3-(4-methoxyphenyl)propoxy]- 4-methoxyphenylethyl}-1H-imidazole hydrochloride) stimulates phosphoinositide hydrolysis in human U373 MG astrocytoma cells

Arias‐Montaño, José‐Antonio; Gibson, W. J.; Young, J. M.

doi:10.1016/s0006-2952(98)00125-7

Cited by 6 publications

(3 citation statements)

References 15 publications

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“…In previous studies this drug was found to inhibit receptor‐stimulated Ca 2+ entry following store depletion in various cell types such as human platelets, neutrophils and endothelial cells (Merritt et al ., 1990), lymphocytes (Mason et al ., 1993), HL‐60 cells (Koch et al ., 1994), Jurkat T cells (Sei et al ., 1995) and in several different smooth muscles (Li et al ., 1997; Wayman et al ., 1997; Takemoto et al ., 1998; Wassdal et al ., 1998; Yang, 1998; Lagaud et al ., 1999). However, SK&F 96365 is neither very potent (the IC 50 in most cases around 10 μ M ) nor selective as it can also inhibit voltage‐gated Ca 2+ channels (Merritt et al ., 1990), K + channels (Schwarz et al ., 1994), the SR Ca 2+ ATPase (Mason et al ., 1993), stimulate phosphoinositide hydrolysis and cause intracellular Ca 2+ release (Arias‐Montano et al ., 1998) and facilitate nicotinic receptor desensitization (Hong & Chang, 1994).…”

Section: Discussionmentioning

confidence: 99%

Voltage‐dependent inhibition of the muscarinic cationic current in guinea‐pig ileal cells by SK&F 96365

Zholos

Tsytsyura

Philyppov

et al. 2000

British J Pharmacology

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1 The eects of SK&F 96365 on cationic current evoked either by activating muscarinic receptors with carbachol or by intracellularly applied GTPgS (in the absence of carbachol) were studied using patch-clamp recording techniques in single guinea-pig ileal smooth muscle cells. 2 SK&F 96365 reversibly inhibited the muscarinic receptor cationic current in a concentration-, time-and voltage-dependent manner producing concomitant alteration of the steady-state I-V relationship shape which could be explained by assuming that increasing membrane positivity increased the anity of the blocker. The inhibition was similar for both carbachol-and GTPgSevoked currents suggesting that the cationic channel rather than the muscarinic receptor was the primary site of the SK&F 96365 action. 3 Increased membrane positivity induced additional rapid inhibition of the cationic current by SK&F 96365 which was more slowly relieved during membrane repolarization. Both the inhibition and disinhibition time course could be well ®tted by a single exponential function with the time constants decreasing with increasing positivity for the inhibition (e-fold per about 12 mV) and approximately linearly decreasing with increasing negativity for the disinhibition. 4 At a constant SK&F 96365 concentration, the degree of cationic current inhibition was a sigmoidal function of the membrane potential with a potential of half-maximal increase positive to about +30 mV and a slope factor of about 713 mV. 5 Increasing the duration of voltage steps at 780 or at 80 mV, increased the percentage inhibition; the degree of inhibition was almost identical at both potentials providing evidence that the same cationic channel was responsible for the cationic current both at negative and at positive potentials. 6 It is concluded that the distinctive and unique mode of SK&F 96365 action on the muscarinic receptor cationic channel is a valuable tool in future molecular biology studies of this channel.

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Section: Discussionmentioning

confidence: 99%

Voltage‐dependent inhibition of the muscarinic cationic current in guinea‐pig ileal cells by SK&F 96365

Zholos

Tsytsyura

Philyppov

et al. 2000

British J Pharmacology

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“…Hence, the effects of histamine on different glial cells have been extensively studied. Histamine has been shown to stimulate phosphoinositide turnover in cultured rat cerebral type 2 astrocytes (Kondou et al 1991) and human U373 MG astrocytoma cells (Arias‐Montaño et al 1994). H 1 receptor‐mediated increases in [Ca 2+ ] i have been reported both in vitro , e.g.…”

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confidence: 99%

Histamine‐induced calcium entry in rat cerebellar astrocytes: evidence for capacitative and non‐capacitative mechanisms

Jung

Pfeiffer

Deitmer

2000

The Journal of Physiology

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We have investigated the effects of histamine on the intracellular calcium concentration ([Ca2+]i) of cultured rat cerebellar astrocytes using fura‐2‐based Ca2+ imaging microscopy. Most of the cells responded to the application of histamine with an increase in [Ca2+]i which was antagonized by the H1 receptor blocker mepyramine. When histamine was applied for several minutes, the majority of the cells displayed a biphasic Ca2+ response consisting of an initial transient peak and a sustained component. In contrast to the initial transient [Ca2+]i response, the sustained, receptor‐activated increase in [Ca2+]i was rapidly abolished by chelation of extracellular Ca2+ or addition of Ni2+, Mn2+, Co2+ and Zn2+, but was unaffected by nifedipine, an antagonist of L‐type voltage‐activated Ca2+ channels. These data indicate that the sustained increase in [Ca2+]i was dependent on Ca2+ influx. When intracellular Ca2+ stores were emptied by prolonged application of histamine in Ca2+‐free conditions, Ca2+ re‐addition after removal of the agonist did not lead to an ‘overshoot’ of [Ca2+]i indicative of store‐operated Ca2+ influx. However, Ca2+ stores were refilled despite the absence of any substantial change in the fura‐2 signal. Depletion of intracellular Ca2+ stores using cyclopiazonic acid in Ca2+‐free saline and subsequent re‐addition of Ca2+ to the saline resulted in an increase in [Ca2+]i that was significantly enhanced in the presence of histamine. The results suggest that besides capacitative mechanisms, a non‐capacitative, voltage‐independent pathway is involved in histamine‐induced Ca2+ entry into cultured rat cerebellar astrocytes.

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“…Iwamuro et al found, for the first time, that SKF 96365 sensitively inhibited the SOCE activated by ET-1 at high concentrations (Iwamuro et al, 1999). As a SOCE inhibitor, SKF 96365 was reported to inhibit cell proliferation in many cancers by inducing cell apoptosis and cell cycle arrest in G2/M phase (Nordström et al, 1992;Lee et al, 1993;Arias-Montaño et al, 1998;Cai et al, 2009;Zeng et al, 2013;Zhang et al, 2015;Jing et al, 2016;Wang W. et al, 2018). Autophagy seems to play different roles in the pharmacological mechanism of SKF 96365.…”

Section: Role Of Store-operated Calcium Entry In Cancermentioning

confidence: 99%

Development of Store-Operated Calcium Entry-Targeted Compounds in Cancer

et al. 2021

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Store-operated Ca2+ entry (SOCE) is the major pathway of Ca2+ entry in mammalian cells, and regulates a variety of cellular functions including proliferation, motility, apoptosis, and death. Accumulating evidence has indicated that augmented SOCE is related to the generation and development of cancer, including tumor formation, proliferation, angiogenesis, metastasis, and antitumor immunity. Therefore, the development of compounds targeting SOCE has been proposed as a potential and effective strategy for use in cancer therapy. In this review, we summarize the current research on SOCE inhibitors and blockers, discuss their effects and possible mechanisms of action in cancer therapy, and induce a new perspective on the treatment of cancer.

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SK&F 96365 (1-{β-[3-(4-methoxyphenyl)propoxy]- 4-methoxyphenylethyl}-1H-imidazole hydrochloride) stimulates phosphoinositide hydrolysis in human U373 MG astrocytoma cells

Cited by 6 publications

References 15 publications

Voltage‐dependent inhibition of the muscarinic cationic current in guinea‐pig ileal cells by SK&F 96365

Voltage‐dependent inhibition of the muscarinic cationic current in guinea‐pig ileal cells by SK&F 96365

Histamine‐induced calcium entry in rat cerebellar astrocytes: evidence for capacitative and non‐capacitative mechanisms

Development of Store-Operated Calcium Entry-Targeted Compounds in Cancer

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