α1-adrenergic receptors activate Ca2+-permeable cationic channels in prostate cancer epithelial cells

Thebault, Stéphanie; Roudbaraki, Morad; Sydorenko, Vadym; Shuba, Yaroslav; Lemonnier, Loïc; Slomianny, Christian; Dewailly, Etienne; Bonnal, J; Mauroy, Brigitte; Skryma, Roman; Prevarskaya, Natalia

doi:10.1172/jci16293

Cited by 66 publications

(24 citation statements)

References 41 publications

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“…First, gadolinium influx was significantly reduced in specific TRPC knockdown monocytes compared with control monocytes. Second, several investigators reported that SKF-96365 is able to reduce cation influx through TRPCs [32,[34][35][36]. In accordance with these findings, in the presence of SKF-96365, gadolinium and sodium influx were significantly reduced in our study.…”

Section: Discussionsupporting

confidence: 92%

Transient receptor potential channels in essential hypertension

Liu

Scholze

Zhu³

et al. 2006

Journal of Hypertension

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Section: Discussionsupporting

confidence: 92%

Transient receptor potential channels in essential hypertension

Liu

Scholze

Zhu³

et al. 2006

Journal of Hypertension

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“…There is evidence in the literature for 2-APB blockade of store-independent calcium entry, including that activated by acetylcholine in PC12 adrenal chromaffin cells (49), by carbachol in murine gastric smooth muscle (27), and by ␣ 1A adrenoceptor agonists in prostate cancer epithelial cells (45,50). 2-APB also inhibits receptor-activated, store-independent calcium entry mediated by TRPC3 overexpressed in HEK293 cells (28,52).…”

Section: Discussionmentioning

confidence: 99%

Calmodulin mediates norepinephrine-induced receptor-operated calcium entry in preglomerular resistance arteries

Facemire

Arendshorst

2005

American Journal of Physiology-Renal Physiology

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Although L-type voltage-dependent calcium channels play a major role in mediating vascular smooth muscle cell contraction in the renal vasculature, non-L-type calcium entry mechanisms represent a significant component of vasoactive agonist-induced calcium entry in these cells as well. To investigate the role of these non-voltage-dependent calcium entry pathways in the regulation of renal microvascular reactivity, we have characterized the function of store- and receptor-operated channels (SOCs and ROCs) in renal cortical interlobular arteries (ILAs) of rats. Using fura 2-loaded, microdissected ILAs, we find that the L-type channel antagonist nifedipine blocks less than half the rise in intracellular calcium concentration ([Ca(2+)](i)) elicited by norepinephrine. SOCs were activated in these vessels using the sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA) inhibitors cyclopiazonic acid and thapsigargin and were dose dependently blocked by the SOC antagonists Gd(3+) and 2-aminoethoxydiphenyl borate (2-APB) and the combined SOC/ROC antagonist SKF-96365. Gd(3+) had no effect on the non-L-type Ca(2+) entry activated by 1 microM NE. A low concentration of SKF-96365 that did not affect thapsigargin-induced store-operated Ca(2+) entry blocked 60-70% of the NE-induced Ca(2+) entry. Two different calmodulin inhibitors (W-7 and trifluoperazine) also blocked the NE-induced Ca(2+) entry. These data suggest that in addition to L-type channels, NE primarily activates ROCs rather than SOCs in ILAs and that this receptor-operated Ca(2+) entry mechanism is regulated by calmodulin. Interestingly, 2-APB completely blocked the NE-induced non-L-type Ca(2+) entry, implying that SOCs and ROCs in preglomerular resistance vessels share a common molecular structure.

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“…However, there are inconsistencies between the sequencing data and functional studies on α 1A -adrenoceptors and muscarinic receptors. Two papers have suggested a role for the α 1A -adrenoceptor in proliferation of LNCaP cells 149 and chemoresistance of DU145 cells; 150 however receptor detection was based on α 1A -drenoceptors antibodies, which are notorious for lack of specificity 151 . The muscarinic receptor agonist carbachol likewise stimulates proliferation of LNCaP cells despite an apparent lack of mRNA for any of the relevant acetylcholine receptor subtypes 135 …”

Section: Prostate Cancermentioning

confidence: 99%

Age-related changes in the innervation of the prostate gland

2013

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The adult prostate gland grows and develops under hormonal control while its physiological functions are controlled by the autonomic nervous system. The prostate gland receives sympathetic input via the hypogastric nerve and parasympathetic input via the pelvic nerve. In addition, the hypogastric and pelvic nerves also provide sensory inputs to the gland. This review provides a summary of the innervation of the adult prostate gland and describes the changes which occur with age and disease. Growth and development of the prostate gland is age dependent as is the occurrence of both benign prostate disease and prostate cancer. In parallel, the activity and influence of both the sympathetic and parasympathetic nervous system changes with age. The influence of the sympathetic nervous system on benign prostatic hyperplasia is well documented and this review considers the possibility of a link between changes in autonomic innervation and prostate cancer progression.

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α1-adrenergic receptors activate Ca2+-permeable cationic channels in prostate cancer epithelial cells

Cited by 66 publications

References 41 publications

Transient receptor potential channels in essential hypertension

Transient receptor potential channels in essential hypertension

Calmodulin mediates norepinephrine-induced receptor-operated calcium entry in preglomerular resistance arteries

Age-related changes in the innervation of the prostate gland

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