Insulin‐like Growth Factors (IGF) I and II Utilize Different Calcium Signaling Pathways in a Primary Human Parathyroid Cell Culture Model

Wong, Chris; Lai, Teresa; Holly, Jeff M.P.; Wheeler, Malcolm H.; Stewart, Claire E.; Farndon, John

doi:10.1007/s00268-005-0339-8

Cited by 12 publications

(12 citation statements)

References 114 publications

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“…Wong et al (59) have described a role for the ryanodine receptors in parathyroid cells in regulating parathyroid hormone (PTH) secretion via the CaSR. Fellner and Arendshorst (24,25,55) have shown that the RyR exists in the renal afferent arteriolar vascular smooth muscle, which is contiguous with the JG cells.…”

Section: Discussionmentioning

confidence: 99%

“…The RyR serves as a signaling gateway for calcium release from the endoplasmic reticulum, and the RyR signaling pathway is important in regulating mobilization of intracellular calcium to be released from endoplasmic reticular stores (2,58). The parathyroid also contains RyR (59). Because of these associations with the contiguous afferent arteriole as well as the parathyroid, we investigated a possible role for the RyR in CaSR-activated, calcium-mediated control of renin release from the JG cells.…”

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confidence: 99%

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Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP₃pathway and the ryanodine receptor

Ortiz-Capisano

Reddy

Méndez

et al. 2013

American Journal of Physiology-Renal Physiology

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The calcium-sensing receptor (CaSR) is a G-coupled protein expressed in renal juxtaglomerular (JG) cells. Its activation stimulates calcium-mediated decreases in cAMP content and inhibits renin release. The postreceptor pathway for the CaSR in JG cells is unknown. In parathyroids, CaSR acts through Gq and/or Gi. Activation of Gq stimulates phospholipase C (PLC), and inositol 1,4,5-trisphosphate (IP3), releasing calcium from intracellular stores. Gi stimulation inhibits cAMP formation. In afferent arterioles, the ryanodine receptor (RyR) enhances release of stored calcium. We hypothesized JG cell CaSR activation inhibits renin via the PLC/IP3 and also RyR activation, increasing intracellular calcium, suppressing cAMP formation, and inhibiting renin release. Renin release from primary cultures of isolated mouse JG cells (n ϭ 10) was measured. The CaSR agonist cinacalcet decreased renin release 56 Ϯ 7% of control (P Ͻ 0.001), while the PLC inhibitor U73122 reversed cinacalcet inhibition of renin (104 Ϯ 11% of control). The IP3 inhibitor 2-APB also reversed inhibition of renin from 56 Ϯ 6 to 104 Ϯ 11% of control (P Ͻ 0.001). JG cells were positively labeled for RyR, and blocking RyR reversed CaSR-mediated inhibition of renin from 61 Ϯ 8 to 118 Ϯ 22% of control (P Ͻ 0.01). Combining inhibition of IP3 and RyR was not additive. Gi inhibition with pertussis toxin plus cinacalcet did not reverse renin inhibition (65 Ϯ 12 to 41 Ϯ 8% of control, P Ͻ 0.001). We conclude stimulating JG cell CaSR activates G q, initiating the PLC/IP3 pathway, activating RyR, increasing intracellular calcium, and resulting in calcium-mediated renin inhibition. calcium; renin; calcium-sensing receptor; inositol-3 phosphate; phospholipase C; protein kinase A; ryanodine receptor THE CALCIUM-SENSING RECEPTOR (CaSR) is a G protein-coupled 7-transmembrane receptor (33) found in the parathyroid gland, blood vessels, and kidney (18). In the parathyroid gland where CaSR was first described, high extracellular calcium results in decreased parathyroid hormone secretion (21). This is mediated by calcium activation of the CaSR, stimulating the G proteins G q and/or G i . In the parathyroid, activation of G q stimulates phospholipase C (PLC), producing diacylglycerol and inositol 1,4,5-trisphosphate (IP 3 ), the latter of which releases calcium from intracellular stores bound in the endoplasmic reticulum (ER) (48). G i stimulation leads to the inhibition of cAMP formation (16,48). Either pathway results in suppressing parathyroid hormone release.In the secretory juxtaglomerular (JG) cells, like the parathyroids, increased calcium results in the suppression of renin secretion (21,43,44). We have previously reported, both in vitro (44) and in vivo (6), that the JG cells contain CaSR, and that increased media calcium or activation of the CaSR with a calcimimetic (6, 43, 44) leads to suppression of renin secretion. JG cells synthesize, store, and release renin, the rate-limiting enzyme involved in the formation of angiotensin II (9). The cyclic nucleotide cAMP ...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP₃pathway and the ryanodine receptor

Ortiz-Capisano

Reddy

Méndez

et al. 2013

American Journal of Physiology-Renal Physiology

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“…The mode of action of TCS as an ED is controversial, and it was recently showed that TCS could exert its effects via several mechanisms, including the modulation of androgen receptor (28), the modulation of the activity of an adenylyl cyclase enzyme (29) and, recently, the activation of calcium signaling (25). The latter effect of TCS is of importance because it is well established that in most cell types, increase in cell calcium (Ca 2þ ) concentrations is associated with cell growth and/or secretory responses (30).…”

Section: Introductionmentioning

confidence: 99%

Activation of TRPA1 Channel by Antibacterial Agent Triclosan Induces VEGF Secretion in Human Prostate Cancer Stromal Cells

Derouiche

Mariot

Warnier

et al. 2017

Cancer Prevention Research

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Accruing evidence indicates that exposure to environmental compounds may adversely affect human health and promote carcinogenesis. Triclosan (TCS), an antimicrobial agent widely used as a preservative in personal care products, has been shown to act as an endocrine disruptor in hormone-dependent tissues. Here, we demonstrate a new molecular mechanism by which TCS stimulates the secretion by human prostate cancer stromal cells of vascular endothelial growth factor (VEGF), a factor known to promote tumor growth. This mechanism involves an increase in intracellular calcium levels due to the direct activation of a membrane ion channel. Using calcium imaging and electrophysiology techniques, we show for the first time that environmentally relevant concentrations of TCS activate a cation channel of the TRP family, TRPA1 (Transient Receptor Potential Ankirin 1), in primary cultured human prostate cancer stromal cells. The TCS-induced TRPA1 activation increased basal calcium in stromal cells and stimulated the secretion of VEGF and epithelial cells proliferation. Interestingly, immunofluorescence labeling performed on formalin-fixed paraffin-embedded prostate tissues showed an exclusive expression of the TRPA1 channel in prostate cancer stromal cells. Our data demonstrate an impact of the environmental factor TCS on the tumor microenvironment interactions, by activating a tumor stroma-specific TRPA1 ion channel. .

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“…Most authors attribute this to its blocking effect on Ca 2+ channels (Yang et al, 2005;Wong et al, 2006), although there is evidence of its direct effect on the genetic system of the cell (Wozniak et al, 2006;Caicedo et al, 2008;Salnikow and Zhitkovich, 2008).…”

Section: Resultsmentioning

confidence: 95%

“…It is considered that Ni 2+ is a nonselective blocker of Ca 2+ channels (Wong et al, 2006). Efficiency of Ni 2+ as a blocker was determined relative to L and T types of Ca 2+ channels, as well as capacitive Ca 2+ channels, controlled by a release of Ca 2+ from the depositary (Clarson et al, 2003;Yang et al, 2005).…”

Section: Resultsmentioning

confidence: 99%

Influence of activator and inhibitors of Ca2+ channels on proliferative activity in Tetrahymena pyriformis infusoria

2012

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It was determined that change in DNA content in macronuclei occurs in the T. pyriformis infuso ria under the influence of an activator (caffeine) and inhibitors of Ca 2+ channels (verapamil), NiCl 2 , and CdCl 2 . Caffeine (10 mM) stimulates DNA synthesis. Verapamil (5 µM), CdCl 2 (125 µM), and NiCl 2 (100 µM) decrease DNA content in macronuclei by 30 min after proliferative stimulation. By 4 h of incuba tion, there is, on average, 10% less DNA in macronuclei of Tetrahymena preprocessed with verapamil than in the control cells. The cells preprocessed with CdCl 2 and NiCl 2 differ from the control cells by lower DNA content almost at all studied periods, but they restore the level of nuclear DNA by 4 h. It is assumed that trans mission of proliferative signals in the T. pyriformis has a Ca 2+ dependent character.

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Insulin‐like Growth Factors (IGF) I and II Utilize Different Calcium Signaling Pathways in a Primary Human Parathyroid Cell Culture Model

Abstract: IGFs I and II induce mitogenesis by different calcium signaling pathways. These data suggest that parathyroid cells may utilize different calcium signaling pathways to distinguish growth factors and serum calcium changes.

Cited by 12 publications

References 114 publications

Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP₃pathway and the ryanodine receptor

Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP₃pathway and the ryanodine receptor

Activation of TRPA1 Channel by Antibacterial Agent Triclosan Induces VEGF Secretion in Human Prostate Cancer Stromal Cells

Influence of activator and inhibitors of Ca2+ channels on proliferative activity in Tetrahymena pyriformis infusoria

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Insulin‐like Growth Factors (IGF) I and II Utilize Different Calcium Signaling Pathways in a Primary Human Parathyroid Cell Culture Model

Abstract: IGFs I and II induce mitogenesis by different calcium signaling pathways. These data suggest that parathyroid cells may utilize different calcium signaling pathways to distinguish growth factors and serum calcium changes.

Cited by 12 publications

References 114 publications

Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP3pathway and the ryanodine receptor

Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP3pathway and the ryanodine receptor

Activation of TRPA1 Channel by Antibacterial Agent Triclosan Induces VEGF Secretion in Human Prostate Cancer Stromal Cells

Influence of activator and inhibitors of Ca2+ channels on proliferative activity in Tetrahymena pyriformis infusoria

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Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP₃pathway and the ryanodine receptor

Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP₃pathway and the ryanodine receptor