Endothelin-B receptor-mediated Ca2+ signaling in human melanocytes

Kang, Hyun-Woo; Kang, Won-Hyoung; Lee, C.-O.

doi:10.1007/pl00008082

Cited by 25 publications

(27 citation statements)

References 23 publications

(25 reference statements)

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“…The signaling pathways activated by ETs are still controversial, with reports pointing to the participation of a G i protein (Imokawa et al, 1996(Imokawa et al, , 1997(Imokawa et al, , 2000, cAMP and PKA (Imokawa et al, 1996(Imokawa et al, , 1997, IP 3 (Kang et al, 1998;Kolch et al, 1993;Yada et al, 1991), Ca 2þ rise (Imokawa et al, 1997;Kang et al, 1998;Kobayashi et al, 2002;Yada et al, 1991), PKC (Imokawa et al, 1996(Imokawa et al, , 1997(Imokawa et al, , 2000, PLC (Imokawa et al, 2000;Kang et al, 1998), and MAPKs (Chen et al, 2007;Imokawa et al, 1996Imokawa et al, , 2000. PKC can phosphorylate and directly activate Raf-1 (Cacace et al, 1996;Kolch et al, 1993;Ueffing et al, 1997), which is one of the components of the MAPK signaling pathway.…”

Section: Introductionmentioning

confidence: 96%

Melanopsin and Clock Genes: Regulation by Light and Endothelin in the Zebrafish ZEM-2S Cell Line

Farhat¹,

Martins²,

Lima³

et al. 2009

LCBI

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It is well known that clocks are present in brain regions other than the suprachiasmatic nucleus and in many peripheral tissues. In the teleost, Danio rerio, peripheral oscillators can be directly synchronized by light. Danio rerio ZEM-2S embryonic cells respond to light with differential growth: cells kept in constant light exhibited a strong inhibition of proliferation, whereas in cells kept in light:dark (LD) cycles (14L:10D and 10L:14D) or in constant darkness (DD), the doubling times were not statistically different. We demonstrated by RT-PCR followed by PCR that ZEM-2S cells express two melanopsins, Opn4x and Opn4m, and the six Cry genes. The presence of the protein OPN4x was demonstrated by immunocytochemistry. The pattern of temporal expression of the genes Opn4x, Per1, Cry1b, and Clock was studied in ZEM-2S cells kept for five days in 12L:12D or DD. In 12L:12D, the clock genes Per 1 and Cry1b exhibited robust circadian expression, while Opn4x and Clock expression seemed to vary in an ultradian pattern. Both Per1 and Cry1b genes had higher expression during the L phase; Clock gene had an increase in expression coincident with the D phase, and during the subjective night. In DD, the temporal variation of Per1 and Cry1b genes was greatly attenuated but not extinguished, and the higher expressions were shifted to the transition times between subjective day and night, demonstrating that Per and Cry1b were synchronized by the LD cycle. Clock and Opn4x kept the ultradian oscillation, but the rhythm was not statistically significant. As endothelins (ET) have been reported to be a potent stimulator of Per genes in rodents, we investigated the effect of endothelin on ZEM-2S cells, which express ETA receptors. Cells were kept in 12D:12L for five days, and then treated with 10(-11) to 10(-8)M ET-1 for 24 h. ET-1 exhibited a biphasic effect on Opn4x expression. At 10(-11)M, the hormone exerted a highly significant stimulation of Opn4x expression during the L phase and introduced a circadian oscillatory pattern. At 10(-10)M, a significant increase was seen at ZT21 and ZT0 (i.e., at the end of the D phase and beginning of the L phase), whereas 10(-9) and 10(-8)M ET-1 inhibited the expression of Opn4x at most ZTs. Clock expression was unaffected by 10(-8)M ET-1; however, in the presence of lower concentrations, the expression was enhanced at some ZTs, strengthening the ultradian oscillation. ET-1 at 10(-11) and 10(-10)M had no effect on Per1 circadian expression; however, 10(-9) and 10(-8)M ET-1 reduced the amplitude of Per1 expression in the beginning of the L phase. ET-1 effects were less evident on Cry 1b. For both genes, the reduction in expression was not sufficient to abolish the circadian oscillatory pattern. Based on these results and data in the literature, a link between ET-1 stimulation of ETA receptors may be established by E4BP4 binding to the promoters and consequent inhibition of gene expression.

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Section: Introductionmentioning

confidence: 96%

Melanopsin and Clock Genes: Regulation by Light and Endothelin in the Zebrafish ZEM-2S Cell Line

Farhat¹,

Martins²,

Lima³

et al. 2009

LCBI

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“…Activation of ET-B receptors leads to phospholipase C-dependent formation of IP 3 and diacylglycerol (Kang et al, 1998;Slominski et al, 2004). IP 3 triggers the IP 3 receptors on the endoplasmic reticulum (ER) and causes transient depletion of ER Ca 2 þ stores.…”

Section: Introductionmentioning

confidence: 99%

ORAI1 Ca2+ Channels Control Endothelin-1-Induced Mitogenesis and Melanogenesis in Primary Human Melanocytes

Stanisz

Stark

Kilch

et al. 2012

Journal of Investigative Dermatology

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UV radiation of the skin triggers keratinocytes to secrete endothelin-1 (ET-1) that binds to endothelin receptors on neighboring melanocytes. Melanocytes respond with a prolonged increase in intracellular Ca(2+) concentration ([Ca(2+)](i)), which is necessary for proliferation and melanogenesis. A major fraction of the Ca(2+) signal is caused by entry through Ca(2+)-permeable channels of unknown identity in the plasma membrane. ORAI Ca(2+) channels are molecular determinants of Ca(2+) release-activated Ca(2+) (CRAC) channels and are expressed in many tissues. Here, we show that ORAI1-3 and their activating partners stromal interaction molecules 1 and 2 (STIM1 and STIM2) are expressed in human melanocytes. Although ORAI1 is the predominant ORAI isoform, STIM2 mRNA expression exceeds STIM1. Inhibition of ORAI1 by 2-aminoethoxydiphenyl borate (2-APB) or downregulation of ORAI1 by small interfering RNA (siRNA) reduced Ca(2+) entry and CRAC current amplitudes in activated melanocytes. In addition, suppression of ORAI1 caused reduction in the ET-1-induced cellular viability, melanin synthesis, and tyrosinase activity. Our results imply a role for ORAI1 channels in skin pigmentation and their potential involvement in UV-induced stress responses of the human skin.

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“…The Ca 2+ release may be mediated by InsP 3 R, as is the case of Ca 2+ oscillations at fertilization of mouse oocytes [29]. Furthermore, in many types of cells, Gprotein-coupled m3AChRs are known to be linked to the PI signaling pathway leading to IICR [14,15,20,34]. To Numbers on the Y-axis represent the Fluo-3 fluorescence intensity confirm the possible involvement of the PI signaling pathway and IICR, we used specific PLC inhibitors and an InsP 3 R antagonist.…”

Section: Effect Of Extracellular Ca 2+ On Ach-induced Ca 2+ Oscillationsmentioning

confidence: 99%

Acetylcholine induces Ca 2+ oscillations via m3/m4 muscarinic receptors in the mouse oocyte

Kang

Park

Han

et al. 2003

Pfl�gers Archiv European Journal of Physiology

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Changes in intracellular Ca2+ concentration are required for the activation of mammalian oocytes. They are caused mainly by Ca2+ release from the endoplasmic reticulum (ER) via Ins P3 receptors (Ins P3R). Several studies have reported that acetylcholine (ACh) is capable of triggering early activation events in mouse oocytes over-expressed with the m1 muscarinic ACh receptor (m1AChR). Here we examined which subtypes of the mAChR (m1 to m4) are involved in the generation of Ca2+ oscillations in native mouse oocytes. ACh (10 microM) elicited regular Ca2+ oscillations similar to those induced by sperm in their temporal characteristics. The Ca2+ oscillations were abolished by application with atropine, the mAChR inhibitor. Within 1 min after treatment of ACh, intracellular Fluo-3 fluorescence intensity increased from 794+/-119 to 2023+/-755 (increase to 250% of original value), indicating a strong rise of cytosolic Ca2+ concentration. 4-DAMP mustard and Tropicamide, specific antagonists of m3AChR and m4AChR, completely abolished ACh-induced Ca2+ oscillations. In the ovulated oocytes, the expression of m3/m4 AChR was clearly detected by RT-PCR analysis. Furthermore, ACh-induced Ca2+ oscillations were also abolished or decreased by PLC inhibitors (U73122 or D609) and an Ins P3-receptor antagonist (xestospongin C), confirming that ACh generates Ca2+ oscillations via the PLC-Ins P3 (PI) pathway. These results strongly suggest that m3/m4AChR is coupled to the generation of Ca2+ oscillations mainly via the PI pathway in mouse oocytes.

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Endothelin-B receptor-mediated Ca2+ signaling in human melanocytes

Cited by 25 publications

References 23 publications

Melanopsin and Clock Genes: Regulation by Light and Endothelin in the Zebrafish ZEM-2S Cell Line

Melanopsin and Clock Genes: Regulation by Light and Endothelin in the Zebrafish ZEM-2S Cell Line

ORAI1 Ca2+ Channels Control Endothelin-1-Induced Mitogenesis and Melanogenesis in Primary Human Melanocytes

Acetylcholine induces Ca 2+ oscillations via m3/m4 muscarinic receptors in the mouse oocyte

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