Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema.

Pentland, Alice P.; Mahoney, Mỹ G.; Jacobs, Sydney; Holtzman, Michael J.

doi:10.1172/jci114746

Cited by 116 publications

(64 citation statements)

References 27 publications

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“…Other mechanisms by which EP 1 and EP 3 receptor signaling could activate PKCζ include through stimulation of 3-phosphoinositide-dependent protein kinase (PDK1), or through TC10, that activates PKCζ through the scaffold proteins Par3 and Par6 [57,58]. Finally, because UVR up-regulates the production and release of lysophosphatidylcholine and prostaglandins by keratinocytes [59][60][61], activation of PKCζ in response to these paracrine factors may be additive and appears to be an important signaling intermediate in the dendritic response of human to melanocytes to UVR. (25 nM) or misoprostol (500 nM).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Scott

Fricke

Fender

et al. 2007

Experimental Cell Research

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Prostaglandins are lipid signaling intermediates released by keratinocytes in response to ultraviolet irradiation (UVR) in the skin. The main prostaglandin released following UVR is PGE 2 , a ligand for 4 related G-protein coupled receptors (EP 1 , EP 2 , EP 3 and EP 4 ). Our previous work established that PGE 2 stimulates melanocyte dendrite formation through activation of the EP 1 and EP 3 receptors. The purpose of the present report is to define the signaling intermediates involved in EP 1 and EP 3 -dependent dendrite formation in human melanocytes. We recently showed that activation of the atypical PKCζ isoform stimulates melanocyte dendricity in response to treatment with lysophosphatidylcholine. We therefore examined the potential contribution of PKCζ activation on EP 1 and EP 3 -dependent dendrite formation in melanocytes. Stimulation of the EP 1 and EP 3 receptors by selective agonists activated PKCζ, and inhibition of PKCζ activation abrogated EP 1 and EP 3 -receptor mediated melanocyte dendricity. Because of the importance of Rho-GTP binding proteins in the regulation of melanocyte dendricity, we also examined the effect of EP 1 and EP 3 receptor activation on Rac and Rho activity. Neither Rac nor Rho was activated upon treatment with EP 1,3 -receptor agonists. We show that melanocytes express only the EP 3A1 isoform, but not the EP 3B receptor isoform, previously associated with Rho activation, consistent with a lack of Rho stimulation by EP 3 agonists. Our data suggest that PKCζ activation plays a predominant role in regulation of PGE 2 -dependent melanocyte dendricity.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Scott

Fricke

Fender

et al. 2007

Experimental Cell Research

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“…A similar mechanism exists in the mouse urinary bladder, where urinary epithelial cell TRPV1 is required for hypoosmolarity-evoked release of ATP (37), which in turn appears to be detected by P2X3 (ATP-gated ion channel subtype three)-containing nerve terminals in the bladder wall (42). Alternative candidate heat-evoked signaling molecules include nitric oxide, which also undergoes TRPV1-dependent release from urinary epithelial cells (43), as well as prostaglandins and platelet-activating factor, which have been shown to be released from keratinocytes in response to UV radiation (44), extreme heating, oxidative stress (25), or, in human keratinocytes, capsaicin-evoked activation of TRPV1 (21). Biochemical analysis of supernatants from warmth-treated keratinocytes would allow the "soluble messenger" hypothesis to be tested experimentally, as would the analysis of thermosensation and thermoregulation in mice lacking TRPV4 selectively in keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

Warm Temperatures Activate TRPV4 in Mouse 308 Keratinocytes

Chung¹,

Lee²,

Caterina³

2003

Journal of Biological Chemistry

261

211

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Mammalian survival requires constant monitoring of environmental and body temperature. Recently, several members of the transient receptor potential vanilloid (TRPV) subfamily of ion channels have been identified that can be gated by increases in temperature into the warm (TRPV3 and TRPV4) or painfully hot (TRPV1 and TRPV2) range. In rodents, TRPV3 and TRPV4 proteins have not been detected in sensory neurons but are highly expressed in skin epidermal keratinocytes. Here, we show that in response to warm temperatures (>32°C), the mouse 308 keratinocyte cell line exhibits nonselective transmembrane cationic currents and Ca 2؉ influx. Both TRPV3 and TRPV4 are expressed in 308 cells. However, the warmth-evoked responses we observe most closely resemble those mediated by recombinant TRPV4 on the basis of their electrophysiological properties and sensitivity to osmolarity and the phorbol ester, 4␣-phorbol-12,13-didecanoate. Together, these data support the notion that keratinocytes are capable of detecting modest temperature elevations, strongly suggest that TRPV4 participates in these responses, and define a system for the cell biological analysis of warmth transduction.The perception of ambient temperature is a physiological process critical to the maintenance of body temperature and the avoidance of painful or dangerous thermal extremes. Since the identification of the heat-sensing ion channel TRPV1 (1), 1 which is activated by temperatures above 42°C, there has been a significant focus on potential thermosensory functions for this and other ion channels of the transient receptor potential family. TRPV2 (2) and TRPV3 (3-5) were first described as heat transducers operative at very hot (Ͼ52°C) and moderately warm (Ͼ34°C) temperatures, respectively. TRPV4, which was originally identified as an osmosensory ion channel (6 -9), can also be activated by warm temperatures (Ͼ34°C) (10, 11). In addition, two TRP proteins outside of the TRPV subfamily, TRPM8 (12, 13) and ANKTM1 (ankyrin repeat/transmembrane-containing ion channel) (14), have been identified as cold-activated ion channels expressed in sensory neurons.In mammals, the skin is extremely important for the transduction of thermal information and its transmission to the central nervous system. Cutaneous thermosensation has been largely attributed to the sensory nerves that innervate the dermal and epidermal layers of the skin. Recent reports, however, have suggested the possibility that other skin components, most notably keratinocytes, might also participate in temperature sensation. TRPV1 and TRPV2 are highly expressed in distinct subsets of sensory neurons (2). In humans, TRPV3 is also expressed in sensory neurons (5). In contrast, attempts to detect TRPV4 (9, 10) and TRPV3 (3) at the protein level in rodent sensory neurons have been unsuccessful. Rather, immunohistochemical studies of mouse and rat skin have revealed that keratinocytes exhibit the greatest degree of cutaneous TRPV3 (3) and TRPV4 (10) expression. In addition, although peripheral sensory neurons ...

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“…Beside these physiological and bene®cial e ects, the solar U.V. light also causes pathological and noxious e ects including skin erythema (Pentland et al, 1990), premature skin aging (Fisher et al, 1996) and skin cancer (Ananthaswamy and Pierceall, 1990). Recently, many studies have been undertaken to elucidate the cellular signaling pathways triggered by U.V.…”

mentioning

confidence: 99%

“…The role of ERKs and SAP kinases activation in U.V.-A and U.V.-B responses is not clearly understood. However, U.V.-induced skin injury is followed by an enhanced prostaglandin synthesis that contributes to the in¯ammatory response (Pentland et al, 1990). The activity of phospholipase A 2 (PLA 2 ) that controls prostaglandin synthesis (Nakazato et al, 1991) has been reported to be stimulated after phosphorylation by MAP kinases (Qiu and Leslie, 1994).…”

mentioning

confidence: 99%

Solar ultraviolet light activates extracellular signal-regulated kinases and the ternary complex factor in human normal keratinocytes

et al. 1998

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Exposure to ultraviolet radiation of solar light is responsible for in¯ammation, premature skin aging and is the main cause of human skin carcinogenesis. While the noxious consequences of U.V. exposure are known, the molecular events triggered by this radiation are poorly understood. We observed that U.V.-A and U.V.-B irradiation of human keratinocytes induces the activation of tyrosine kinase pathways leading to the tyrosine phosphorylation of several cellular proteins. We also observed a stimulation of the Stress Activated Protein kinases (SAPKs), p38 and JNK, and an activation of the transcription factors AP-1 in response to U.V.-A and U.V.-B radiation. Furthermore, we clearly demonstrated that physiological U.V. doses are able to activate the Extracellular signal-Regulated Kinases, ERK1 and ERK2, which could explain the activation of the Ternary Complex Factor. Thus, in human keratinocytes, solar U.V. light activates multiple signalling pathways that could be involved in skin in¯ammation following U.V.-induced skin injury or in U.V.-induced skin carcinogenesis.

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Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema.

Cited by 116 publications

References 27 publications

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Prostaglandin E2 regulates melanocyte dendrite formation through activation of PKCζ

Warm Temperatures Activate TRPV4 in Mouse 308 Keratinocytes

Solar ultraviolet light activates extracellular signal-regulated kinases and the ternary complex factor in human normal keratinocytes

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