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CXC chemokine melanocyte

Murielle Mimeault, Surinder K Batra
Cutaneous malignant melanoma is the most aggressive form of skin cancer with an extremely poor survival rate for the patients diagnosed with locally invasive and metastatic disease states. Intensive research has led in last few years to an improvement of the early detection and curative treatment of primary cutaneous melanomas that are confined to the skin by tumor surgical resection. However, locally advanced and disseminated melanomas are generally resistant to conventional treatments, including ionizing radiation, systemic chemotherapy, immunotherapy and/or adjuvant stem cell-based therapies, and result in the death of patients...
March 10, 2012: World Journal of Clinical Oncology
K Y Lee, S Y Jeon, J W Hong, K W Choi, C Y Lee, S J Choi, J H Kim, K H Song, K H Kim
BACKGROUND: Vitiligo is an acquired pigmentary disorder caused by the destruction of melanocytes. Two of the major theories regarding the pathogenesis of vitiligo are the autoimmune theory and autocytotoxicity theory, but, the precise pathogenetic mechanism is still not clarified. OBJECTIVES: We investigated the effects of ET-1, tacrolimus and tumour necrosis factor-α (TNF-α) on proliferation and migration of cultured normal human melanocytes (NHMs). We also sought to clarify the theoretical rationale underlying the topical tacrolimus monotherapy or tacrolimus-UV combination therapy as tools for vitiligo treatment...
May 2013: Journal of the European Academy of Dermatology and Venereology: JEADV
Linda W Horton, Yingchun Yu, Snjezana Zaja-Milatovic, Robert M Strieter, Ann Richmond
The Duffy antigen receptor for chemokines (DARC) has been classified as a "silent" receptor, as it can bind CXC and CC chemokines to undergo ligand-induced receptor internalization, but is not coupled to trimeric G proteins required for the classic G protein-coupled receptor-mediated signaling. CXC chemokine receptor-2 (CXCR2) has been shown to play a major role in tumor angiogenesis. To test the hypothesis that these two chemokine receptors might play opposing roles in the growth of melanoma tumors, we developed a transgenic mouse model, where the preproendothelin promoter/enhancer (PPEP) is used to drive expression of either murine DARC (mDARC) or murine CXCR2 (mCXCR2) in endothelial cells...
October 15, 2007: Cancer Research
Sunil K Manna, Abira Sarkar, Yashin Sreenivasan
Considering the role of interleukin-8 (IL-8) in a large number of acute and chronic inflammatory diseases, the regulation of IL-8-mediated biological responses is important. Alpha-melanocyte-stimulating hormone (alpha-MSH), a tridecapeptide, inhibits most forms of inflammation by an unknown mechanism. In the present study, we have found that alpha-MSH interacts predominantly with melanocortin-1 receptors and inhibits several IL-8-induced biological responses in macrophages and neutrophils. It down-regulated receptors for IL-8 but not for TNF, IL-4, IL-13 or TNF-related apoptosis-inducing ligand (TRAIL) in neutrophils...
March 2006: European Journal of Immunology
Catherine R Mangahas, Gelo V dela Cruz, George Friedman-Jiménez, Sumayah Jamal
The endothelin pathway plays a critical role in melanoma tumor progression by a variety of mechanisms that enhance tumor cell growth, invasion, and metastasis. Here, we investigate the effect of this pathway on CXC chemokine expression in human melanoma cells and melanocytes. As determined by ELISA, endothelin-1 (ET-1) induces CXCL1 and CXCL8 secretion in three human melanoma cell lines in a concentration-dependent fashion. These responses are mediated by the endothelin-B receptor and are sustained over a 40 h time course...
August 2005: Journal of Investigative Dermatology
Joerg Wenzel, Barbara Bekisch, Manfred Uerlich, Otto Haller, Thomas Bieber, Thomas Tüting
We studied 253 primary melanomas of the skin for histologic signs of regression. Detailed immunohistologic analyses, including expression of MxA (an antiviral protein specifically induced by type I interferons), the chemokine IP10/CXCL10, the chemokine receptor CXCR3, and the cytotoxic molecule granzyme B, were performed for 14 typical regressive tumors and 20 control samples (congenital nevi, halo nevi, unaffected skin). We found high expression of MxA, indicating local type I interferon production, in inflamed regressive melanocytic lesions, along with large numbers of natural interferon-producing plasmacytoid dendritic cells, CXCR3+ lymphocytes, and granzyme B+ lymphocytes...
July 2005: American Journal of Clinical Pathology
Maja Mockenhaupt, Frank Peters, Ildiko Schwenk-Davoine, Yared Herouy, Ingrid Schraufstätter, Peter Elsner, Johannes Norgauer
The CXC-chemokines 1 and 8 (CXCL1 and CXCL8) are ligands for the G protein-coupled CXC-chemokine receptor 2 (CXCR2). Both chemokines and CXCR2 are components of a potent autocrine growth factor loop in human melanoma cells. Currently, expression and biological function of both chemokines in normal human melanocytes is poorly defined. Here we describe that cocktails of melanocyte growth factors consisting of basic fibroblast growth factor (bFGF), endothelin 1 (ET-1) and alpha-melanocyte-stimulating hormone (alpha-MSH) stimulated release of CXCL1 and CXCL8, but did not influence expression of CXCR2 in human melanocytes...
October 2003: International Journal of Molecular Medicine
S J Getting, M Perretti
To date five melanocortin receptors (MC-R) have been cloned, identified and shown to have a wide distribution throughout the body and likely many diverse functions. MC1-R, found on melanocytes, is involved in pigmentation, while MC2-R is the classic adrenocorticotropic (ACTH) receptor found on the adrenal cortex and adipocytes. MC3-R, MC4-R and MC5-R are in their infancy with regard to their characterization. MC4-R has generated wide interest for its involvement in obesity, whereas our own studies have indicated a role for MC3-R in experimental inflammation...
February 2000: Drug News & Perspectives
Johannes Norgauer, Stefan Dichmann, Frank Peters, Maja Mockenhaupt, Ingrid Schraufst tter, Yared Herouy
The CXC-chemokines Groalpha and interleukin-8 (IL-8) are ligands for two different G protein-coupled receptors, named CXC-chemokine receptor I & II (CXCRI & II). Both cytokines are potent growth factors for human melanoma cells, with only limited proliferative activity towards normal melanocytes. Here we analysed the influence of various cytokines on the expression of CXCRI & II and the CXC-chemokine-induced proliferation in human melanocytes. Flow cytometric studies revealed no protein expression of CXCRI and low protein expression of CXCRII at the cell surface of normal melanocytes...
March 2003: European Journal of Dermatology: EJD
Stephen J Getting, Helen C Christian, Connie W Lam, Felicity N E Gavins, Roderick J Flower, Helgi B Schiöth, Mauro Perretti
The issue of which melanocortin receptor (MC-R) is responsible for the anti-inflammatory effects of melanocortin peptides is still a matter of debate. Here we have addressed this aspect using a dual pharmacological and genetic approach, taking advantage of the recent characterization of more selective agonists/antagonists at MC1 and MC3-R as well as of the existence of a naturally defective MC1-R mouse strain, the recessive yellow (e/e) mouse. RT-PCR and ultrastructural analyses showed the presence of MC3-R mRNA and protein in peritoneal macrophages (M phi) collected from recessive yellow (e/e) mice and wild-type mice...
March 15, 2003: Journal of Immunology
Punita Dhawan, Ann Richmond
The CXC chemokine, CXCL1 (melanoma growth-stimulatory activity/growth-regulated protein alpha), plays a major role in inflammation, angiogenesis, tumorigenesis, and wound healing. Recently, chemokines have been extensively related to cellular transformation, tumor growth, homing, and metastasis. CXCL1 and its mouse homologue MIP-2 have been shown to be involved in the process of tumor formation. When chemokines such as CXCL1 and CXCL8 (IL-8) become disregulated so that they are chronically expressed, tissue damage, angiogenesis, and tumorigenesis can follow...
July 2002: Journal of Leukocyte Biology
Benton R Middleman, Michael Friedman, David H Lawson, Patricia B DeRose, Cynthia Cohen
Malignant melanoma (MM) cells do not require all exogenous growth factors of normal melanocytes. It is hypothesized that they make their own growth factors including melanoma growth stimulatory activity (MGSA). Cultured melanoma cells respond to MGSA with increased growth and angiogenesis suggesting a role for MGSA in MM proliferation, differentiation, and progression. We assessed the prognostic significance of MGSA expression in 37 primary MM immunostained for MGSA. Immunostains were graded for intensity (0-3+), percentage of cells immunostained, and location of immunostain (intraepidermal, junctional, or dermal)...
May 2002: Modern Pathology
Punita Dhawan, Ann Richmond
Constitutive activation of NF-kappa B is an emerging hallmark of various types of tumors including breast, colon, pancreatic, ovarian, and melanoma. In melanoma cells, the basal expression of the CXC chemokine, CXCL1, is constitutively up-regulated. This up-regulation can be attributed in part to constitutive activation of NF-kappa B. Previous studies have shown an elevated basal I kappa B kinase (IKK) activity in Hs294T melanoma cells, which leads to an increased rate of I kappa B phosphorylation and degradation...
March 8, 2002: Journal of Biological Chemistry
J Yang, J Luan, Y Yu, C Li, R A DePinho, L Chin, A Richmond
The molecular and genetic events that contribute to the genesis and progression of cutaneous malignant melanoma are poorly understood, attributable in large part to the different genetic alterations accompanying tumorigenesis. Inhibitor of kinase 4a (INK4a) is often inactivated in families with hereditary melanoma. Loss of INK4a/alternate reading frame (ARF) in mice is associated with increased incidence of other tumors such as lymphoma and fibrosarcoma. However, the incidence of melanoma in INK4a/ARF-deficient mice is very low...
November 15, 2001: Cancer Research
J Yang, A Richmond
Constitutive IKK activity associated with increased IkappaBalpha phosphorylation and degradation contribute to the high level of endogenous nuclear factor-kappaB (NF-kappaB) activation in Hs294T melanoma cells as compared with RPE cells (R. L. Shattuck-Brandt and A. Richmond, Cancer Res., 57: 3032-3039, 1997; M. N. Devalaraja et al., Cancer Res., 59: 1372-1377, 1999). To determine whether this endogenous NF-kappaB activation was characteristic of melanoma, we examined the level of constitutive activation of NF-kappaB in a number of melanoma cell lines...
June 15, 2001: Cancer Research
C Nirodi, S NagDas, S P Gygi, G Olson, R Aebersold, A Richmond
The melanoma growth stimulatory activity/growth-regulated protein, CXCL1, is constitutively expressed at high levels during inflammation and progression of melanocytes into malignant melanoma. It has been shown previously that CXCL1 overexpression in melanoma cells is due to increased transcription as well as stability of the CXCL1 message. The transcription of CXCL1 is regulated through several cis-acting elements including Sp1, NF-kappaB, HMGI(Y), and the immediate upstream region (IUR) element (nucleotides -94 to -78), which lies immediately upstream to the nuclear factor kappaB (NF-kappaB) element...
March 23, 2001: Journal of Biological Chemistry
D Wang, A Richmond
Melanoma growth stimulatory activity/growth-regulated protein (MGSA/GRO), a CXC chemokine, plays an important role in inflammation, wound healing, growth regulation, angiogenesis, and tumorigenesis. Constitutive expression of MGSA/GROalpha in melanoma tumors is associated with constitutive nuclear factor (NF)-kappaB activity. We show here that either exogenous addition or continuous expression of MGSA/GROalpha in immortalized melanocytes enhances NF-kappaB activation, as well as mitogen-activated protein (MAP) kinase kinase kinase (MEKK) 1, MAP kinase kinase (MEK) 3/6, and p38 MAP kinase activation...
February 2, 2001: Journal of Biological Chemistry
D Wang, W Yang, J Du, M N Devalaraja, P Liang, K Matsumoto, K Tsubakimoto, T Endo, A Richmond
The MGSA/GRO protein is endogenously expressed in almost 70% of the melanoma cell lines and tumors, but not in normal melanocytes. We have previously demonstrated that over-expression of human MGSA/GROalpha, beta or gamma in immortalized murine melanocytes (melan-a cells) enables these cells to form tumors in SCID and nude mice. To examine the possibility that the MGSA/GRO effect on melanocyte transformation requires expression of other genes, differential display was performed. One of the mRNA's identified in the screen as overexpressed in MGSA/GRO transformed melan-a clones was the newly described M-Ras or R-Ras3 gene, a member of the Ras gene superfamily...
September 21, 2000: Oncogene
T E Scholzen, T Brzoska, D H Kalden, M Hartmeyer, M Fastrich, T A Luger, C A Armstrong, J C Ansel
Human dermal microvascular endothelial cells (HDMEC) are capable of mediating leukocyte-endothelial interactions by the expression of cellular adhesion molecules and the release of proinflammatory cytokines and chemokines during cutaneous inflammation. Recent studies support the important role for proopiomelanocortin (POMC) peptides, such as alpha-melanocyte stimulating hormone (alpha-MSH), as immunomodulators in the cutaneous immune system. The purpose of the studies described here was to determine whether HDMEC serves as both target and source for POMC peptides...
October 20, 1999: Annals of the New York Academy of Sciences
T Brzoska, D H Kalden, T Scholzen, T A Luger
The neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH) is recognized as a potent mediator of immune and inflammatory reactions. Accordingly, alpha-MSH in vitro, as well as in vivo, antagonizes the proinflammatory activities of cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha (TNF alpha). Since the molecular basis of these antiinflammatory effects is not well known, the influence of alpha-MSH on IL-1 beta-induced chemokine production and transcription factor activation was investigated in human keratinocytes...
October 20, 1999: Annals of the New York Academy of Sciences
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