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Systemic and hepatic chemerin, and chemerin receptor activation were not changed in hepatocellular carcinoma. Chemerin protein was induced in liver in NASH, but was unchanged in HCC tissues. Hepatic and serum chemerin and ex vivo analyzed chemerin receptor activation do not differ in murine NASH-associated HCC when compared to NASH.
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endogenously secreted chemerin plays an autocrine/paracrine role in white adipose tissue, identifying chemerin as a therapeutic target to modulate adipose remodelling.
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elevated levels of chemerin were found in colons of mice with experimental colitis, and a neutralizing anti-chemerin antibody improved intestinal inflammation
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Data suggest a potential role for chemerin and CMKLR1 in the regulation of inflammatory responses in the tumor microenvironment.
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Suggest reduction of chemerin could contribute to the antiobesity/antidiabetic properties described for alpha-lipoic acid.
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Study indicates that Chemerin plays a role in the negative cross-talk between skeletal muscle and adipose tissue. Specifically, Chemerin promotes the adipogenic differentiation potential and alters the myoblast cell fate from myogenesis to adipogenesis.
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Data indicate that chemerin may play an important role in regulating mitochondrial remodelling and function in skeletal muscle.
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The chemerin15 (C15) precursor, chemerin, and its receptor, ChemR23, are both upregulated after skin damage and the receptor is expressed by macrophages, neutrophils, and keratinocytes. C15 delivery dampens immediate inflammatory events.
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findings reveal previously uncharacterized regulators of chemerin expression in skin and identify a physiologic role for chemerin in skin barrier defense against microbial pathogens.
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A novel autocrine/paracrine role for chemerin in regulating osteoclast differentiation of hematopoietic stem cells
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this study reports that retinoic acid-activated endothelial cells can promote myeloid and plasmacytoid dendritic cell transmigration across endothelial cell monolayers through the endogenous production of chemerin
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Data suggest that chemerin/ChemR23 (chemokine-like receptor 1) signaling is not essential for adipocyte differentiation, but it appears to play a role in control of body weight and energy metabolism as overweight/obesity progresses.
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Studies using isolated islets and perfused pancreas revealed impaired glucose-dependent insulin secretion (GSIS) in chemerin-deficient mice. Conversely, chemerin transgenic mice revealed enhanced GSIS and improved glucose tolerance.
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Following TNFalpha treatment, increased elastase and tryptase modify the balance between activation and deactivation, elevating active chemerin concentration in adipocyte media and subsequent CMKLR1 activation.
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results of this study indicate that chemerin plays a role in the negative cross-talk between skeletal muscle and adipose tissue to regulate myogenesis
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Downstream targets of Chemerin/ChemR23 signaling are phosphorylated in vitro and are expressed in mouse tooth development, suggesting roles for Chemerin/ChemR23-mediated epithelial-mesenchymal cell signaling during tooth morphogenesis.
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These results rule out the direct anti-inflammatory effect of chemerin on macrophages ex vivo, described previously in the literature, despite the expression of a functional ChemR23 receptor in these cells.
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Chemerin increases in airways during viral infection; Chemerin appears to have anti-inflammatory properties, by acting on ChemR23 expressed by non-leukocytic cells dampening the inflammatory response promoted by the viral infection; the chemerin/ChemR23 system plays important roles in the physiopathology of viral pneumonia
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a fundamental role for chemerin/CMKLR1 signaling in clonal expansion during adipocyte differentiation as well as a role for PPARgamma in regulating chemerin expression.
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The current data show that adipocyte hypertrophy and chronic inflammation are equally important in inducing chemerin synthesis.
