CXCL14 enhances insulin-dependent glucose uptake in adipocytes and is related to high-fat diet-induced obesity

Takahashi, Michiko; Takahashi, Yutaka; Takahashi, Ken­ichi; Zolotaryov, Fyodor N.; Hong, Kyongsu; Iida, Keiji; Okimura, Yasuhiko; Kaji, Hidesuke; Chihara, Kazuo

doi:10.1016/j.bbrc.2007.10.120

Cited by 35 publications

(32 citation statements)

References 27 publications

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“…However, CXCL14 was found to be dispensable for dendritic-cell and macrophage function under in vivo inflammatory conditions (20). CXCL14 also has a role in insulin signaling (21,22). A general association between activation of mesenchymal cells and CXCL14 up-regulation, in agreement with the present and earlier findings, are also supported by the finding of CXCL14 up-regulation in activated stellate cells (23).…”

Section: Discussionsupporting

confidence: 82%

CXCL14 is an autocrine growth factor for fibroblasts and acts as a multi-modal stimulator of prostate tumor growth

Augsten

Hägglöf

Olsson

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

207

218

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This study explored the role of secreted fibroblast-derived factors in prostate cancer growth. Analyses of matched normal and tumor tissue revealed up-regulation of CXCL14 in cancer-associated fibroblasts of a majority of prostate cancer. Fibroblasts overexpressing CXCL14 promoted the growth of prostate cancer xenografts, and increased tumor angiogenesis and macrophage infiltration. Mechanistic studies demonstrated that autocrine CXCL14-stimulation of fibroblasts stimulate migration and ERKdependent proliferation of fibroblasts. CXCL14-stimulation of monocyte migration was also demonstrated. Furthermore, CXCL14-producing fibroblasts, but not recombinant CXCL14, enhanced in vitro proliferation and migration of prostate cancer cells and in vivo angiogenesis. These studies thus identify CXCL14 as a novel autocrine stimulator of fibroblast growth and migration, with multi-modal tumor-stimulatory activities. In more general terms, our findings suggest autocrine stimulation of fibroblasts as a previously unrecognized mechanism for chemokine-mediated stimulation of tumor growth, and suggest a novel mechanism whereby cancer-associated fibroblasts achieve their pro-tumorigenic phenotype.cancer-associated fibroblasts ͉ prostate cancer ͉ tumor stroma

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Section: Discussionsupporting

confidence: 82%

CXCL14 is an autocrine growth factor for fibroblasts and acts as a multi-modal stimulator of prostate tumor growth

Augsten

Hägglöf

Olsson

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

207

218

View full text Add to dashboard Cite

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“…This reduction in the body weight may support the previously postulated hormone-like roles of CXCL14 [7].…”

Section: Resultssupporting

confidence: 66%

“…Moreover, mice infected with neuroinvasive West-Nile virus (WNV) showed increased levels of CXCL14 in the brain and spleen 3 days postinfection [5], which suggests the involvement of this chemokine in the innate immune responses. Apart from leukocyte-specific functions, CXCL14 takes part in the developmental processes of the brain [6] and it also presents homeostatic functions in a hormone-like manner [7]. Interestingly, CXCL14 may enhance and suppress the growth of different types of tumors through a variety of mechanisms [2].…”

Section: Introductionmentioning

confidence: 99%

CXCL14 deficiency does not impact the outcome of influenza or Escherichia coli infections in mice

Sidahmed

Leόn

Banner

et al. 2014

J Infect Dev Ctries

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Introduction: Chemokines are small proteins that regulate different cellular functions, such as leukocyte activation, chemoattraction and inflammation. The chemokine CXCL14 (BRAK) is a highly conserved gene among species and through evolution. It has been shown that CXCL14 is locally upregulated during viral infections, also, it has been found that this chemokine possesses direct antibacterial activities. Nonetheless, the exact role that CXCL14 plays during infection remains elusive. Methodology: CXCL14 deficient mice were generated in a C57B6/129 background and followed by phenotypic characterization. Later, the effect of CXCL14 deficiency during influenza infection and E. coli challenge was assessed. Results: Other than a slight weight reduction, CXCL14 deficient mice exhibited no phenotypic alterations. CXCL14 deficiency did not influence the outcome of influenza virus infection or challenge with E. coli, and no statistically significant differences in clinical signs, cellular responses and histopathological findings were observed. Conclusions: CXCL14 does not seem to play a pivotal role during influenza and E. coli infections of the lung; these results are suggestive of functional overlap between CXCL14 and other chemokines that are present during lung infection.

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“…The glucose uptake assay was performed essentially as described previously [16]. First, cells were washed several times with Hanks' solution and treated with 100 µmol/l 2-deoxy- D -[1- 14 C] glucose (2-NBDG) with or without 10 -7 mol/l insulin for 30 min at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Chemerin Induces Insulin Resistance in Rat Cardiomyocytes in Part through the ERK1/2 Signaling Pathway

et al. 2014

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Aims: Chemerin is a novel adipokine that is closely associated with cardiovascular diseases and glucose homeostasis. This study aimed to investigate the effects of chemerin on insulin resistance in rat cardiomyocytes. Methods: Rat cardiomyocytes were treated with high concentrations of glucose and tumor necrosis factor-alpha (TNF-E), and chemerin and chemokine-like receptor 1 (CMKLR1) were measured by Western blot analysis. Then, the cardiomyocytes were treated with chemerin and insulin. Glucose uptake was evaluated using a fluorescence microplate reader. Western blot analysis was used to evaluate the phosphorylation of Akt, insulin receptor substrate-1, p38 mitogen-activated protein kinase (MAPK), as well as extracellular signal-regulated kinase (ERK)1/2. Results: Chemerin and CMKLR1 were found to be expressed in rat cardiomyocytes. Pretreatment with chemerin caused decreases in glucose uptake and phosphorylation of Akt in insulin-stimulated cardiomyocytes. Furthermore, chemerin activated the phosphorylation of p38 MAPK and ERK1/2 in insulin-stimulated cardiomyocytes. Inhibition of ERK partially rescued chemerin-induced insulin resistance. Conclusion: Chemerin is a novel adipokine that induces insulin resistance in rat cardiomyocytes in part through the ERK1/2 pathway. i 2014 S. Karger AG, Basel

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CXCL14 enhances insulin-dependent glucose uptake in adipocytes and is related to high-fat diet-induced obesity

Cited by 35 publications

References 27 publications

CXCL14 is an autocrine growth factor for fibroblasts and acts as a multi-modal stimulator of prostate tumor growth

CXCL14 is an autocrine growth factor for fibroblasts and acts as a multi-modal stimulator of prostate tumor growth

CXCL14 deficiency does not impact the outcome of influenza or Escherichia coli infections in mice

Chemerin Induces Insulin Resistance in Rat Cardiomyocytes in Part through the ERK1/2 Signaling Pathway

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