Lipocalin 2 is a Regulator Of Macrophage Polarization and NF-κB/STAT3 Pathway Activation

Guo, Hong; Jin, Daozhong; Chen, Xiaoli

doi:10.1210/me.2014-1092

Cited by 105 publications

(93 citation statements)

References 58 publications

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“…In this regard, an upregulation of LCN2 by insulin in adipose tissue explants and increased circulating levels after hyperinsulinemic induction in humans have been described (Tan et al 2009). The positive correlation between both circulating and gene expression levels of LCN-2 with inflammatory markers detected in the present study may be related to the role of LCN-2 as an anti-inflammatory regulator described not only on adipocytes but also on macrophage activation (Guo et al 2014;Zhang et al 2008). …”

Section: Discussionsupporting

confidence: 62%

“…The family of adipokines is highly diverse in structure and function. Whereas LCN-2 seems to act as an antagonist to the effect of inflammatory molecules (Guo et al 2014;Zhang et al 2008), OPN and YKL-40 are directly related to increased inflammation and insulin resistance via impaired extracellular matrix remodeling (Johansen et al 2000;Lancha et al 2014).…”

Section: Introductionmentioning

confidence: 99%

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Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

et al. 2015

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Inflammation is a critical contributor to the pathogenesis of metabolic disorders with adipose tissue being crucial in the inflammatory response by releasing multiple adipokines with either pro-or anti-inflammatory activities with potential functions as metabolic regulators. Peripheral blood mononuclear cells (PBMC) have been proposed as representative of the inflammatory status in obesity. The aim of the present study was to evaluate the contribution of PBMC to the obesity-associated chronic inflammation analyzing the expression of novel adipokines. Samples obtained from 69 subjects were used in the study. Real-time PCR determinations were performed to quantify gene expression levels in PBMC of novel adipokines including chemerin, chitinase-3-like protein 1 (YKL-40), lipocalin-2 (LCN-2) and osteopontin (OPN), and their circulating concentrations were also determined by ELISA. We show, for the first time, that PBMC gene expression levels of chemerin (P \ 0.0001), chitinase-3-like protein 1 (P = 0.010), lipocalin-2 (P \ 0.0001) and osteopontin (P \ 0.0001) were strongly upregulated in obesity independently of the glycemic state. Circulating concentrations of these adipokines followed the same trend being significantly higher (P \ 0.05) in obese normoglycemic and type 2 diabetic patients compared to lean volunteers and also associated (P \ 0.05) with their corresponding mRNA levels in PBMC. These results provide evidence that alterations in inflammation-related adipokines are manifest in PBMC, which might contribute to the low-grade chronic inflammation that characterizes obesity.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

et al. 2015

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“…STAT3 plays an important role in inflammation and tumorigenesis by regulating cell proliferation, differentiation and metabolism [25,26]. The immunosuppressive activities of TAMs correlate with overactivated STAT3 signaling in the cells and disrupting STAT3 activity in TAMs can enhance the rat immune response to breast cancer [27].…”

Section: Discussionmentioning

confidence: 99%

M2 polarized macrophages induced by CSE promote proliferation, migration, and invasion of alveolar basal epithelial cells

Shi

et al. 2015

International Immunopharmacology

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“…Lipocalin-2 (LCN2), also known as neutrophil gelatinase-associated lipocalin (NGAL), neu-related lipocalin, oncogene 24p3, siderocalin, and uterocalin, is a secretory glycoprotein member of 25 kDa of the highly heterogeneous family of lipocalins that was originally isolated from secondary granules of human neutrophils (164). LCN2 is a component of the innate immune system that acts as an iron carrier protein and plays a key role in acute-phase response to infection (73) and in regulation of macrophage polarization (108). LCN2 has been also identified as an adipokine secreted from murine and human adipose tissue involved in the regulation of energy metabolism and glucose and lipid homeostasis, as well as in insulin resistance (38,332,354).…”

Section: Recruitment Of Proinflammatory Immune Cells In Obesity Perpementioning

confidence: 99%

Revisiting the adipocyte: a model for integration of cytokine signaling in the regulation of energy metabolism

Rodrı́guez

Ezquerro

Méndez‐Giménez

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

241

186

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Adipose tissue constitutes an extremely active endocrine organ with a network of signaling pathways enabling the organism to adapt to a wide range of different metabolic challenges, such as starvation, stress, infection, and short periods of gross energy excess. The functional pleiotropism of adipose tissue relies on its ability to synthesize and release a huge variety of hormones, cytokines, complement and growth factors, extracellular matrix proteins, and vasoactive factors, collectively termed adipokines. Obesity is associated with adipose tissue dysfunction leading to the onset of several pathologies including type 2 diabetes, dyslipidemia, nonalcoholic fatty liver, or hypertension, among others. The mechanisms underlying the development of obesity and its associated comorbidities include the hypertrophy and/or hyperplasia of adipocytes, adipose tissue inflammation, impaired extracellular matrix remodeling, and fibrosis together with an altered secretion of adipokines. Recently, the potential role of brown and beige adipose tissue in the protection against obesity has been also recognized. In contrast to white adipocytes, which store energy in the form of fat, brown and beige fat cells display energy-dissipating capacity through the promotion of triacylglycerol clearance, glucose disposal, and generation of heat for thermogenesis. Identification of the morphological and molecular changes in white, beige, and brown adipose tissue during weight gain is of utmost relevance for the identification of pharmacological targets for the treatment of obesity and its associated metabolic diseases. white and brown adipogenesis; fat browning; adipocyte hypertrophy and hyperplasia; adipose tissue inflammation; extracellular matrix remodeling THE ADIPOSE ORGAN REPRESENTS a special loose connective tissue containing adipocytes and several cell types surrounded by capillary and innervation networks (47, 79, 82). Adipocytes comprise ϳ35-70% of adipose mass, and the other cell types found in the stroma-vascular fraction include preadipocytes, mesenchymal stem cells, macrophages and other immune cells, and endothelial and smooth muscle cells, among others (79). The classical functions of adipose tissue are the storage of energy in the form of triacylglycerols (TG) and as thermal insulator. Adipocytes were formerly classified into two main types: white adipocytes, which store energy in the form of fat, and brown adipocytes, which induce thermogenesis (82). The current classification scheme includes a third category of adipocytes, termed beige or brite (brown-in-white) adipocytes, which can be considered inducible brown-like cells with thermogenic properties (340). Since the identification of leptin in 1994 (359), adipose tissue has emerged as an extremely active endocrine organ that secretes a huge variety of hormones, cytokines, growth factors, and vasoactive factors that are collectively termed adipokines (67, 81,235,262). Over the last three decades, overwhelming evidence has proven that adipokines not only influence adipobiol...

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Lipocalin 2 is a Regulator Of Macrophage Polarization and NF-κB/STAT3 Pathway Activation

Cited by 105 publications

References 58 publications

Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

M2 polarized macrophages induced by CSE promote proliferation, migration, and invasion of alveolar basal epithelial cells

Revisiting the adipocyte: a model for integration of cytokine signaling in the regulation of energy metabolism

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