Mesenteric Adipose Tissue‐Derived Monocyte Chemoattractant Protein‐1 Plays a Crucial Role in Adipose Tissue Macrophage Migration and Activation in Obese Mice

Yu, Rina; Kim, Chu-Sook; Kwon, Byoung Soo; Kawada, Teruo

doi:10.1038/oby.2006.153

Cited by 162 publications

(142 citation statements)

References 19 publications

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Section: Chemokinesmentioning

confidence: 86%

“…They likewise observed increased gene expression of the macrophage markers F4/80 and CD68 in AT beds [59]. In addition, they performed in vitro migration experiments showing increased macrophage migration to mesenteric AT-conditioned media, which was blocked in response to an antibody for MCP-1 [59].…”

Section: Chemokinesmentioning

confidence: 99%

“…Expression of the macrophage chemokines monocyte chemotactic protein (MCP)-1 and MIP-1α have been shown to be increased in the white AT of LepR db/db , Lep ob/ob and DIO mice [1,10,13,[57][58][59][60]. Other chemokines upregulated in AT from DIO and/or Lep ob/ob mice are MCP-2 [12], MCP-3 [12], RANTES [5] and CXCL14 [60].…”

Section: Chemokinesmentioning

confidence: 99%

“…Yu et al demonstrated that MCP-1 was upregulated at the mRNA and protein levels in the mesenteric, epididymal, subcutaneous and perirenal white AT of DIO mice, with the highest upregulation being in the mesenteric fat [59]. They likewise observed increased gene expression of the macrophage markers F4/80 and CD68 in AT beds [59]. In addition, they performed in vitro migration experiments showing increased macrophage migration to mesenteric AT-conditioned media, which was blocked in response to an antibody for MCP-1 [59].…”

Section: Chemokinesmentioning

confidence: 99%

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Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

2008

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It has long been known that adipose tissue in obesity is in a heightened state of inflammation. Recently, our understanding of this has been transformed by the knowledge that immune cells such as macrophages and T cells can infiltrate adipose tissue and are responsible for the majority of inflammatory cytokine production. These seminal findings have opened up a new area in biology that is garnering the interest of scientists involved in research relating to cell motility, inflammation, obesity, physiology, diabetes and cardiovascular disease. Some important general questions relevant to this field are: how are macrophages recruited to adipose tissue in obesity? What are the physiological consequences of macrophage-adipocyte interactions? Do these inflammatory macrophages contribute to pathophysiological conditions associated with obesity, such as insulin resistance, dyslipidemia, diabetes and cardiovascular disease? This review focuses on the first of these important questions. Keywords activation; adipose tissue; chemokines; crown-like structures; hypoxia; inflammation; insulin resistance; leptin; lymphocytes; macrophages During the past two decades, the complex nature of adipose tissue (AT) has become an area of intense investigation. This is in part due to the growing worldwide obesity epidemic, and in part to the identification of leptin as an adipokine secreted from AT. Since the discovery of leptin, many other adipokines, such as adiponectin, resistin, visfatin and omentin, have also been identified. These discoveries have led to the first revolution in the field of AT biology, the identification of AT as an endocrine organ. More recently, it has been discovered that not only adipocytes, but also immune cells, such as macrophages [1,2] and T lymphocytes [3][4][5], reside in AT, and that these cells may induce insulin resistance by promoting a proinflammatory milieu within the AT. This discovery has led to the second revolution in the field of AT biology,

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Section: Chemokinesmentioning

confidence: 86%

Section: Chemokinesmentioning

confidence: 99%

Section: Chemokinesmentioning

confidence: 99%

Section: Chemokinesmentioning

confidence: 99%

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Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

2008

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“…5). In general, intra-abdominal AT of rodents and humans is more susceptible to M⌽ infiltration, is a greater source of inflammatory mediators, and may contribute more to some metabolic complications of obesity than subcutaneous AT (25,26,(41)(42)(43)(44). Removal of intra-abdominal AT in rodents ameliorates DIO-associated insulin resistance (26) and prevents insulin resistance and glucose intolerance of aging (25).…”

Section: Discussionmentioning

confidence: 99%

Adipocyte Death, Adipose Tissue Remodeling, and Obesity Complications

Strissel

Stancheva²,

Miyoshi³

et al. 2007

Diabetes

850

807

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OBJECTIVE-We sought to determine the role of adipocyte death in obesity-induced adipose tissue (AT) inflammation and obesity complications.RESEARCH DESIGN AND METHODS-Male C57BL/6 mice were fed a high-fat diet for 20 weeks to induce obesity. Every 4 weeks, insulin resistance was assessed by intraperitoneal insulin tolerance tests, and epididymal (eAT) and inguinal subcutaneous AT (iAT) and livers were harvested for histological, immunohistochemical, and gene expression analyses.RESULTS-Frequency of adipocyte death in eAT increased from Ͻ0.1% at baseline to 16% at week 12, coincident with increases in 1) depot weight; 2) AT macrophages (ATM⌽s) expressing F4/80 and CD11c; 3) mRNA for tumor necrosis factor (TNF)-␣, monocyte chemotactic protein (MCP)-1, and interleukin (IL)-10; and 4) insulin resistance. ATM⌽s in crown-like structures surrounding dead adipocytes expressed TNF-␣ and IL-6 proteins. Adipocyte number began to decline at week 12. At week 16, adipocyte death reached ϳ80%, coincident with maximal expression of CD11c and inflammatory genes, loss (40%) of eAT mass, widespread collagen deposition, and accelerated hepatic macrosteatosis. By week 20, adipocyte number was restored with small adipocytes, coincident with reduced adipocyte death (fourfold), CD11c and MCP-1 gene expression (twofold), and insulin resistance (35%). eAT weight did not increase at week 20 and was inversely correlated with liver weight after week 12 (r ϭ Ϫ0. 85, P Ͻ 0.001). In iAT, adipocyte death was first detected at week 12 and remained Յ3%.CONCLUSIONS-These results implicate depot-selective adipocyte death and M⌽-mediated AT remodeling in inflammatory and metabolic complications of murine obesity. Diabetes

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Hypothalamic lipid‐laden astrocytes induce microglia migration and activation

Kwon

Kim

et al. 2017

FEBS Letters

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Obesity-induced hypothalamic inflammation is closely associated with various metabolic complications and neurodegenerative disorders. Astrocytes, the most abundant glial cells in the central nervous system, play a crucial role in pathological hypothalamic inflammatory processes. Here, we demonstrate that hypothalamic astrocytes accumulate lipid droplets under saturated fatty acid-rich conditions, such as obese environment, and that the lipid-laden astrocytes increase astrogliosis markers and inflammatory cytokines (TNFα, IL-1β, IL-6, MCP-1) at the transcript and/or protein level. Medium conditioned by the lipid-laden astrocytes stimulate microglial chemotactic activity and upregulate transcripts of the microglia activation marker Iba-1 and inflammatory cytokines. These findings indicate that the lipid-laden astrocytes formed in free fatty acid-rich obese condition may participate in obesity-induced hypothalamic inflammation through promoting microglia migration and activation.

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Mesenteric Adipose Tissue‐Derived Monocyte Chemoattractant Protein‐1 Plays a Crucial Role in Adipose Tissue Macrophage Migration and Activation in Obese Mice

Cited by 162 publications

References 19 publications

Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

Adipocyte Death, Adipose Tissue Remodeling, and Obesity Complications

Hypothalamic lipid‐laden astrocytes induce microglia migration and activation

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