Adipose-specific Monocyte Chemotactic Protein-1 Deficiency Reduces Pulmonary Metastasis of Lewis Lung Carcinoma in Mice

Sundaram, Shanthy; Yan, Lin

doi:10.21873/anticanres.13279

Cited by 8 publications

(5 citation statements)

References 46 publications

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“…Mediated the infiltration of monocyte and macrophage to the site of inflammation Its expression correlates with body BMI and adiposity [40] Fetuin-A Promotes IR by inhibition of insulin receptor's tyrosine kinase activity Mainly secreted by the liver and taken up by AT AT secreted fetuin-A increases in metabolic syndrome [34] [41] [42] generated in WAT from a non-myf-5 lineage [48]. Both types of brown adipocyte express uncoupling protein 1 (UCP1) on the inner mitochondrial membrane.…”

Section: Adipose Tissue Structure and Biologymentioning

confidence: 99%

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

Komi

Shafaghat

Christian

2020

Clinic Rev Allerg Immunol

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Excessive fatty acids and glucose uptake support the infiltration of adipose tissue (AT) by a variety of immune cells including neutrophils, pro-inflammatory M1 macrophages, and mast cells (MCs). These cells promote inflammation by releasing proinflammatory mediators. The involvement of MCs in AT biology is supported by their accumulation in the AT of obese individuals along with significantly higher serum levels of MC-derived tryptase. AT-resident MCs under the influence of locally derived adipokines such as leptin become activated and release pro-inflammatory cytokines including TNFα that worsens the inflammatory state. MCs support angiogenesis in AT by releasing chymase and inducing preadipocyte differentiation and also the proliferation of adipocytes through 15-deoxy-delta PGJ2/PPARγ interaction. Additionally, they contribute to the remodeling of the AT extracellular matrix (ECM) and play a role in the recruitment and activation of leukocytes. MC degranulation has been linked to brown adipocyte activation, and evidence indicates an important link between MCs and the appearance of BRITE/beige adipocytes in white AT. Cell crosstalk between MCs and AT-resident cells, mainly adipocytes and immune cells, shows that these cells play a critical role in the regulation of AT homeostasis and inflammation.

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Section: Adipose Tissue Structure and Biologymentioning

confidence: 99%

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

Komi

Shafaghat

Christian

2020

Clinic Rev Allerg Immunol

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“…We have reported that adipose specific Mcp-1 knockout reduces high-fat diet-enhanced mammary tumorigenesis in female mice ( 24 ) and metastasis of Lewis lung carcinoma ( 25 ) in male mice. However, the role of adipose-derived MCP-1 in male breast cancer remains unelucidated.…”

Section: Introductionmentioning

confidence: 99%

Mammary Tumorigenesis and Metabolome in Male Adipose Specific Monocyte Chemotactic Protein-1 Deficient MMTV-PyMT Mice Fed a High-Fat Diet

et al. 2021

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Male breast cancer, while uncommon, is a highly malignant disease. Monocyte chemotactic protein-1 (MCP-1) is an adipokine; its concentration in adipose tissue is elevated in obesity. This study tested the hypothesis that adipose-derived MCP-1 contributes to male breast cancer. In a 2x2 design, male MMTV-PyMT mice with or without adipose-specific Mcp-1 knockout [designated as Mcp-1-/- or wild-type (WT)] were fed the AIN93G standard diet or a high-fat diet (HFD) for 25 weeks. Mcp-1-/- mice had lower adipose Mcp-1 expression than WT mice. Adipose Mcp-1 deficiency reduced plasma concentrations of MCP-1 in mice fed the HFD compared to their WT counterparts. Mcp-1-/- mice had a longer tumor latency (25.2 weeks vs. 18.0 weeks) and lower tumor incidence (19% vs. 56%), tumor progression (2317% vs. 4792%), and tumor weight (0.23 g vs. 0.64 g) than WT mice. Plasma metabolomics analysis identified 56 metabolites that differed among the four dietary groups, including 22 differed between Mcp-1-/- and WT mice. Pathway and network analyses along with discriminant analysis showed that pathways of amino acid and carbohydrate metabolisms are the most disturbed in MMTV-PyMT mice. In conclusion, adipose-derived MCP-1 contributes to mammary tumorigenesis in male MMTV-PyMT. The potential involvement of adipose-derived MCP-1 in metabolomics warrants further investigation on its role in causal relationships between cancer metabolism and mammary tumorigenesis in this male MMTV-PyMT model.

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“…The close link between MCP-1 and inflammation was revealed by adipose-specific Mcp-1 knockdown mice displaying lowered plasma concentrations of several proinflammatory adipokines viz. leptin, plasminogen activator inhibitor-1 and resistin compared to wild-type controls (16). We believe that the two chemotactic signals, FetA and MCP-1, copiously generated in lipid-enriched AT milieu, can significantly influence ATM content and activation.…”

Section: Introductionmentioning

confidence: 85%

Fetuin-A regulates adipose tissue macrophage content and activation in insulin resistant mice through MCP-1 and iNOS: involvement of IFNγ-JAK2-STAT1 pathway

Chattopadhyay

Das

Guria

et al. 2021

Biochemical Journal

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In the context of obesity-induced adipose tissue (AT) inflammation, migration of macrophages and their polarization from predominantly anti-inflammatory to proinflammatory subtype is considered a pivotal event in the loss of adipose insulin sensitivity. Two major chemoattractants, monocyte chemoattractant protein-1 (MCP-1) and Fetuin-A (FetA), have been reported to stimulate macrophage migration into inflamed AT instigating inflammation. Moreover, FetA could notably modulate macrophage polarization, yet the mechanism(s) is unknown. The present study was undertaken to elucidate the mechanistic pathway involved in the actions of FetA and MCP-1 in obese AT. We found that FetA knockdown in high fat diet (HFD) fed mice could significantly subdue the augmented MCP-1 expression and reduce adipose tissue macrophage (ATM) content thereby indicating that MCP-1 is being regulated by FetA. Additionally, knockdown of FetA in HFD mice impeded the expression of inducible nitric oxide synthase (iNOS) reverting macrophage activation from mostly proinflammatory to anti-inflammatory state. It was observed that the stimulating effect of FetA on MCP-1 and iNOS was mediated through interferon γ (IFNγ) induced activation of JAK2-STAT1-NOX4 pathway. Furthermore, we detected that the enhanced IFNγ expression was accounted by the stimulatory effect of FetA upon the activities of both cJun and JNK. Taken together, our findings revealed that obesity-induced FetA acts as a master upstream regulator of AT inflammation by regulating MCP-1 and iNOS expression through JNK-cJun-IFNγ-JAK2-STAT1 signaling pathway. This study opened a new horizon in understanding the regulation of ATM content and activation in conditions of obesity-induced insulin resistance.

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Adipose-specific Monocyte Chemotactic Protein-1 Deficiency Reduces Pulmonary Metastasis of Lewis Lung Carcinoma in Mice

Cited by 8 publications

References 46 publications

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

Mammary Tumorigenesis and Metabolome in Male Adipose Specific Monocyte Chemotactic Protein-1 Deficient MMTV-PyMT Mice Fed a High-Fat Diet

Fetuin-A regulates adipose tissue macrophage content and activation in insulin resistant mice through MCP-1 and iNOS: involvement of IFNγ-JAK2-STAT1 pathway

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