114 TRIB3-mediated regulation of macrophage phenotype. (June 2018)

• Record Type: Journal Article
• Authors: Campesino, Laura Martinez; Johnston, Jessica; Kiss-Toth, Endre; Wilson, Heather
• Is Part Of: Heart. Volume 104(2018)Supplement 6
• Page Start: A89
• Page End: A89
• Publication Date: 2018-06
• Subjects: Tribbles -- Macrophages -- Inflammation; Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/heartjnl-2018-BCS.113
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Background: Chronic inflammation is one of the key processes in the development of metabolic dysfunction under obesity which represents a major risk for cardiovascular disease. The metabolic and immune responses to obesity affect many organs and particularly the adipose tissue where macrophages are key effector cells modulating inflammation through the signals received from adipocytes. The Tribbles (Trib) family of proteins has been described as major regulators of inflammation and energy metabolism. Specifically, Trib3 participates in a wide range of inflammatory and metabolic signalling pathways. We propose that Trib3 may modulate macrophage polarisation and therefore modulate the immune response to promote obesity. Methodology: Trib3 full body knock out (Trib3KO) mice were used to study morphological changes in the adipose tissue. To investigate whether Trib3 regulates the polarisation state of macrophages, bone marrow derived macrophages (BMDMs) were isolated and polarised in vitro to further characterise their pro- or anti- inflammatory properties. Adipose tissue macrophages (CD11b+ATMs) were isolated from adipose tissue using magnetics beads and the expression of polarisation markers was evaluated by qPCR. Results: Trib3 deficiency increased subcutaneous adipose tissue mass. Cell content showed that adipocytes were the same size compared to wild-type. However, adipocyte and macrophage numbers were increased in the Trib3KO mice. No significant differences in gene expression of classical polarisation markers were found in ATMs, however differential gene expression of proteins involved in macrophage function and phenotype was found in Trib3KO BMDMs compared to wild type results among the different polarisation states. Conclusion: The results obtained in this pilot study suggest a role for Trib3 in macrophages due to expression differences measured in Trib3 deficient BMDMs, linked to a pro-inflammatory macrophage phenotype.