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TGS1/PIMT regulates pro-inflammatory macrophage mediated paracrine insulin resistance: Crosstalk between macrophages and skeletal muscle cells. | LitMetric

TGS1/PIMT regulates pro-inflammatory macrophage mediated paracrine insulin resistance: Crosstalk between macrophages and skeletal muscle cells.

Biochim Biophys Acta Mol Basis Dis

Centre for Innovation in Molecular and Pharmaceutical Sciences (CIMPS), Dr. Reddy's Institute of Life sciences, University of Hyderabad Campus, Hyderabad 500046, Telangana, India. Electronic address:

Published: January 2024

AI Article Synopsis

Article Abstract

Macrophage-driven chronic low-grade inflammatory response is intimately associated with pathogenesis of insulin resistance and type 2 diabetes (T2D). However, the molecular basis for skewing of pro-inflammatory macrophage is still elusive. Here, we describe the mechanism and significance of TGS1/PIMT (PRIP-Interacting protein with Methyl Transferase domain) in regulating macrophage activation and polarization and its impact on the development of insulin resistance in skeletal muscle cells. We show altered expression of TGS1 in M1 polarized cultured macrophages, bone marrow-derived (BMDM) and adipose tissue macrophages. Moreover, in High Fat Diet (HFD)-fed mice enhanced TGS1 expression is predominantly localized to the nucleus of adipose tissue macrophages suggesting its potential functional role. Gain and loss of TGS1 expression in macrophage further established its role in the secretion of pro-inflammatory mediators. Mechanistically, TGS1 controls the transcription of numerous genes linked to inflammation by forming a complex with Histone Acetyl Transferase (HAT)-containing transcriptional co-activators CBP and p300. Functionally, TGS1 mediated macrophage inflammatory response induces the development of insulin resistance in skeletal muscle cells and adipocytes. Our findings thus demonstrate an unexpected contribution of TGS1 in the regulation of macrophage mediated inflammation and insulin resistance highlighting that TGS1 antagonism could be a promising therapeutic target for the management of inflammation and insulin resistance in T2D.

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Source
http://dx.doi.org/10.1016/j.bbadis.2023.166878DOI Listing

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