The endoplasmic reticulum stress protein GRP94 modulates cathepsin L activity in M2 macrophages in conditions of obesity-associated inflammation and contributes to their pro-inflammatory profile.

Date publication

février 2024

Journal

International journal of obesity (2005)

Auteurs

Membres identifiés du Cancéropôle Est :
Dr GARRIDO Carmen , Pr NARCE Michel , Pr KOHLI Evelyne

Tous les auteurs :
Wang F, Baverel V, Chaumonnot K, Bourragat A, Bellenger J, Bellenger S, Zhou W, Narce M, Garrido C, Kohli E

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/38351251

Résumé

Adipose tissue macrophages (ATM) are key actors in the pathophysiology of obesity-related diseases. They have a unique intermediate M2-M1 phenotype which has been linked to endoplasmic reticulum (ER) stress. We previously reported that human M2 macrophages treated with the ER stress inducer thapsigargin switched to a pro-inflammatory phenotype that depended on the stress protein GRP94. In these conditions, GRP94 promoted cathepsin L secretion and was co-secreted with complement C3. As cathepsin L and complement C3 have been reported to play a role in the pathophysiology of obesity, in this work we studied the involvement of GRP94 in the pro-inflammatory phenotype of ATM.

Référence

Int J Obes (Lond). 2024 02 13;: