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.
Fiche publication
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
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;: