Open AccessMacrophages are Novel Sites of Expression and Regulation of Retinol Binding Protein-4 (RBP4)
Author(s) -
Montserrat Broch,
Rafael Vidal Tamayo Ramírez,
Michel Auguet,
María José Alcaide,
Carmen Aguilar,
Antonio GarcíaEspaña,
C Richart
Publication year - 2010
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931714
Subject(s) - retinol binding protein 4 , adipokine , adipose tissue , tumor necrosis factor alpha , inflammation , endocrinology , lipopolysaccharide , medicine , monocyte , retinol binding protein , biology , insulin resistance , chemistry , immunology , obesity , retinol , vitamin
Obesity is linked to a low-level chronic inflammatory state thatmay contribute to the development of associated metaboliccomplications. Retinol-binding protein 4 (RBP4) is an adipokineassociated with parameters of obesity including insulin resistanceindices, body mass index, waist circumference, lipid profile, andrecently, with circulating inflammatory factors. Due to theinfiltration of adipose tissue in obesity by macrophages derivedfrom circulating monocytes and, on the other hand, the existenceof a close genetic relationship between adipocytes andmacrophages, we decided to examine if RBP4 is expressed inmonocytes and/or primary human macrophages. While we didnot detect expression of RBP4 in undifferentiated monocytes,RBP4 expression became evident during the differentiation ofmonocytes into macrophages and was highest in differentiatedmacrophages. Once we demonstrated the expression of RBP4 inmacrophages, we checked if RBP4 expression could be regulatedby inflammatory stimuli such as tumor necrosis factor-alpha(TNF-α), interleukin-6 (IL-6), or the endotoxin lipopolysaccharide(LPS). We observed that while RBP4 expression was stronglyinhibited by TNF-α and LPS, it was not affected by IL-6. Ourresults highlight the complexity behind the regulation of thisadipokine and demonstrate that RBP4 expression in macrophagescould be modulated by inflammatory stimuli.