CCL2 mediates anti-fibrotic effects in human fibroblasts independently of CCR2
2014 (English)In: International Immunopharmacology, ISSN 1567-5769, E-ISSN 1878-1705, Vol. 20, no 1, 66-73 p.Article in journal (Refereed) Published
CCL2 is known for its major role as a chemoattractant of monocytes for immunological surveillance and to site of inflammation. CCL2 acts mainly through the G-protein-coupled receptor CCR2 but has also been described to mediate its effects independently of this receptor in vitro and in vivo. Emerging pieces of evidence indicate that the CCL2/CCR2 axis is involved in fibrotic diseases, such as increased plasma levels of CCL2 and the presence of CCL2-hyperresponsive fibroblasts explanted from patients with systemic sclerosis and idiopathic pulmonary fibrosis. One of the profibrotic key mediators is the myofibroblast characterized by overexpression of alpha-smooth muscle actin and collagen I. However, the correlation between the CCL2/CCR2 axis and the activation of fibroblasts is not yet fully understood. We have screened human fibroblasts of various origins, human pulmonary fibroblasts (HPF), human fetal lung fibroblasts (HFL-1) and primary preadipocytes (SPF-1) in regard to CCL2 stimulated fibrotic responses. Surprisingly we found that CCL2 mediates anti-fibrotic effects independently of CCR2 in human fibroblasts of different origins.
Place, publisher, year, edition, pages
2014. Vol. 20, no 1, 66-73 p.
CCL2, CCR2, Fibroblast, Preadipocyte, Fibrosis
Immunology in the medical area
IdentifiersURN: urn:nbn:se:kth:diva-147051DOI: 10.1016/j.intimp.2014.02.020ISI: 000336337900009ScopusID: 2-s2.0-84896350707OAI: oai:DiVA.org:kth-147051DiVA: diva2:728451
FunderScience for Life Laboratory - a national resource center for high-throughput molecular bioscience
QC 201406242014-06-242014-06-232014-06-24Bibliographically approved