Premium
Relaxin Promotes Clustering, Migration, and Activation States of Mononuclear Myelocytic Cells
Author(s) -
Figueiredo Kevin A.,
Rossi Gina,
Cox Michael E.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.03843.x
Subject(s) - relaxin , monocyte , microbiology and biotechnology , cytokine , macrophage , downregulation and upregulation , inflammation , chemistry , dendritic cell , biology , immune system , cancer research , immunology , receptor , in vitro , biochemistry , gene
Monocytes are leukocytic precursors of macrophages, dendritic cells, and osteoclasts, with critical roles in inflammation and tumor biology. Tumors can elicit signals that activate monocytes to extravasate, infiltrate tumors, and differentiate into tumor‐associated macrophages (TAMs), which can modulate host immune surveillance. In order to assess whether relaxin can influence monocyte activation status, we assessed its ability to alter cell–cell clustering and cytokine expression of the monocytic cell line THP‐1. Here we report that relaxin can induce time‐ and substrate‐dependent homotypic cell–cell clustering of monocytes. In addition, we demonstrate that relaxin can suppress macrophage migration in an adenylate cyclase‐independent, nitric oxide synthase‐dependent fashion. We confirm relaxin‐induced upregulation of vascular endothelial growth factor expression and regulation of M1/M2 cytokine profiles. By stimulating monocyte activation and modulating inflammatory cytokine expression and migratory activity of resulting macrophages in response to endotoxin exposure, relaxin may be a critical regulator of the macrophage activation state that regulates the TAM phenotype.