Does human relaxin-2 affect peripheral blood mononuclear cells to increase inflammatory mediators in pathologic bone loss?
This study was designed to test the hypothesis that relaxin stimulates bone resorption by regulating the production of several mediators that stimulate osteoclast formation. The levels of mediators were measured in response to differing relaxin concentrations in supernatants from peripheral blood mononuclear cells (PBMCs), MCF-7 breast cancer cells, and normal human osteoblasts. Although all cell types expressed mRNA for the relaxin receptor (LGR7), only PBMCs responded to relaxin at physiologic levels by increasing tumor necrosis factor-alpha and interleukin-1beta secretion. The findings indicate that PBMCs should be studied in relation to the effect of relaxin on inflammation and bone destruction caused by osteoclasts.
Kristiansson
P
P
Department of Public Health and Caring Sciences, Uppsala University, SE-751 85 Uppsala, Sweden. per.kristiansson@pubcare.uu.se
Holding
C
C
Hughes
S
S
Haynes
D
D
D001862:Bone Resorption / Q000378:metabolism* / Q000473:pathology*; D002478:Cells, Cultured; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007375:Interleukin-1 / Q000378:metabolism*; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D012065:Relaxin / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D018836:Inflammation Mediators; D007375:Interleukin-1; C095068:RLN2 protein, human; D014409:Tumor Necrosis Factor-alpha; D012065:Relaxin