Expression of serum amyloid A in chondrocytes and myoblasts differentiation and inflammation: possible role in cholesterol homeostasis.
Serum amyloid A (SAA) is synthesized by the liver during the acute phase. Local expression of SAA mRNA has been reported also in non-liver cells, a potential local source of SAA protein not related to the systemic acute phase response. SAA function has not been established yet. In the present study, we identified SAA as a protein expressed by chondrocytes and myoblasts in response to inflammatory stimula. In both cell systems, SAA mRNA and protein expression is strongly stimulated by bacterial lipopolysaccharide treatment. SAA mRNA expression is also enhanced during terminal differentiation of cells of the chondrogenic and myogenic lineage; mRNA is barely detectable in prechondrogenic cells and is highly expressed in differentiated hyperthrophic chondrocytes. An increased level of SAA mRNA was also observed in vivo when we compared mRNA extracted from tibiae of 10 day embryos, still fully cartilaginous, with tibiae from 18 day embryos, a stage when the endochondral ossification process has already started. p38 activation, a well-known event of the chondrogenesis signaling cascade, controls expression of SAA in cartilage following inflammatory stimuli. SAA secreted by stimulated chondrocytes is associated with cholesterol. Cholesterol is synthesized by the same chondrocytes and is also increased in inflammatory conditions. A role of SAA in cholesterol homeostasis in chondrocytes is proposed.
Zerega
Barbara
B
Istituto Nazionale per la Ricerca sul Cancro Genova, Italy.
Pagano
Aldo
A
Pianezzi
Ada
A
Ulivi
Valentina
V
Camardella
Laura
L
Cancedda
Ranieri
R
Cancedda
Fiorella Descalzi
FD
D000818:Animals; D002454:Cell Differentiation; D002478:Cells, Cultured; D002642:Chick Embryo; D002784:Cholesterol / Q000378:metabolism*; D019902:Chondrocytes / Q000378:metabolism* / Q000473:pathology*; D020219:Chondrogenesis; D004789:Enzyme Activation; D020869:Gene Expression Profiling; D006706:Homeostasis; D007249:Inflammation / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008099:Liver / Q000378:metabolism; D024510:Muscle Development; D032446:Myoblasts / Q000378:metabolism* / Q000473:pathology*; D011485:Protein Binding; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D000685:Serum Amyloid A Protein / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D013977:Tibia / Q000378:metabolism; D013997:Time Factors; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D012333:RNA, Messenger; D000685:Serum Amyloid A Protein; D002784:Cholesterol; D048051:p38 Mitogen-Activated Protein Kinases