title: Fluid shear stress increases interleukin-11 expression in human osteoblast-like cells: its role in osteoclast induction.
abstract: It is unclear how mechanical stress influences bone cells. Mechanical stress causes fluid shear stress (FSS) in the bone. Osteoblast lineage cells are thought to sense FSS and regulate bone remodeling. We therefore investigated the effects of FSS on human osteoblast-like osteosarcoma cells: SaOS-2 cells in vitro. The conditioned medium of the SaOS-2 cells after 24 h of FSS (24 h-FSS CM) showed such osteoclastic phenotype inductions as significantly increasing the number of tartrate-resistant acid phosphatase (TRAP) positive multinuclear cells in rat bone marrow cells and TRAP-positive cells in human preosteoclastic cells: FLG 29.1 cells. An enzyme-linked immunosorbent assay showed interleukin-11 (IL-11) protein to increase 7-fold in the 24 h-FSS CM. A Northern analysis showed that IL-11 mRNA increased 4-fold in the SaOS-2 cells after 6 h-FSS; however, no IL-6 mRNA expression was detected. Furthermore, the anti-human IL-11 antibody significantly neutralized the osteoclastic phenotype induction of the 24 h-FSS CM. The IL-11 mRNA up-regulation in SaOS-2 cells by the 6 h-FSS was not inhibited by the anti-human transforming growth factor-beta1 antibody, but it was significantly inhibited by indomethacin. An enzymeimmunoassay showed prostaglandin E2 to increase 7-fold in the 1 h-FSS CM. These findings thus suggest that FSS induces osteoblasts to produce IL-11 (mediated by prostaglandins) and thus stimulates bone remodeling.
authors.affiliation: Department of Orthopaedic Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Sakai
authors.forename: M
authors.initials: M
authors.lastname: Mohtai
authors.forename: J
authors.initials: J
authors.lastname: Shida
authors.forename: K
authors.initials: K
authors.lastname: Harimaya
authors.forename: S
authors.initials: S
authors.lastname: Benvenuti
authors.forename: M L
authors.initials: ML
authors.lastname: Brandi
authors.forename: T
authors.initials: T
authors.lastname: Kukita
authors.forename: Y
authors.initials: Y
authors.lastname: Iwamoto
mesh_terms: D000135:Acid Phosphatase; D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D016723:Bone Remodeling / Q000187:drug effects*; D017077:Culture Media, Conditioned; D015232:Dinoprostone / Q000378:metabolism; D000091344:Filaggrin Proteins; D005786:Gene Expression Regulation; D006651:Histocytochemistry; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D017370:Interleukin-11 / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D007527:Isoenzymes; D010006:Osteoblasts / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D013314:Stress, Mechanical; D000071681:Tartrate-Resistant Acid Phosphatase; D016212:Transforming Growth Factor beta / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D000906:Antibodies; D017077:Culture Media, Conditioned; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D017370:Interleukin-11; D007527:Isoenzymes; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D015232:Dinoprostone; D007213:Indomethacin