Duong L T, Lakkakorpi P T, Nakamura I, Machwate M, Nagy R M, Rodan G A
Department of Bone Biology and Osteoporosis, Merck Research Laboratories, West Point, Pennsylvania 19486, USA.
J Clin Invest. 1998 Sep 1;102(5):881-92. doi: 10.1172/JCI3212.
Osteoclast activation is initiated by adhesion to the bone surface, followed by cytoskeletal rearrangement, the formation of the sealing zone, and a polarized ruffled membrane. This study shows that PYK2/CAKbeta/RAFTK, a cytoplasmic kinase related to the focal adhesion kinase, is highly expressed in rat osteoclasts in vivo. Using murine osteoclast-like cells (OCLs) or their mononuclear precursors (pOCs), generated in a coculture of bone marrow and osteoblastic MB1.8 cells, we show: (a) tyrosine phosphorylation of PYK2 upon ligation of beta3 integrins or adhesion of pOCs to serum, vitronectin, osteopontin, or fibronectin but not to laminin or collagen; (b) coimmunoprecipitation of PYK2 and c-Src from OCLs; (c) PYK2 binding to the SH2 domains of Src; (d) marked reduction in tyrosine phosphorylation and kinase activity of PYK2 in OCLs derived from Src (-/-) mice, which do not form actin rings and do not resorb bone; (e) PYK2 phosphorylation by exogeneous c-Src; (f) translocation of PYK2 to the Triton X-100 insoluble cytoskeletal fraction upon adhesion; (g) localization of PYK2 in podosomes and the ring-like structures in OCLs plated on glass and in the sealing zone in OCLs plated on bone; and (h) activation of PYK2, in the presence of MB1.8 cells, parallels the formation of sealing zones and pit resorption in vitro and is reduced by echistatin or calcitonin and cytochalasin D. Taken together, these findings suggest that Src-dependent tyrosine phosphorylation of PYK2 is involved in the adhesion-induced formation of the sealing zone, required for osteoclastic bone resorption.
破骨细胞的激活始于其与骨表面的黏附,随后是细胞骨架重排、封闭区的形成以及极化的皱褶膜的形成。本研究表明,与粘着斑激酶相关的细胞质激酶PYK2/CAKbeta/RAFTK在大鼠破骨细胞中高表达。利用在骨髓与成骨细胞MB1.8细胞共培养中产生的小鼠破骨细胞样细胞(OCLs)或其单核前体细胞(pOCs),我们发现:(a)β3整合素连接或pOCs黏附于血清、玻连蛋白、骨桥蛋白或纤连蛋白而非层粘连蛋白或胶原蛋白时,PYK2发生酪氨酸磷酸化;(b)从OCLs中共免疫沉淀PYK2和c-Src;(c)PYK2与Src的SH2结构域结合;(d)源自Src(-/-)小鼠的OCLs中,PYK2的酪氨酸磷酸化和激酶活性显著降低,这些OCLs不形成肌动蛋白环且不吸收骨;(e)外源性c-Src使PYK2磷酸化;(f)黏附时PYK2易位至Triton X-100不溶性细胞骨架组分;(g)PYK2定位于接种在玻璃上的OCLs中的足体和环状结构以及接种在骨上的OCLs中的封闭区;(h)在MB1.8细胞存在的情况下,PYK2的激活与体外封闭区的形成和凹坑吸收平行,且可被echistatin、降钙素和细胞松弛素D降低。综上所述,这些发现表明,Src依赖的PYK2酪氨酸磷酸化参与了破骨细胞骨吸收所需的黏附诱导的封闭区形成。