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Type XII collagen regulates osteoblast polarity and communication during bone formation

2011; Rockefeller University Press; Volume: 193; Issue: 6 Linguagem: Inglês

10.1083/jcb.201010010

1540-8140

Yayoi Izu, Mei Sun, Daniela Zwolanek, Guido Veit, Valerie Williams, Byeong Cha, Karl J. Jepsen, Manuel Koch, David E. Birk,

Bone health and osteoporosis research

Differentiated osteoblasts are polarized in regions of bone deposition, demonstrate extensive cell interaction and communication, and are responsible for bone formation and quality. Type XII collagen is a fibril-associated collagen with interrupted triple helices and has been implicated in the osteoblast response to mechanical forces. Type XII collagen is expressed by osteoblasts and localizes to areas of bone formation. A transgenic mouse null for type XII collagen exhibits skeletal abnormalities including shorter, more slender long bones with decreased mechanical strength as well as altered vertebrae structure compared with wild-type mice. Col12a−/− osteoblasts have decreased bone matrix deposition with delayed maturation indicated by decreased bone matrix protein expression. Compared with controls, Col12a−/− osteoblasts are disorganized and less polarized with disrupted cell–cell interactions, decreased connexin43 expression, and impaired gap junction function. The data demonstrate important regulatory roles for type XII collagen in osteoblast differentiation and bone matrix formation.