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Absence of beta3 integrin accelerates early skeletal repair
Author(s) -
Hu Diane,
Lu Chuanyong,
Sapozhnikova Anna,
Barnett Michael,
Sparrey Carolyn,
Miclau Theodore,
Marcucio Ralph S.
Publication year - 2010
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.20955
Subject(s) - integrin , angiogenesis , bone healing , cartilage , microbiology and biotechnology , extracellular matrix , transmembrane protein , biology , cell , medicine , anatomy , receptor , genetics
Integrins are heterodimeric transmembrane proteins that mediate cell–matrix interactions and modulate cell behavior. Beta3 subunit is a component of αIIβ3 and αVβ3 integrins. In this study, we first determined that β3 transcripts are expressed by cells within fracture calluses at 7 and 10 days after injury in a mouse model. We then analyzed fracture healing in mice deficient of β3 integrin with molecular, histomorphometric, and biomechanical techniques. We found that lack of β3 integrin results in an extended bleeding time and leads to more bone formation and accelerated cartilage maturation at 7 days after injury. However, β3 deficiency does not appear to affect later fracture healing. At days 14 and 21, histological appearance or biomechanical properties of fracture calluses are similar between wild type and mutant mice. We also found that altered fracture healing in β3‐null mice is not associated with accelerated angiogenesis, because no significant difference of length density and surface density of blood vessels in fracture limbs was detected at 3 days after injury between wild type and β3‐null mice. In conclusion, our findings demonstrate that β3 integrin plays an important role during early fracture healing. Further research is required to determine the underlying mechanisms. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:32–37, 2010