The mechanical phenotype of biglycan-deficient mice is bone- and gender-specific

Joseph M. Wallace, Rupak M. Rajachar, Xiao Dong Chen, Songtao Shi, Matthew Allen, Susan A. Bloomfield, Clifford M. Les, Pamela G. Robey, Marian F. Young, David H. Kohn

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Biglycan (bgn) is a small leucine-rich proteoglycan (SLRP) enriched in the extracellular matrix of skeletal tissues. While bgn is known to be involved in the growth and differentiation of osteoblast precursor cells and regulation of collagen fibril formation, it is unclear how these functions impact bone's geometric and mechanical properties, properties which are integral to the structural function of bone. Because the genetic control of bone structure and function is both local- and gender-specific and because there is evidence of gender-specific effects associated with genetic deficiencies, it was hypothesized that the engineered deletion of the gene encoding bgn would result in a cortical bone mechanical phenotype that was bone- and gender-specific. In 11-week-old C57BL6/129 mice, the cortical bone in the mid-diaphyses of the femora and tibiae of both genders was examined. Phenotypic changes in bgn-deficient mice relative to wild type controls were assayed by four-point bending tests to determine mechanical properties at the whole bone (structural) and tissue levels, as well as analyses of bone geometry and bone formation using histomorphometry. Of the bones examined, bgn deficiency most strongly affected the male tibiae, where enhanced cross-sectional geometric properties and bone mineral density were accompanied by decreased tissue-level yield strength and pre-yield structural deformation and energy dissipation. Because pre-yield properties alone were impacted, this implies that the gene deletion causes important alterations in mineral and/or the matrix/mineral ultrastructure and suggests a new understanding of the functional role of bgn in regulating bone mineralization in vivo.

Original languageEnglish (US)
Pages (from-to)106-116
Number of pages11
JournalBone
Volume39
Issue number1
DOIs
StatePublished - Jul 2006
Externally publishedYes

Fingerprint

Biglycan
Phenotype
Bone and Bones
Gene Deletion
Tibia
Minerals
129 Strain Mouse
Physiologic Calcification
Diaphyses
Osteoblasts
Osteogenesis
Bone Density
Femur
Extracellular Matrix
Collagen
Growth

Keywords

  • Histomorphometry
  • Mechanical properties
  • Mineralization
  • pQCT
  • Transgenic

ASJC Scopus subject areas

  • Physiology
  • Hematology

Cite this

Wallace, J. M., Rajachar, R. M., Chen, X. D., Shi, S., Allen, M., Bloomfield, S. A., ... Kohn, D. H. (2006). The mechanical phenotype of biglycan-deficient mice is bone- and gender-specific. Bone, 39(1), 106-116. https://doi.org/10.1016/j.bone.2005.12.081

The mechanical phenotype of biglycan-deficient mice is bone- and gender-specific. / Wallace, Joseph M.; Rajachar, Rupak M.; Chen, Xiao Dong; Shi, Songtao; Allen, Matthew; Bloomfield, Susan A.; Les, Clifford M.; Robey, Pamela G.; Young, Marian F.; Kohn, David H.

In: Bone, Vol. 39, No. 1, 07.2006, p. 106-116.

Research output: Contribution to journalArticle

Wallace, JM, Rajachar, RM, Chen, XD, Shi, S, Allen, M, Bloomfield, SA, Les, CM, Robey, PG, Young, MF & Kohn, DH 2006, 'The mechanical phenotype of biglycan-deficient mice is bone- and gender-specific', Bone, vol. 39, no. 1, pp. 106-116. https://doi.org/10.1016/j.bone.2005.12.081
Wallace JM, Rajachar RM, Chen XD, Shi S, Allen M, Bloomfield SA et al. The mechanical phenotype of biglycan-deficient mice is bone- and gender-specific. Bone. 2006 Jul;39(1):106-116. https://doi.org/10.1016/j.bone.2005.12.081
Wallace, Joseph M. ; Rajachar, Rupak M. ; Chen, Xiao Dong ; Shi, Songtao ; Allen, Matthew ; Bloomfield, Susan A. ; Les, Clifford M. ; Robey, Pamela G. ; Young, Marian F. ; Kohn, David H. / The mechanical phenotype of biglycan-deficient mice is bone- and gender-specific. In: Bone. 2006 ; Vol. 39, No. 1. pp. 106-116.
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abstract = "Biglycan (bgn) is a small leucine-rich proteoglycan (SLRP) enriched in the extracellular matrix of skeletal tissues. While bgn is known to be involved in the growth and differentiation of osteoblast precursor cells and regulation of collagen fibril formation, it is unclear how these functions impact bone's geometric and mechanical properties, properties which are integral to the structural function of bone. Because the genetic control of bone structure and function is both local- and gender-specific and because there is evidence of gender-specific effects associated with genetic deficiencies, it was hypothesized that the engineered deletion of the gene encoding bgn would result in a cortical bone mechanical phenotype that was bone- and gender-specific. In 11-week-old C57BL6/129 mice, the cortical bone in the mid-diaphyses of the femora and tibiae of both genders was examined. Phenotypic changes in bgn-deficient mice relative to wild type controls were assayed by four-point bending tests to determine mechanical properties at the whole bone (structural) and tissue levels, as well as analyses of bone geometry and bone formation using histomorphometry. Of the bones examined, bgn deficiency most strongly affected the male tibiae, where enhanced cross-sectional geometric properties and bone mineral density were accompanied by decreased tissue-level yield strength and pre-yield structural deformation and energy dissipation. Because pre-yield properties alone were impacted, this implies that the gene deletion causes important alterations in mineral and/or the matrix/mineral ultrastructure and suggests a new understanding of the functional role of bgn in regulating bone mineralization in vivo.",
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