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J Dev Biol. 2015;3(4):158-176. Epub 2015 Dec 16.

Col11a1 Regulates Bone Microarchitecture during Embryonic Development.

Author information

1
Biomolecular Research Center, Boise State University, 1910 University Drive, Boise, ID 83706-1511, USA.
2
Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA.
3
Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA; College of Dental Medicine, Roseman University, South Jordan, UT 84095, USA.

Abstract

Collagen XI alpha 1 (Col11a1) is an extracellular matrix molecule required for embryonic development with a role in both nucleating the formation of fibrils and regulating the diameter of heterotypic fibrils during collagen fibrillar assembly. Although found in many different tissues throughout the vertebrate body, Col11a1 plays an essential role in endochondral ossification. To further understand the function of Col11a1 in the process of bone formation, we compared skeletal mineralization in wild-type (WT) mice and Col11a1-deficient mice using X-ray microtomography (micro-CT) and histology. Changes in trabecular bone microstructure were observed and are presented here. Additionally, changes to the periosteal bone collar of developing long bones were observed and resulted in an increase in thickness in the case of Col11a1-deficient mice compared to WT littermates. Vertebral bodies were incompletely formed in the absence of Col11a1. The data demonstrate that Col11a1 depletion results in alteration to newly-formed bone and is consistent with a role for Col11a1 in mineralization. These findings indicate that expression of Col11a1 in the growth plate and perichondrium is essential for trabecular bone and bone collar formation during endochondral ossification. The observed changes to mineralized tissues further define the function of Col11a1.

KEYWORDS:

Col11a1; Collagen XI; X-ray microtomography; chondrodysplasia; mineralization

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