Tgfbi deficiency leads to a reduction in skeletal size and degradation of the bone matrix

Jung Mi Lee, Eun Hye Lee, In-San Kim, Jung Eun Kim

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Transforming growth factor-β-induced gene product-h3 (TGFBI/BIGH3) is an extracellular matrix protein expressed in a wide variety of tissues. TGFBI binds to type I, II, and IV collagens, as well as to biglycan and decorin and plays important roles in cell-to-cell, cell-tocollagen, and cell-to-matrix interactions. Furthermore, TGFBI is involved in cell growth and migration, tumorigenesis, wound healing, and apoptosis. To investigate whether TGFBI is involved in the maintenance of skeletal tissues, Tgfbi knockout mice were generated by crossing male and female Tgfbi heterozygous mice. Skeletal preparation showed that the skeletal size in Tgfbi knockout mice was smaller than in wild-type and heterozygous mice. However, chondrocytic cell alignment in the growth plates, bone mineral density, and bone forming rates were similar in Tgfbi knockout, wild-type, and heterozygous mice. Alterations in skeletal tissue arrangements in Tgfbi knockout mice were estimated from safranin O staining, trichrome staining, and immunohistochemistry for type II and X collagen, and matrix metalloproteinase 13 (MMP13). Cartilage matrix degradation was observed in the articular cartilage of Tgfbi knockout mice. Although the detection of type II collagen in the articular cartilage was lower in Tgfbi knockout mice than wild-type mice, the detection of MMP13 was markedly higher, indicating that Tgfbi deficiency is associated with the degradation of cartilage matrix. These results suggest that TGFBI plays an important role in maintaining skeletal tissues and the cartilage matrix in mice.

Original languageEnglish
Pages (from-to)56-64
Number of pages9
JournalCalcified Tissue International
Volume96
Issue number1
DOIs
Publication statusPublished - 2014 Dec 2
Externally publishedYes

Fingerprint

Bone Matrix
Knockout Mice
Collagen Type II
Cartilage
Articular Cartilage
Biglycan
Collagen Type X
Matrix Metalloproteinase 13
Staining and Labeling
Decorin
Growth Plate
Collagen Type IV
Extracellular Matrix Proteins
Transforming Growth Factors
Collagen Type I
Bone Density
Wound Healing
Cell Movement
Carcinogenesis
Immunohistochemistry

Keywords

  • Knockout
  • Matrix degradation
  • Skeletal size
  • TGFBI
  • Tgfbi

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Orthopedics and Sports Medicine
  • Endocrinology

Cite this

Tgfbi deficiency leads to a reduction in skeletal size and degradation of the bone matrix. / Lee, Jung Mi; Lee, Eun Hye; Kim, In-San; Kim, Jung Eun.

In: Calcified Tissue International, Vol. 96, No. 1, 02.12.2014, p. 56-64.

Research output: Contribution to journalArticle

@article{0d57aa68ea874954b0357e98c99c08cf,
title = "Tgfbi deficiency leads to a reduction in skeletal size and degradation of the bone matrix",
abstract = "Transforming growth factor-β-induced gene product-h3 (TGFBI/BIGH3) is an extracellular matrix protein expressed in a wide variety of tissues. TGFBI binds to type I, II, and IV collagens, as well as to biglycan and decorin and plays important roles in cell-to-cell, cell-tocollagen, and cell-to-matrix interactions. Furthermore, TGFBI is involved in cell growth and migration, tumorigenesis, wound healing, and apoptosis. To investigate whether TGFBI is involved in the maintenance of skeletal tissues, Tgfbi knockout mice were generated by crossing male and female Tgfbi heterozygous mice. Skeletal preparation showed that the skeletal size in Tgfbi knockout mice was smaller than in wild-type and heterozygous mice. However, chondrocytic cell alignment in the growth plates, bone mineral density, and bone forming rates were similar in Tgfbi knockout, wild-type, and heterozygous mice. Alterations in skeletal tissue arrangements in Tgfbi knockout mice were estimated from safranin O staining, trichrome staining, and immunohistochemistry for type II and X collagen, and matrix metalloproteinase 13 (MMP13). Cartilage matrix degradation was observed in the articular cartilage of Tgfbi knockout mice. Although the detection of type II collagen in the articular cartilage was lower in Tgfbi knockout mice than wild-type mice, the detection of MMP13 was markedly higher, indicating that Tgfbi deficiency is associated with the degradation of cartilage matrix. These results suggest that TGFBI plays an important role in maintaining skeletal tissues and the cartilage matrix in mice.",
keywords = "Knockout, Matrix degradation, Skeletal size, TGFBI, Tgfbi",
author = "Lee, {Jung Mi} and Lee, {Eun Hye} and In-San Kim and Kim, {Jung Eun}",
year = "2014",
month = "12",
day = "2",
doi = "10.1007/s00223-014-9938-4",
language = "English",
volume = "96",
pages = "56--64",
journal = "Calcified Tissue International",
issn = "0171-967X",
publisher = "Springer New York",
number = "1",

}

TY - JOUR

T1 - Tgfbi deficiency leads to a reduction in skeletal size and degradation of the bone matrix

AU - Lee, Jung Mi

AU - Lee, Eun Hye

AU - Kim, In-San

AU - Kim, Jung Eun

PY - 2014/12/2

Y1 - 2014/12/2

N2 - Transforming growth factor-β-induced gene product-h3 (TGFBI/BIGH3) is an extracellular matrix protein expressed in a wide variety of tissues. TGFBI binds to type I, II, and IV collagens, as well as to biglycan and decorin and plays important roles in cell-to-cell, cell-tocollagen, and cell-to-matrix interactions. Furthermore, TGFBI is involved in cell growth and migration, tumorigenesis, wound healing, and apoptosis. To investigate whether TGFBI is involved in the maintenance of skeletal tissues, Tgfbi knockout mice were generated by crossing male and female Tgfbi heterozygous mice. Skeletal preparation showed that the skeletal size in Tgfbi knockout mice was smaller than in wild-type and heterozygous mice. However, chondrocytic cell alignment in the growth plates, bone mineral density, and bone forming rates were similar in Tgfbi knockout, wild-type, and heterozygous mice. Alterations in skeletal tissue arrangements in Tgfbi knockout mice were estimated from safranin O staining, trichrome staining, and immunohistochemistry for type II and X collagen, and matrix metalloproteinase 13 (MMP13). Cartilage matrix degradation was observed in the articular cartilage of Tgfbi knockout mice. Although the detection of type II collagen in the articular cartilage was lower in Tgfbi knockout mice than wild-type mice, the detection of MMP13 was markedly higher, indicating that Tgfbi deficiency is associated with the degradation of cartilage matrix. These results suggest that TGFBI plays an important role in maintaining skeletal tissues and the cartilage matrix in mice.

AB - Transforming growth factor-β-induced gene product-h3 (TGFBI/BIGH3) is an extracellular matrix protein expressed in a wide variety of tissues. TGFBI binds to type I, II, and IV collagens, as well as to biglycan and decorin and plays important roles in cell-to-cell, cell-tocollagen, and cell-to-matrix interactions. Furthermore, TGFBI is involved in cell growth and migration, tumorigenesis, wound healing, and apoptosis. To investigate whether TGFBI is involved in the maintenance of skeletal tissues, Tgfbi knockout mice were generated by crossing male and female Tgfbi heterozygous mice. Skeletal preparation showed that the skeletal size in Tgfbi knockout mice was smaller than in wild-type and heterozygous mice. However, chondrocytic cell alignment in the growth plates, bone mineral density, and bone forming rates were similar in Tgfbi knockout, wild-type, and heterozygous mice. Alterations in skeletal tissue arrangements in Tgfbi knockout mice were estimated from safranin O staining, trichrome staining, and immunohistochemistry for type II and X collagen, and matrix metalloproteinase 13 (MMP13). Cartilage matrix degradation was observed in the articular cartilage of Tgfbi knockout mice. Although the detection of type II collagen in the articular cartilage was lower in Tgfbi knockout mice than wild-type mice, the detection of MMP13 was markedly higher, indicating that Tgfbi deficiency is associated with the degradation of cartilage matrix. These results suggest that TGFBI plays an important role in maintaining skeletal tissues and the cartilage matrix in mice.

KW - Knockout

KW - Matrix degradation

KW - Skeletal size

KW - TGFBI

KW - Tgfbi

UR - http://www.scopus.com/inward/record.url?scp=84926664232&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84926664232&partnerID=8YFLogxK

U2 - 10.1007/s00223-014-9938-4

DO - 10.1007/s00223-014-9938-4

M3 - Article

VL - 96

SP - 56

EP - 64

JO - Calcified Tissue International

JF - Calcified Tissue International

SN - 0171-967X

IS - 1

ER -