TY - JOUR
T1 - Nonreducible crosslink formation in tibial dyschondroplastic growth plate cartilage from broiler chicks fed homocysteine
AU - Orth, M. W.
AU - Martinez, D. A.
AU - Cook, M. E.
AU - Vailas, A. C.
N1 - Funding Information:
The authors would like to thank Yisheng Bai, Pete Anderla, and Bikram Sawney for their technical assistance. Research was partially supported by NASA Grant# NAG-2568, Federal Hatch Grant# 0302, and the College of Agriculture and Life Sciences at the University of Wisconsin.
PY - 1991/9/30
Y1 - 1991/9/30
N2 - In the study of tibial dyschondroplasia, scientists have for a long time thought that an altered extracellular matrix might be involved in the etiology of the disease. The results presented in this paper show that the collagen content was increased in the dyschondroplastic cartilage when compared to normal growth plate and day-old hypertrophic cartilage. Furthermore, nonreducible crosslinks were found only in dyschondroplastic cartilage, with the greatest amounts occurring in the distal region of the lesion, approximately 10-fold higher than that found in the dyschondroplastic growth plate. Thus, intermolecular collagen bonding is altered in the extracellular matrix of dyschondroplastic cartilage. Possible models for the etiology of the disease are discussed.
AB - In the study of tibial dyschondroplasia, scientists have for a long time thought that an altered extracellular matrix might be involved in the etiology of the disease. The results presented in this paper show that the collagen content was increased in the dyschondroplastic cartilage when compared to normal growth plate and day-old hypertrophic cartilage. Furthermore, nonreducible crosslinks were found only in dyschondroplastic cartilage, with the greatest amounts occurring in the distal region of the lesion, approximately 10-fold higher than that found in the dyschondroplastic growth plate. Thus, intermolecular collagen bonding is altered in the extracellular matrix of dyschondroplastic cartilage. Possible models for the etiology of the disease are discussed.
UR - http://www.scopus.com/inward/record.url?scp=0026048093&partnerID=8YFLogxK
U2 - 10.1016/0006-291X(91)91754-Z
DO - 10.1016/0006-291X(91)91754-Z
M3 - Article
C2 - 1930198
AN - SCOPUS:0026048093
VL - 179
SP - 1582
EP - 1586
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -