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Identification of novel osteochondrosis— Associated genes
Author(s) -
Mirams Michiko,
Ayodele Babatunde A.,
Tatarczuch Liliana,
Henson Frances M.,
Pagel Charles N.,
Mackie Eleanor J.
Publication year - 2016
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.23033
Subject(s) - cartilage , osteochondrosis , pathology , chondrocyte , suppression subtractive hybridization , lumican , biology , aggrecan , gene , gene expression , osteoarthritis , proteoglycan , medicine , anatomy , genetics , cdna library , articular cartilage , alternative medicine , decorin
During the early stages of articular osteochondrosis, cartilage is retained in subchondral bone, but the pathophysiology of this condition of growing humans and domestic animals is poorly understood. A subtractive hybridization study was undertaken to compare gene expression between the cartilage of early experimentally induced equine osteochondrosis lesions and control cartilage. Of the many putative differentially expressed genes identified, eight were confirmed by quantitative PCR analysis as differentially expressed, in addition to those already known to be associated with early lesions. Genes encoding vacuolar H + ‐ATPase V 0 subunit d 2 (ATP6V0D2), cathepsin K, integrin‐binding sialoprotein, integrin αV, low density lipoprotein receptor‐related protein 4, lumican, osteopontin, and thymosin β4 (TMSB4) were expressed at higher levels in lesions than in control cartilage. These genes included 34 genes not previously identified in cartilage. Some genes identified as associated with early lesions are known chondrocyte hypertrophy‐associated genes, and in transmission electron microscopy studies normal hypertrophic chondrocytes were observed in lesions. Differential expression of ATP6V0D2 and TMSB4 in the cartilage of early naturally occurring osteochondrosis lesions was confirmed by immunohistochemistry. These results identify novel osteochondrosis‐associated genes and provide evidence that articular osteochondrosis does not necessarily result from failure of chondrocytes to undergo hypertrophy. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:404–411, 2016.