D N Clements1, S D Carter, J F Innes, W E R Ollier, P J R Day. 1. Musculoskeletal Research Group, Faculty of Veterinary Science, University of Liverpool, Liverpool, L69 3BX, UK. dylan.clements@liverpool.ac.uk
Abstract
OBJECTIVE: To identify genes which may be involved in the development of anterior cruciate ligament (ACL) laxity and rupture in a naturally occurring canine osteoarthritis (OA) model. DESIGN: Three groups of dog were studied: (1) dogs with ACL rupture; (2) dogs with intact ACLs from a breed predisposed to ACL rupture; (3) dogs with intact ACLs from a breed at very low risk of rupture. The transcriptomes of the ACLs from each group were compared using a whole genome microarray and quantitative reverse transcriptase polymerase chain reaction. Differential gene expression in ruptured canine ACLs was compared with that published in the literature for ruptured human ACLs. RESULTS: No significant differences were identified between the gene expression profiles of normal ACLs of a breed predisposed to ACL rupture when compared to a breed relatively resistant to ACL rupture. A general pattern of increased protease and extracellular structural matrix gene expression was identified in the ruptured ACLs when compared to intact ACLs. The gene expression profiles of ruptured canine ACLs demonstrate similar patterns to those previously reported for ruptured human ACLs. CONCLUSIONS: A transcriptomic basis to breed specific risk for the development of canine ACL rupture was not identified. Although changes in matrix associated gene expression in the ruptured ACL are similar between humans and dogs, the molecular events which may predispose to ACL laxity and rupture were not defined.
OBJECTIVE: To identify genes which may be involved in the development of anterior cruciate ligament (ACL) laxity and rupture in a naturally occurring canineosteoarthritis (OA) model. DESIGN: Three groups of dog were studied: (1) dogs with ACL rupture; (2) dogs with intact ACLs from a breed predisposed to ACL rupture; (3) dogs with intact ACLs from a breed at very low risk of rupture. The transcriptomes of the ACLs from each group were compared using a whole genome microarray and quantitative reverse transcriptase polymerase chain reaction. Differential gene expression in ruptured canine ACLs was compared with that published in the literature for ruptured human ACLs. RESULTS: No significant differences were identified between the gene expression profiles of normal ACLs of a breed predisposed to ACL rupture when compared to a breed relatively resistant to ACL rupture. A general pattern of increased protease and extracellular structural matrix gene expression was identified in the ruptured ACLs when compared to intact ACLs. The gene expression profiles of ruptured canine ACLs demonstrate similar patterns to those previously reported for ruptured human ACLs. CONCLUSIONS: A transcriptomic basis to breed specific risk for the development of canine ACL rupture was not identified. Although changes in matrix associated gene expression in the ruptured ACL are similar between humans and dogs, the molecular events which may predispose to ACL laxity and rupture were not defined.
Authors: Joe N Kornegay; Janet R Bogan; Daniel J Bogan; Martin K Childers; Juan Li; Peter Nghiem; David A Detwiler; C Aaron Larsen; Robert W Grange; Ratna K Bhavaraju-Sanka; Sandra Tou; Bruce P Keene; James F Howard; Jiahui Wang; Zheng Fan; Scott J Schatzberg; Martin A Styner; Kevin M Flanigan; Xiao Xiao; Eric P Hoffman Journal: Mamm Genome Date: 2012-01-05 Impact factor: 2.957
Authors: Stephanie M Frahs; Julia Thom Oxford; Erica E Neumann; Raquel J Brown; Cynthia R Keller-Peck; Xinzhu Pu; Trevor J Lujan Journal: Ann Biomed Eng Date: 2018-06-05 Impact factor: 3.934
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