Gene expression in intestinal mucosal biopsy specimens obtained from dogs with chronic enteropathy

Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE). Animals—18 dogs with CE and 6 healthy control dogs. Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed. Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis. Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity. Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease

Gene expression in intestinal mucosal biopsy specimens obtained from dogs with chronic enteropathy

Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE). Animals—18 dogs with CE and 6 healthy control dogs. Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed. Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis. Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity. Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease

Comparative Gene Approach to the Investigation of SNPs within the Tenascin-C Gene in Achilles Tendon Injury in the Canine Patient

Objective: To evaluate for single nucleotide polymorphisms (SNPs) within the tenascin-C (TNC) gene in a population of dogs with atraumatic Achilles tendon rupture.Background: In humans, Achilles tendinopathy has been extensively studied for numerous polymorphisms within several genes and has been associated with polymorphisms in collagen (COL5A1) and the TNC genes.Evidentiary value: This study serves as a starting point for evaluating a genetic component of Achilles tendinopathy in the dog.Methods: Whole blood from twenty dogs with atraumatic Achilles tendon rupture and 14 matched control samples were used. DNA was extracted from whole blood run with primers designed around two SNPs previously identified to be related to Achilles tendinopathy in humans. One SNP was located in exon 29, and one exon 17 of the canine TNC gene. Polymerase chain reaction (PCR) was run on the samples and they were sequenced. Sequences of the affected canine population were compared to the control sample sequences.Results: There were no significant differences in genotype or allele frequency of the SNPs rs13321 and rs2104772 between any of the affected and control subjects with a p-value of 1.0.Conclusion: This study evaluated a population of canines with atraumatic Achilles tendon rupture for SNPs in the TNC gene. We found no difference in gene sequence for the study population compared to age, sex, and breed matched controls.Application: Though the data from this study did not show a correlation between the specific polymorphisms investigated, it is possible that other SNPs within the TNC gene or other genes involved in tendon composition and repair such as collagen may be associated with atraumatic Achilles tendon injury in the dog.  <img src="https://www.veterinaryevidence.org/rcvskmod/icons/pr-icon.jpg" alt="Peer Reviewed" /

Inheritance of rupture of the cranial cruciate ligament in Newfoundlands

Objective - To determine prevalence, level of inbreeding, heritability, and mode of inheritance for rupture of the cranial cruciate ligament (RCCL) in Newfoundlands. Design - Retrospective and recruitment study. Animals - 574 client-owned Newfoundlands. Procedure - Medical records from January 1, 1996, to December 31, 2002, were evaluated for prevalence of RCCL. A pedigree was constructed by use of recruited Newfoundlands with RCCL status based on results of veterinary examination; level of inbreeding, heritability, and mode of inheritance were calculated. Results - Hospital prevalence for RCCL was 22%; dogs in the pedigree from the recruitment study had a mean level of inbreeding of 1.19 X 10–4, heritability of 0.27, and a possible recessive mode of inheritance with 51% penetrance for RCCL. Conclusions and Clinical Relevance - Identification of a genetic basis for RCCL in Newfoundlands provided evidence that investigators can now focus on developing methods to identify carriers to reduce the prevalence of RCCL