Paul J Hauser1, Samuel B VanGordon1, Jonathan Seavey2, Troy M Sofinowski3, Mohammad Ramadan1, Shivon Abdullah4, C A Tony Buffington5, Robert E Hurst6. 1. Department of Urology, College of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma. 2. Department of Urology, College of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma; General Surgery Department, Walter Reed National Military Medical Center, Bethesda, Maryland. 3. Department of Urology, College of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma; Murfreesboro Medical Clinic and Surgicenter, Murfreesboro, Tennessee. 4. Department of Urology, College of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma; Department of Anesthesiology, College of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma. 5. Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Ohio State University, Columbus, Ohio. 6. Department of Urology, College of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma; Department of Biochemistry and Molecular Biology, College of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma. Electronic address: Robert-hurst@ouhsc.edu.
Abstract
PURPOSE: We analyzed the urothelium of cats diagnosed with feline interstitial cystitis to determine whether abnormalities in protein expression patterns could be detected and whether the expression pattern was similar to that in patients with human interstitial cystitis/bladder pain syndrome. The proteins analyzed are involved in cell adhesion and barrier function, comprise the glycosaminoglycan layer or are differentiation markers. MATERIALS AND METHODS: Formalin fixed biopsies from 8 cats with feline interstitial cystitis and from 7 healthy control cats were labeled by immunohistochemistry and scored with a modified version of a system previously used for human samples. Cluster analysis was performed to investigate relationships between markers and samples. RESULTS: Of the feline interstitial cystitis bladders 89% showed abnormal protein expression and chondroitin sulfate patterns while only 27% of normal tissues showed slight abnormalities. Abnormalities were found in most feline interstitial cystitis samples, including biglycan in 87.5%, chondroitin sulfate, decorin, E-cadherin and keratin-20 in 100%, uroplakin in 50% and ZO-1 in 87.5%. In feline interstitial cystitis bladders about 75% of chondroitin sulfate, biglycan and decorin samples demonstrated absent luminal staining or no staining. Cluster analysis revealed that feline interstitial cystitis and normal samples could be clearly separated into 2 groups, showing that the urothelium of cats with feline interstitial cystitis is altered from normal urothelium. CONCLUSIONS: Feline interstitial cystitis produces changes in luminal glycosaminoglycan and several proteins similar to that in patients, suggesting some commonality in mechanism. Results support the use of feline interstitial cystitis as a model of human interstitial cystitis.
PURPOSE: We analyzed the urothelium of cats diagnosed with feline interstitial cystitis to determine whether abnormalities in protein expression patterns could be detected and whether the expression pattern was similar to that in patients with humaninterstitial cystitis/bladder pain syndrome. The proteins analyzed are involved in cell adhesion and barrier function, comprise the glycosaminoglycan layer or are differentiation markers. MATERIALS AND METHODS:Formalin fixed biopsies from 8 cats with feline interstitial cystitis and from 7 healthy control cats were labeled by immunohistochemistry and scored with a modified version of a system previously used for human samples. Cluster analysis was performed to investigate relationships between markers and samples. RESULTS: Of the feline interstitial cystitis bladders 89% showed abnormal protein expression and chondroitin sulfate patterns while only 27% of normal tissues showed slight abnormalities. Abnormalities were found in most feline interstitial cystitis samples, including biglycan in 87.5%, chondroitin sulfate, decorin, E-cadherin and keratin-20 in 100%, uroplakin in 50% and ZO-1 in 87.5%. In feline interstitial cystitis bladders about 75% of chondroitin sulfate, biglycan and decorin samples demonstrated absent luminal staining or no staining. Cluster analysis revealed that feline interstitial cystitis and normal samples could be clearly separated into 2 groups, showing that the urothelium of cats with feline interstitial cystitis is altered from normal urothelium. CONCLUSIONS: Feline interstitial cystitis produces changes in luminal glycosaminoglycan and several proteins similar to that in patients, suggesting some commonality in mechanism. Results support the use of feline interstitial cystitis as a model of humaninterstitial cystitis.
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