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Published on: June 14, 2016
Desmin disorganisation: A key feature in feline hypertrophic cardiomyopathy
Wan-Ching Cheng1, Charlotte Lawson2, Lois Wilkie1
1Department of Clinical Science and Services, Royal Veterinary College, Hatfield, Hertfordshire, United Kingdom.
Insights
Hypertrophic cardiomyopathy (HCM) in cats shows similar subcellular changes as in humans, including protein aggregates and disorganization of cardiomyocyte connections. This suggests a shared cellular response to HCM across species.
Area of Science:
- Veterinary Pathology
- Cardiovascular Research
- Cell Biology
Background:
- Hypertrophic cardiomyopathy (HCM) is histologically defined by increased ventricular wall thickness and myocyte disarray.
- Subcellular alterations in human and rodent HCM involve the intermediate filament cytoskeleton (desmin) and proteins crucial for cardiomyocyte connections (beta-catenin, connexin-43).
Purpose of the Study:
- To investigate if similar subcellular alterations observed in human and rodent HCM are present in feline HCM samples.
- To compare the expression and organization of desmin, αB-crystallin, beta-catenin, and connexin-43 in feline HCM.
Main Methods:
- Histological examination of feline HCM samples.
- Immunohistochemistry and protein expression analysis to detect desmin, αB-crystallin, beta-catenin, and connexin-43.
Main Results:
- Feline HCM samples exhibit prominent desmin and αB-crystallin aggregates with increased protein expression.
- Disorganization of beta-catenin and connexin-43 was observed, with aberrant signals at the lateral cardiomyocyte surfaces.
- These findings indicate subcellular changes analogous to those seen in human and rodent HCM.
Conclusions:
- The subcellular response in cardiomyocytes to HCM is conserved between cats and humans.
- This study highlights shared pathological mechanisms of HCM across species.
- Findings may inform comparative approaches to HCM research and treatment.
Abstract:
Hypertrophic cardiomyopathy is usually characterised histologically by increased ventricular wall thickness and myocyte disarray. In human and rodent HCM, subcellular alterations were detected that involve the intermediate filament cytoskeleton (mainly desmin) and proteins that are important for mechanical and electrochemical connection of the cardiomyocytes (beta-catenin and connexin-43, respectively). We demonstrate here that similar changes can be visualised in HCM samples from cats, with prominent desmin and αB-crystallin aggregates that are accompanied by increased expression at the protein level. In addition, there is a disorganisation of beta-catenin and connexin-43, which display additional aberrant signals at the lateral surface of cardiomyocytes. This suggests that the subcellular response in cardiomyocytes to HCM is shared by humans and cats.
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