Histopathologic changes in the valves of DMVD dogs include damage to the endothelial valvular cell lining. In human and veterinary medicine, serotonin and serotonin-related pathways have been associated with cardiac disease serotonininduced valvular lesions resemble many gross and histologic DMVD descriptions, and serotonin has recently been suggested to have a role in the progression of DMVD in dogs. Several studies have reported the molecular mechanisms underlying DMVD pathophysiology. Absence of transmembrane processing may result in increased and persistent serotonin receptor interactions and increased valvular mitogenic activity and extracellular matrix production in SERT-knockout mice. A previous study showed that interference with serotonin transmembrane processing via knocking out SERT gene resulted in valvulopathy in mice, establishing a link between SERT and the development of cardiac fibrosis and valvulopathy in vivo. SERT expression facilitates the intercellular processing of serotonin after receptor interactions and is responsible for serotonin uptake and consequent inactivation of amine. In addition, expression of the SERT gene ( SLC6A4) was significantly higher among dogs with clinical DMVD. Furthermore, carcinoid tumors that produce serotonin and the administration of serotonergic drugs have been shown to be associated with valvulopathy in humans. Cardiac fibrosis and valvulopathy occur in mice without serotonin transporter (SERT) protein expression through an increase in serotonin production, localized serotonin re-uptake by SERT, and a decrease in serotonin metabolism. In a previous study, rats that received serotonin injections over a long period developed valvular lesions. This increases serotonin signaling or decreases serotonin clearance, which may induce valvular lesions. Furthermore, components of the cardiovascular system, such as vascular endothelium, smooth muscles, and heart tissue, easily bind to and transport serotonin. The carcinoid syndrome, which is developed by the secretion of serotonin and other vasoactive substances from a tumor, results in endocardial damage.
Serotonin has a crucial role in various cardiovascular disorders. Keywords: canine, mitral valve, polymorphism, serotonin transporter This is the first study of SERT mutation in Maltese dogs with DMVD and is considered a pilot study into clinical genetic examination for early DMVD diagnosis. This study identified six polymorphisms of the SERT gene in Maltese dogs with DMVD, suggesting an association between the SERT gene and canine DMVD. Three of the five polymorphisms were predicted to be probable causes of damage to protein function and confirmed by protein structure model verification. Protein structure and function of the five nonsynonymous genetic variations were predicted. Genetic variations, including five nonsynonymous genetic variations, were detected in five exons. The resulting genetic sequences were aligned and analyzed for variations by comparing with reference sequences the predicted secondary structures of these variations were modeled and cross-verified by applying computational methods. Genomic DNA was extracted from blood samples collected from 20 client-owned DMVD Maltese dogs and 10 healthy control dogs, and each exon of the SERT gene was amplified via polymerase chain reaction. This study evaluated the relationship between genetic variations in the serotonin transporter (SERT) gene of Maltese dogs and DMVD. Degenerative mitral valve disease (DMVD) is the most commonly acquired cardiac disease in dogs.
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