Pulmonary hypertension (PH) is defined as an increase in pulmonary vascular pressure. It is one of the most common complications that occur as a result of degenerative mitral valve disease (DMVD) in dogs. Serotonin (5-HT) can trigger the development of PH. Accordingly, this study investigated the changes in the expression of genes and proteins associated with local 5-HT signaling in the lungs and pulmonary arteries (PA) of dogs with PH secondary to DMVD. Lung and PA tissue samples were collected from the cadavers of fourteen small-breed dogs and divided into normal (n = 4), DMVD (n = 5) and DMVD with PH (n = 5) groups. Gene expression (tph1, slc6a4 and htr2a) was analyzed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The expression of proteins (TPH-1, SERT, 5-HTR2A, ERK1/2 and pERK1/2) was examined by Western blot analysis and immunohistochemical staining. The results showed that the expression of genes and proteins evaluated by qRT-PCR and Western blot analysis in lung and PA tissues did not differ among groups. However, the expression of proteins related to 5-HT signaling tended to be upregulated in PA tissues from DMVD dogs with and without PH. Immunohistochemical examination revealed the overexpression of these proteins in the DMVD and DMVD with PH groups in lung tissue. These findings suggest a local effect of 5-HT signaling in DMVD dogs with and without PH.

Cardiac disease is common in cats, and concurrent pleural effusion can worsen the prognosis. However, the definitive diagnosis of feline cardiac disease by echocardiography is limited in some areas. This study was designed to determine the indicators from fluid analysis obtained from pleural effusion to help diagnose cardiac disease in cats.

Background: Pulmonary hypertension (PH) can cause medial thickening, a hallmark of pulmonary arterial remodeling. The serotonin (5HT) pathway has been suggested as a factor associated with PH by inducing pulmonary arterial smooth muscle cells (SMCs) proliferation, a major cause of medial thickening. This study aims to demonstrate the expression of molecules in the 5HT pathway in the pulmonary artery of dogs affected with PH secondary to degenerative mitral valve disease (DMVD) compared to DMVD and healthy control dogs. Materials and Methods: The study included lung samples from the carcasses of 19 older small-breed dogs (Control n = 5, DMVD n = 7, DMVD+PH n = 7). Lung tissue sections were performed Hematoxylin and Eosin staining for measuring the percentage of medial thickness and immunohistochemistry for evaluating the expression of proteins in the 5HT pathway including serotonin transporter (SERT), serotonin 2A receptor (5HT2A), tryptophan hydroxylase 1 (TPH1), extracellular regulated kinase 1/2 (ERK1/2), and phosphorylated ERK1/2 (pERK1/2). Results: Medial thickening of the pulmonary arteries was found in the DMVD and DMVD+PH groups compared to the control. The medial thickening of the DMVD+PH group was increased significantly compared to that in the DMVD group. Intracytoplasmic expression of proteins related to the 5HT pathway was mainly presented in the medial layer of the pulmonary arteries. The control group showed a low expression of proteins related to the 5HT pathway. An intensive expression of SERT, 5HT2A, TPH1, and ERK1/2 protein was seen in the DMVD and DMVD+PH groups. Interestingly, pERK1/2 was strongly represented only in the DMVD+PH group. Conclusions: Overexpression of proteins related to the 5HT pathway including SERT, 5HT2A, TPH1, ERK1/2, and pERK1/2 was associated with medial remodeling in dogs affected with secondary to DMVD.

In dogs with degenerative mitral valve disease (DMVD), pulmonary hypertension (PH) is a common complication characterized by abnormally elevated pulmonary arterial pressure (PAP). Pulmonary arterial remodeling is the histopathological changes of pulmonary artery that has been recognized in PH. The underlying mechanisms that cause this arterial remodeling are poorly understood. This study aimed to perform shotgun proteomics to investigate changes in protein expression in pulmonary arteries and lung tissues of DMVD dogs with PH compared to normal control dogs and DMVD dogs without PH. Tissue samples were collected from the carcasses of 22 small-sized breed dogs and divided into three groups: control (n = 7), DMVD (n = 7) and DMVD+PH groups (n = 8). Differentially expressed proteins were identified, and top three upregulated and downregulated proteins in the pulmonary arteries of DMVD dogs with PH including SIK family kinase 3 (SIK3), Collagen type I alpha 1 chain (COL1A1), Transforming growth factor alpha (TGF-α), Apoptosis associated tyrosine kinase (AATYK), Hepatocyte growth factor activator (HGFA) and Tyrosine-protein phosphatase non-receptor type 13 (PTPN13) were chosen. Results showed that some of the identified proteins may play a role in the pathogenesis of pulmonary arterial remodeling. This study concluded shotgun proteomics has potential as a tool for exploring candidate proteins associated with the pathogenesis of PH secondary to DMVD in dogs.

Pulmonic stenosis (PS) is the most common congenital heart disease in dogs. This condition causes right ventricle (RV) overload and disrupts overall systolic function. The aim of this study was to examine the alterations of cardiac electrical activity and mechanical function in dogs with PS compared to normal healthy dogs.