Expression levels of angiogenic growth factors in feline squamous cell carcinoma.

Squamous cell carcinoma (SCC) is the most common malignant neoplasm of the skin in cats. Tumour angiogenesis is the pivotal event for tumour progression and metastasis. We assessed protein and gene expression of angiogenic growth factors including bFGF, VEGF-C, TGF-ß, PDGF-A, PDGF-C and PDGFR-α that possibly contribute to the angiogenic phenotype of feline SCC (FSCC) and could, therefore, be a good target in the treatment of SCC. In the present study, a total of 27 FSCC cases were investigated. Tumour cases were histopathologically classified as well differentiated (10/27), moderately differentiated (5/27), and poorly differentiated (12/27). The expression levels of the growth factors were detected using immunohistochemistry and assessed semi-quantitatively. Growth factor expression levels were evaluated at different locations: in the oral region, in areas exposed to solar UV radiation including the ears, eyelids and nasal planum, and other miscellaneous locations. Our findings have revealed that FSCC arising from different anatomical sites of the body and showing differences in aggressiveness, metastasis, and prognosis may be angiogenesis dependent, and angiogenic key regulators could play a role in the development of FSCC.

The Effects of Periostin in a Rat Model of Isoproterenol: Mediated Cardiotoxicity.

Periostin is an extracellular matrix protein from fasciclin family, and it plays an important role in the cell adhesion, migration, and growth of the organism. Periostin prevents apoptosis while stimulating cardiomyocytes. The present study was designed to investigate cardioprotective effects of the recombinant murine periostin peptide administration in a rat model of isoproterenol (ISO)-induced myocardial injury. The experiment was performed on 84 adult male Sprague Dawley rats in 4 groups (n = 21): control group (1), periostin-treated group (2), ISO-treated group (3), and ISO + periostin-treated group (4). The groups were further divided into three subgroups based on the duration of the experiment in which rats were killed on days 1, 7, and 28 (n = 7). Growth factors (VEGF, ANGPT, FGF-2, TGFß), mitosis and apoptosis (Bcl-2, Bax, PCNA, Ki-67, phospho-histone H3), cell cycle activators and inhibitors (cyclin D1, D2, A2, Cdc2), the origin of regenerating cells (cKit and CD45) mRNA were detected using quantitative real-time polymerase chain reaction (PCR) and PCR array. Immunohistochemistry staining was used to directly detect protein level and distribution in the heart tissues. Administration of periostin following ISO-induced cardiotoxicity revealed that periostin alleviated deleterious effects of ISO through several pathways: (1) periostin induced mitotic activity of endothelial/fibroblastic cells, (2) periostin drives cardiomyocytes into S and M phases, thus promoting proliferation of cardiomyocytes, (3) periostin contributed to collagen degradation, tissue remodeling, and reduced cardiac fibrosis during the healing process following myocardial damage while preserving tissue matrix, (4) periostin stimulated angiogenesis by upregulating THBS1, TGFB2, and HGF genes, (5) periostin regulated cell growth and proliferation while maintaining cell shape and cellular muscle contractions (ACTB) and functioned as chemoattractant factor (CCL2) at the beginning of myocardial damage.