The peroxisome proliferator-activated receptors (PPARs) belong to nuclear receptor superfamily acting as transcription factors related to lipid and glucose metabolism. There are 3 subtypes including PPARα, PPAR, and PPAR. PPARα and PPAR activations can inhibit tumor cell proliferation and differentiation in many cell types. However, the expressions of these receptors in canine mammary tissue are still unknown. This study was performed to investigate the expressions of PPARα and PPAR in normal, benign, and malignant canine mammary tissues. Twenty four bitches at the age of 5-15 years old, which undergone unilateral mastectomy, were used in the study. Mammary tissues were sectioned and histologically diagnosed by H&E staining, 12 were benign and another 12 were malignant. In each dog, tissues were collected from both normal and tumor area. Immunohistochemical staining has demonstrated that both PPARα and PPAR express mainly in cytoplasm, perinucleolar region, and some nuclei of glandular epithelial cells, ductal epithelial cells, and myoepithelial cells. Lower expression of the receptors were found in fibroblasts, macrophages, endothelial cells and smooth muscle cells of blood vessels. Cytoplasmic immunoreactivities of these receptors were calculated into H-score. H-score of PPARα in benign type and PPAR in malignant type were significantly higher than in normal tissue (P<0.05). According to the expression of these receptors in normal canine mammary tissue and receptor upregulation in tumor cells suggested that PPARα and PPAR may play a role in canine mammary gland function and might be related to the pathogenesis or progression of canine mammary gland tumors.
Faculty of Veterinary Science, Chulalongkorn University
Klomkleaw, Wuthichai and Raksaseri, Promporn
"Immunohistochemical staining of peroxisome proliferatoractivated receptor alpha and gamma in normal, benign, and malignant canine mammary tissues,"
The Thai Journal of Veterinary Medicine: Vol. 48:
3, Article 11.
Available at: https://digital.car.chula.ac.th/tjvm/vol48/iss3/11