Differential expression of growth factors and their receptors indicates their involvement in the inverted teat defect in pigs.
In this study 8 genes of growth factors and their receptors were investigated that are known to play a significant role in signaling pathways involved in the ontogenetic, but also tumorigenic, development of breast and mammary glands. Differential expression of fibroblast growth factor receptor 2 (FGFR2), GH receptor (GHR), hepatocyte growth factor (HGF), hepatocyte growth factor receptor (HGFR), platelet-derived growth factor alpha (PDGFA), platelet-derived growth factor receptor alpha (PDGFRA), platelet-derived growth factor beta (PDGFB), and vascular endothelial growth factor (VEGF) was analyzed in mesenchymal and epithelial teat tissue of peripubertal pigs affected and nonaffected by the inverted teat defect. Comparisons were made at the level where pigs were affected between samples derived from nonaffected animals and affected animals, including specimens of normal and inverted teats. In addition, comparisons were made at the level of the teat phenotype with normal teats of nonaffected animals vs. either the normal or the inverted teat of affected animals. All genes tested, except HGFR, showed significant differential expression at P < 0.05 in the mesenchymal or the epithelial teat tissue or both. In general, we observed more pronounced differences when comparing samples obtained from inverted tissues vs. samples from normal ones. Therefore, results of our study suggest that gene expression of the growth factors and their receptors associates directly with the teat phenotype rather than with the affection status of the investigated animals, suggesting that local processes and tissue-specific compensation by means of differential expression of growth factors and their receptors are responsible for the development of impaired teat phenotypes.
Tetzlaff
S
S
Research Institute for the Biology of Farm Animals, Research Unit Molecular Biology, Wilhelm-Stahl-Allee 2, 18196 Dummerstorf, Germany.
Murani
E
E
Schellander
K
K
Ponsuksili
S
S
Wimmers
K
K
D000818:Animals; D005260:Female; D020869:Gene Expression Profiling; D017228:Hepatocyte Growth Factor / Q000096:biosynthesis / Q000235:genetics; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis / Q000235:genetics*; D008297:Male; D008321:Mammary Glands, Animal / Q000002:abnormalities*; D010982:Platelet-Derived Growth Factor / Q000096:biosynthesis / Q000235:genetics; D019859:Proto-Oncogene Proteins c-met / Q000096:biosynthesis / Q000235:genetics; D020574:Proto-Oncogene Proteins c-sis / Q000096:biosynthesis / Q000235:genetics; D051497:Receptor, Fibroblast Growth Factor, Type 2 / Q000096:biosynthesis / Q000235:genetics; D020796:Receptor, Platelet-Derived Growth Factor alpha / Q000096:biosynthesis / Q000235:genetics; D020797:Receptor, Platelet-Derived Growth Factor beta / Q000096:biosynthesis / Q000235:genetics; D017978:Receptors, Growth Factor / Q000096:biosynthesis / Q000235:genetics*; D011986:Receptors, Somatotropin / Q000096:biosynthesis / Q000235:genetics*; D040262:Receptors, Vascular Endothelial Growth Factor / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D034421:Sus scrofa / Q000235:genetics*; D013553:Swine Diseases / Q000235:genetics*; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000235:genetics
D036341:Intercellular Signaling Peptides and Proteins; D010982:Platelet-Derived Growth Factor; D020574:Proto-Oncogene Proteins c-sis; D017978:Receptors, Growth Factor; D011986:Receptors, Somatotropin; D042461:Vascular Endothelial Growth Factor A; C075278:platelet-derived growth factor A; D017228:Hepatocyte Growth Factor; D019859:Proto-Oncogene Proteins c-met; D051497:Receptor, Fibroblast Growth Factor, Type 2; D020796:Receptor, Platelet-Derived Growth Factor alpha; D020797:Receptor, Platelet-Derived Growth Factor beta; D040262:Receptors, Vascular Endothelial Growth Factor