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Current IssueEditorial BoardOnline First Articles
Indian Journal of
Animal Research
Print ISSN: 0367-6722
Online ISSN: 0976-0555
NASS Rating
6.40
SJR
0.233
CiteScore
0.606

Chief Editor:
M. R. Saseendranath
Kerala Veterinary and Animal Science University, Mannuthy, Thrissur, INDIA
Frequency:Monthly
Indexing:
Science Citation Index Expanded, BIOSIS Preview, ISI Citation Index, Biological Abstracts, Scopus, ...

Research Article

Indian Journal of Animal Research, volume 53 issue 11 (november 2019) : 1440-1444

Immunohistochemical detection of alpha-smooth muscle actin and S-100 in bovine mammary gland with mastitis

Geeta Devi Leishangthem, Nittin Dev Singh, Amarjit Singh
1Animal Disease Research Centre, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana-141 004, Punjab, India.
Cite article:- Leishangthem Devi Geeta, Singh Dev Nittin, Singh Amarjit (2019). Immunohistochemical detection of alpha-smooth muscle actin and S-100 in bovine mammary gland with mastitis. Indian Journal of Animal Research. 53(11): 1440-1444. doi: 10.18805/ijar.B-3674.

ABSTRACT

Fibrosis is a common finding in chronic mastitis. Epithelial-mesenchymal transition (EMT) plays a prominent role in fibrogenesis in adult tissues. The aim of this study was to investigate whether EMT occurs in bovine mastitis by assessing the expression or localization of alpha-smooth muscle actin (alpha-SMA), S-100 protein and caspase-3. Two normal bovine mammary gland tissue samples and five mastitic samples were used in the study. Antibodies to alpha-SMA, S-100 and caspase-3 were used for immunohistochemical studies. In mastitis there was increased expression of S-100 in the alveolar epithelial cells. Alpha-SMA was highly expressed in the areas where there is fibrosis in chronic mastitis. Further caspase-3 was observed in alveolar cells in mastitic tissue. Overexpression of S-100 and alpha-SMA directly correlates to the severity of mastitis.S-100 and alpha-SMA may serve as biomarkers to know the extent of tissue structural changes in mastitis. EMT could be one of the mechanistic pathways underlying the pathogenesis of fibrosis in mastitis. 

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