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Solexa sequencing and custom micro RNA chip reveal repertoire of micro RNA s in mammary gland of bovine suffering from natural infectious mastitis
Author(s) -
Ju Zhihua,
Jiang Qiang,
Liu Gang,
Wang Xiuge,
Luo Guojing,
Zhang Yan,
Zhang Jibin,
Zhong Jifeng,
Huang Jinming
Publication year - 2018
Publication title -
animal genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.756
H-Index - 81
eISSN - 1365-2052
pISSN - 0268-9146
DOI - 10.1111/age.12628
Subject(s) - biology , mastitis , microrna , immune system , innate immune system , immunology , inflammation , dna microarray , gene , gene expression , genetics , microbiology and biotechnology
Summary Identification of microRNAs (mi RNA s), target genes and regulatory networks associated with innate immune and inflammatory responses and tissue damage is essential to elucidate the molecular and genetic mechanisms for resistance to mastitis. In this study, a combination of Solexa sequencing and custom mi RNA chip approaches was used to profile the expression of mi RNA s in bovine mammary gland at the late stage of natural infection with Staphylococcus aureus , a widespread mastitis pathogen. We found 383 loci corresponding to 277 known and 49 putative novel mi RNA s, two potential mitrons and 266 differentially expressed mi RNA s in the healthy and mastitic cows’ mammary glands. Several interaction networks and regulators involved in mastitis susceptibility, such as ALCAM , COL 1A1, APOP 4, ITIH 4, CRP and fibrinogen alpha ( FGA ), were highlighted. Significant down‐regulation and location of bta‐miR‐26a, which targets FGA in the mastitic mammary glands, were validated using quantitative real‐time PCR, in situ hybridization and dual‐luciferase reporter assays. We propose that the observed mi RNA variations in mammary glands of mastitic cows are related to the maintenance of immune and defense responses, cell proliferation and apoptosis, and tissue injury and healing during the late stage of infection. Furthermore, the effect of bta‐miR‐26a in mastitis, mediated at least in part by enhancing FGA expression, involves host defense, inflammation and tissue damage.