Abstract
More than 99% of ovarian follicles undergo atresia in mammals, but the mechanism of follicular atresia remains to be elucidated. In this study, we explored microRNA (miRNA) regulation of follicular atresia in porcine ovary. A miRNA expression profile was constructed for healthy, early atretic, and progressively atretic follicles, and the differentially expressed miRNAs were selected and analyzed. We found that miR-26b, which was upregulated during follicular atresia, increased the number of DNA breaks and promoted granulosa cell apoptosis by targeting the ataxia telangiectasia mutated gene directly in vitro.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Apoptosis*
-
Ataxia Telangiectasia Mutated Proteins
-
Cell Cycle Proteins / metabolism*
-
DNA Damage
-
DNA-Binding Proteins / metabolism*
-
Estradiol / metabolism
-
Female
-
Follicular Atresia / metabolism*
-
Follicular Fluid / metabolism
-
Gene Expression Profiling
-
Granulosa Cells / cytology*
-
Luminescence
-
MicroRNAs / biosynthesis*
-
MicroRNAs / genetics
-
Ovarian Follicle / metabolism
-
Ovary / metabolism*
-
Progesterone / metabolism
-
Protein Serine-Threonine Kinases / metabolism*
-
Swine
-
Tissue Distribution
-
Tumor Suppressor Proteins / metabolism*
-
Up-Regulation
Substances
-
Cell Cycle Proteins
-
DNA-Binding Proteins
-
MicroRNAs
-
Tumor Suppressor Proteins
-
Progesterone
-
Estradiol
-
Ataxia Telangiectasia Mutated Proteins
-
Protein Serine-Threonine Kinases