miR-181b-induced SMAD7 downregulation controls granulosa cell apoptosis through TGF-β signaling by interacting with the TGFBR1 promoter

J Cell Physiol. 2018 Sep;233(9):6807-6821. doi: 10.1002/jcp.26431. Epub 2018 Mar 25.

Abstract

SMAD7 disrupts the TGF-β signaling pathway by influencing TGFBR1 stability and by blocking the binding of TGFBR1 to SMAD2/3. In this study, we showed that SMAD7 attenuated the TGF-β signaling pathway in ovarian granulosa cells (GCs) by regulating TGFBR1 transcriptional activity. To function as a transcription factor, SMAD7 downregulated the mRNA levels of TGFBR1 via direct binding to the SMAD-binding elements (SBEs) within the promoter region of pig TGFBR1. We also showed that SMAD7 enhanced porcine GC apoptosis by interrupting TGFBR1 and the TGF-β signaling pathway. Interestingly, miR-181b, a microRNA that is downregulated during porcine follicular atresia, was identified to be directly targeting SMAD7 at its 3'-UTR. By inhibiting SMAD7, miR-181b could inhibit GC apoptosis by activating the TGF-β signaling pathway. Our findings provide new insights into the mechanisms underlying the regulation of the TGF-β signaling pathway by SMAD7 and miR-181b.

Keywords: SMAD7; TGF-β signaling pathway; granulosa cell apoptosis; miR-181b.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions / genetics
  • Animals
  • Apoptosis / genetics*
  • Cell Line
  • Down-Regulation / genetics*
  • Female
  • Gene Expression Regulation / genetics
  • Granulosa Cells / physiology*
  • Humans
  • MicroRNAs / genetics*
  • Ovary / physiology
  • Promoter Regions, Genetic / genetics
  • RNA, Messenger / genetics
  • Receptor, Transforming Growth Factor-beta Type I / genetics*
  • Signal Transduction / genetics
  • Smad7 Protein / genetics*
  • Swine
  • Transforming Growth Factor beta / genetics*

Substances

  • 3' Untranslated Regions
  • MicroRNAs
  • RNA, Messenger
  • Smad7 Protein
  • Transforming Growth Factor beta
  • Receptor, Transforming Growth Factor-beta Type I