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YY1-induced lncRNA XIST inhibits cartilage differentiation of BMSCs by binding with TAF15 to stabilizing FUT1

Jian-Ying He1, Min Cheng2, Jia-Lian Ye2

  • 1Orthopedics Department, JiangXi Provinvcial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, 330006, Jiangxi Province, PR China.

Regenerative Therapy
|April 11, 2022
PubMed
Abstract

Insights

The long non-coding RNA XIST is upregulated in osteoarthritis and inhibits bone marrow mesenchymal stem cell differentiation. Targeting the YY1/XIST/TAF15/FUT1 pathway may offer a new therapeutic strategy for osteoarthritis.

Area of Science:

  • Molecular Biology
  • Stem Cell Biology
  • Osteoarthritis Research

Background:

  • Osteoarthritis (OA) is a degenerative joint disease.
  • Bone marrow mesenchymal stem cells (BMSCs) play a role in cartilage repair.
  • The long non-coding RNA XIST (X inactive specific transcript) is implicated in various diseases, but its role in OA and BMSC chondrogenesis is not fully understood.

Purpose of the Study:

  • To elucidate the functional role and mechanism of XIST in osteoarthritis.
  • To investigate the effect of XIST on the chondrogenic differentiation of BMSCs.
  • To identify potential therapeutic targets for OA.

Main Methods:

  • Quantitative RT-PCR and Western blot to detect gene and protein expression.
  • Histological staining (HE, Safranin O-fast green, Alcian-Blue, Alizarin red S) to assess cartilage damage and BMSC differentiation.
  • RNA immunoprecipitation and Luciferase reporter assays to analyze molecular interactions.
  • Chromatin immunoprecipitation to study DNA-protein interactions.
  • Establishment of an OA mouse model to evaluate XIST function *in vivo*.

Main Results:

  • XIST, TAF15, and FUT1 were upregulated in OA cartilage.
  • XIST levels decreased during BMSC chondrogenic differentiation, and its overexpression inhibited this process.
  • Silencing FUT1 reversed the inhibitory effects of XIST overexpression on BMSC differentiation.
  • YY1 induced XIST expression, which in turn regulated FUT1 mRNA stability via TAF15.
  • XIST silencing alleviated cartilage injury in OA mice.

Conclusions:

  • YY1-induced XIST is closely linked to BMSC chondrogenic differentiation and OA progression.
  • The TAF15/FUT1 axis is a key component of the XIST regulatory mechanism in OA.
  • XIST represents a potential novel therapeutic target for osteoarthritis.
Keywords:
ACAN, aggrecanBMSCsBMSCs, bone marrow-derived mesenchymal stem cellsChIP, chromatin immunoprecipitationChondrogenic differentiationFUT1, fucosyltransferase 1H&E, hematoxylin and eosinMSCs, mesenchymal stem cellsOA, osteoarthritisOsteoarthritisRIP, RNA immunoprecipitationRT, room temperatureSOX9, sex-determining region Y (SRY)-box 9TAF15, TATA-box-binding protein-associated factor 15TFs, transcription factorsXISTXIST, X inactive specific transcriptYY1YY1, ying yang 1lncRNAs, long noncoding RNAsqRT-PCR, quantitative real-time polymerase chain reaction

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