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PPAR Gamma-Regulated MicroRNA 199a-5p Underlies Bone Marrow Adiposity in Aplastic Anemia

Xianning Zhang1, Lulu Liu1, Cuiyun Dou2

  • 1Central Laboratory, Affiliated Hospital of Jining Medical University, Jining 272029, Shandong Province, China.

Molecular Therapy. Nucleic Acids
|August 11, 2019
PubMed

Insights

MicroRNA 199a-5p promotes fat cell differentiation in bone marrow mesenchymal stem cells (BM-MSCs) in aplastic anemia (AA). This process, regulated by PPAR gamma and inhibiting TGFBI, offers potential therapeutic targets for AA.

Area of Science:

  • Stem cell biology
  • Molecular mechanisms of disease
  • Hematopoiesis

Background:

  • Aplastic anemia (AA) is linked to increased adipogenesis of bone marrow-derived mesenchymal stem cells (BM-MSCs), leading to fatty bone marrow and impaired hematopoiesis.
  • The molecular pathways driving this aberrant adipogenic differentiation in AA remain largely unelucidated.

Purpose of the Study:

  • To investigate the role of microRNA 199a-5p (miR-199a-5p) in the adipogenic differentiation of BM-MSCs in the context of aplastic anemia.
  • To elucidate the molecular mechanism by which miR-199a-5p influences adipogenesis and its relationship with key regulatory factors.

Main Methods:

  • Comparative analysis of miR-199a-5p expression in BM-MSCs from AA patients and healthy controls.
  • Lentivirus-mediated overexpression of miR-199a-5p in BM-MSCs to assess its functional impact on adipogenic differentiation.
  • Investigation of the regulatory relationship between PPAR gamma (PPARγ), miR-199a-5p, and transforming growth factor beta induced (TGFBI) using molecular assays.
  • Validation of TGFBI as a regulator of adipogenesis.

Main Results:

  • miR-199a-5p expression is significantly upregulated in AA BM-MSCs compared to normal controls.
  • Overexpression of miR-199a-5p enhances adipogenic differentiation of BM-MSCs.
  • miR-199a-5p is regulated by PPARγ in a transcription-independent manner and targets TGFBI expression.
  • TGFBI acts as a negative regulator of adipogenesis, and its expression is inversely correlated with miR-199a-5p levels.
  • A positive correlation between PPARγ and miR-199a-5p, and an inverse correlation between miR-199a-5p and TGFBI were observed in both normal and AA BM-MSCs.

Conclusions:

  • PPARγ-regulated miR-199a-5p promotes BM-MSC adipogenesis by inhibiting TGFBI expression.
  • This pathway represents a novel mechanism contributing to bone marrow adiposity in aplastic anemia.
  • Targeting the PPARγ-miR-199a-5p-TGFBI axis offers potential therapeutic strategies for AA treatment.
Keywords:
Aplastic anemiaBM-MSCsPPARγTGFBImiR-199a-5p

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