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Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues
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Micro-RNAS Regulate Metabolic Syndrome-induced Senescence in Porcine Adipose Tissue-derived Mesenchymal Stem Cells

Y Meng1,2, A Eirin1, X-Y Zhu1

  • 11 Divisions of Nephrology and Hypertension, Mayo Clinic, Rochester, USA.

Cell Transplantation
|September 7, 2018
PubMed

Insights

Metabolic syndrome impairs mesenchymal stem cells (MSCs) by altering microRNAs (miRNAs) that regulate senescence. Inhibiting miR-27b in MSCs reduced senescence markers and improved migration, suggesting a role for miRNAs in metabolic syndrome-induced MSC aging.

Area of Science:

  • Stem cell biology
  • Molecular biology
  • Metabolic syndrome research

Background:

  • Mesenchymal stem cells (MSCs) are crucial for tissue repair but can be compromised by cardiovascular risk factors.
  • Metabolic syndrome (MetS) negatively impacts adipose tissue-derived MSCs, reducing their vitality.
  • The role of microRNAs (miRNAs) in regulating MSC senescence within the context of MetS is not well understood.

Purpose of the Study:

  • To investigate the hypothesis that MetS upregulates miRNA expression in MSCs, targeting senescence-associated genes.
  • To identify specific miRNAs and their target genes involved in MetS-induced MSC senescence.
  • To elucidate the functional impact of specific miRNAs, such as miR-27b, on MSC senescence and function.

Main Methods:

  • MSCs were isolated from swine fed either a lean or obese diet for 16 weeks.
  • Next-generation miRNA sequencing (miRNA-seq) was employed to compare miRNA expression profiles between MetS-MSCs and Lean-MSCs.
  • Senescence was assessed using biomarkers (p16, p21, H2AX, SA-β-Galactosidase activity), and gene expression of key senescence-related genes (p16, p21, MAPK3, MAPK14) was analyzed.
  • The functional effects of miR-27b inhibition on MSC senescence and migration were evaluated.

Main Results:

  • MetS-MSCs exhibited significantly elevated senescence biomarkers compared to Lean-MSCs.
  • Seven miRNAs were upregulated, including miR-27b, and three were downregulated in MetS-MSCs.
  • These differentially expressed miRNAs targeted 35 senescence-associated genes, with a notable enrichment in MAPK signaling pathways.
  • Inhibition of miR-27b in cultured MSCs led to decreased expression of p16 and MAPK3, and enhanced MSC migration.

Conclusions:

  • Metabolic syndrome alters the expression of senescence-associated miRNAs in MSCs, contributing to their senescence.
  • The p16 signaling pathway appears to be a key mediator in MetS-induced MSC senescence.
  • Targeting specific miRNAs, like miR-27b, may offer a therapeutic strategy to counteract MetS-induced MSC dysfunction.
Keywords:
mesenchymal stem cellsmetabolic syndromemicroRNAsenescence

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