The miR-30 family microRNAs confer epithelial phenotype to human pancreatic cells

Mugdha V Joglekar1, Deepak Patil, Vinay M Joglekar

  • 1Stem Cells and Diabetes Section, National Center for Cell Science, Ganeshkhind Road, Pune, India.

Islets
|November 25, 2010
PubMed

Insights

Reduced miR-30 family microRNAs drive mesenchymal transition in human pancreatic cells. These microRNAs normally suppress this transition, crucial in development and disease.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Epithelial-to-mesenchymal transition (EMT) is vital for embryonic development.
  • EMT is also implicated in pathological conditions, including fibrosis.
  • The specific role of microRNAs in pancreatic EMT is not fully understood.

Purpose of the Study:

  • To investigate the role of miR-30 family microRNAs in human pancreatic epithelial cells.
  • To determine if miR-30 family microRNAs regulate EMT in pancreatic cells.
  • To explore the therapeutic potential of modulating miR-30 levels in pancreatic diseases.

Main Methods:

  • Primary culture of human pancreatic epithelial cells.
  • Manipulation of miR-30 family microRNA levels using anti-miRs and overexpression vectors.
  • Analysis of mesenchymal gene expression and protein translation.
  • Study of miR-30 expression in differentiating pancreatic cells and diseased pancreas.

Main Results:

  • Reduction in miR-30 family microRNAs induces mesenchymal transition in human pancreatic epithelial cells.
  • miR-30 family microRNAs target and translationally repress mesenchymal gene transcripts.
  • Depletion of miR-30 promotes EMT, while overexpression maintains the epithelial phenotype.
  • miR-30 family microRNAs are upregulated during pancreatic islet cell differentiation and downregulated in fibrotic pancreatitis lesions.

Conclusions:

  • miR-30 family microRNAs are key regulators of EMT in human pancreatic epithelial cells.
  • These microRNAs act as suppressors of the mesenchymal phenotype.
  • Dysregulation of miR-30 family microRNAs may contribute to pancreatic fibrosis and disease.