Notch1 signaling mediated dysfunction of bone marrow mesenchymal stem cells derived from cyanotic congenital heart disease

Biochem Biophys Res Commun. 2020 Jul 5;527(4):847-853. doi: 10.1016/j.bbrc.2020.04.129. Epub 2020 May 16.

Abstract

Bone marrow mesenchymal stem cells (BMSCs) derived from cyanotic congenital heart disease (CCHD) exhibit deficient multi-lineage differentiation potential due to the abnormal accumulation of D-galactose. However, the underlying mechanisms have not yet been explored. Here, the multi-lineage differentiation potential of the BMSCs from CCHD and non-CCHD (NCHD) patients were assessed. BMSCs from CCHD patients exhibited inferior multi-lineage differentiation potential with reduced Notch1 protein and mRNA level. Bisulfite sequencing PCR results showed the methylation level of Notch1 promoter was raised, which inhibited the binding of NF-Ya. Exposure BMSCs from NCHD patients with D-galactose under hypoxia (4% O2) decreased the expression of Notch1. And activating Notch1 partially restored the deficient BMSCs of CCHD patients. In conclusion, the impaired multi-lineage differentiation potential of BMSCs from CCHD patients is owing to the decreased Notch1 level with a remarkable hypermethylation in its promoter region. Activated Notch1 signaling pathway could partially restore the deficient BMSCs in the CCHD patients, which may provide a new method on cell therapy in patients with CCHD.

Keywords: Bone marrow mesenchymal stem cells; Cyanotic congenital heart disease; D-galactose; Hypermethylation; Notch1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Child
  • Child, Preschool
  • DNA Methylation
  • Down-Regulation
  • Female
  • Heart Defects, Congenital / genetics
  • Heart Defects, Congenital / metabolism
  • Heart Defects, Congenital / pathology*
  • Humans
  • Infant
  • Male
  • Mesenchymal Stem Cells / metabolism
  • Mesenchymal Stem Cells / pathology*
  • Promoter Regions, Genetic
  • Receptor, Notch1 / genetics
  • Receptor, Notch1 / metabolism*
  • Signal Transduction*

Substances

  • NOTCH1 protein, human
  • Receptor, Notch1