Abi3bp regulates cardiac progenitor cell proliferation and differentiation

Circ Res. 2014 Dec 5;115(12):1007-16. doi: 10.1161/CIRCRESAHA.115.304216. Epub 2014 Oct 8.

Abstract

Rationale: Cardiac progenitor cells (CPCs) are thought to differentiate into the major cell types of the heart: cardiomyocytes, smooth muscle cells, and endothelial cells. We have recently identified ABI family, member 3 (NESH) binding protein (Abi3bp) as a protein important for mesenchymal stem cell biology. Because CPCs share several characteristics with mesenchymal stem cells, we hypothesized that Abi3bp would similarly affect CPC differentiation and proliferation.

Objective: To determine whether Abi3bp regulates CPC proliferation and differentiation.

Methods and results: In vivo, genetic ablation of the Abi3bp gene inhibited CPC differentiation, whereas CPC number and proliferative capacity were increased. This correlated with adverse recovery after myocardial infarction. In vitro, CPCs, either isolated from Abi3bp knockout mice or expressing an Abi3bp shRNA construct, displayed a higher proliferative capacity and, under differentiating conditions, reduced expression of both early and late cardiomyocyte markers. Abi3bp controlled CPC differentiation via integrin-β1, protein kinase C-ζ, and v-akt murine thymoma viral oncogene homolog.

Conclusions: We have identified Abi3bp as a protein important for CPC differentiation and proliferation.

Keywords: extracellular matrix; integrin-β.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Cell Differentiation*
  • Cell Proliferation*
  • Cells, Cultured
  • Disease Models, Animal
  • Integrin beta1 / metabolism
  • Isoenzymes / metabolism
  • Male
  • Mesenchymal Stem Cells / metabolism*
  • Mesenchymal Stem Cells / pathology
  • Mice, Knockout
  • Myocardial Contraction
  • Myocardial Infarction / genetics
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology
  • Myocardial Infarction / physiopathology
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • Protein Kinase C / metabolism
  • Protein Kinase C-theta
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA Interference
  • Recovery of Function
  • Regeneration
  • Signal Transduction
  • Stroke Volume
  • Time Factors
  • Transfection

Substances

  • Carrier Proteins
  • Integrin beta1
  • Isoenzymes
  • TARSH protein, mouse
  • Proto-Oncogene Proteins c-akt
  • Prkcq protein, mouse
  • Protein Kinase C
  • Protein Kinase C-theta