Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2014 Jun 7;18(9):1785–1796. doi: 10.1111/jcmm.12305

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

PMC Copyright notice

Fig. 6 — Cardiac GPR17⁺/Sca-1⁺/CD31⁻/CD45⁻ cells represent a myo-fibroblast (MF) progenitor cell population. (A) the GPR17⁺/Sca-1⁺/CD31⁻/CD45⁻ cell line obtained from normal hearts (Fig. S6 and S7) was treated with a differentiation medium (DM) containing TGF-β to induce MF differentiation. The treatment caused up-regulation of MF marker αSMA and, although not significantly, Collagen-I. The increase in αSMA expression was also confirmed by the analysis of the mean fluorescence intensity (MFI), as well as by western blotting. DDR2 expression remained low, while CD44 did not change. (B) Immunofluorescence with a Ki-67 antibody (upper panels) and αSMA and GPR17 antibodies (lower panels) in maintenance (MM) and differentiation (DM) media revealed that the stromal cell line acquired MF characteristics as characterized by formation of αSMA fibres. Differentiation occurred in concert with a reduction in KI-67⁺ cell number (arrowheads). By contrast, GPR17 was not down-regulated.