English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  The inability of the adult mammalian heart to replace cells lost after severe cardiac injury compromises organ function. Although the heart is one of the least regenerative organs in the body, evidence accumulated in recent decades indicates a certain degree of renewal after injury. We have evaluated the role of cardiac  Bmi1   +   progenitor cells ( Bmi1 -CPC) following acute myocardial infarction (AMI).    Methods   Bmi1  Cre/+ ; Rosa26  YFP/+  ( Bmi1 -YFP) mice were used for lineage tracing strategy. After tamoxifen (TM) induction, yellow fluorescent protein (YFP) is expressed under the control of  Rosa26  regulatory sequences in  Bmi1   +   cells. YFP +  cells were tracked following myocardial infarction. Additionally, whole transcriptome analysis of isolated YFP +  cells was performed in unchallenged hearts and after myocardial infarction.    Results  Deep-sequencing analysis of  Bmi1 -CPC from unchallenged hearts suggests that this population expresses high levels of pluripotency markers. Conversely, transcriptome evaluation of  Bmi1 -CPC following AMI shows a rich representation of genes related to cell proliferation, movement, and cell cycle. Lineage-tracing studies after cardiac infarction show that the progeny of  Bmi1 -expressing cells contribute to de novo cardiomyocytes (CM) (13.8 ± 5 % new YFP +  CM compared to 4.7 ± 0.9 % in age-paired non-infarcted hearts). However, apical resection of TM-induced day 1  Bmi1 -YFP pups indicated a very minor contribution of  Bmi1 -derived cells to de novo CM.    Conclusions  Cardiac  Bmi1  progenitor cells respond to cardiac injury, contributing to the generation of de novo CM in the adult mouse heart.    Electronic supplementary material  The online version of this article (doi:10.1186/s13287-016-0355-7) contains supplementary material, which is available to authorized users.

Bmi1 + cardiac progenitor cells contribute to myocardial repair following acute injury