ATP-binding cassette transporter Abcg2 lineage contributes to the cardiac vasculature after oxidative stress

Abstract

CM. ATP-binding cassette transporter Abcg2 lineage contributes to the cardiac vasculature after oxidative stress.

Abcg2-Labeled Cells Contribute to Different Cell Populations in the Embryonic and Adult Heart

“…In contrast to our findings with the cardiac lineage, we did not observe a difference in Abcg2 lineage-labeled endothelial cells when tamoxifen was delivered at different time points. This observation is consistent with prior observations that the Abcg2 lineage contributes significantly to endothelial cells [15].…”

“…There was no difference in survival between treatment and control groups both before and after ligation (data not shown). In our prior study, using the same tamoxifen and PQ delivery strategy, we observed no cardiac damage in the absence of injury [15].…”

“…Using this lineage-tracing technique, Fatima et al demonstrated that Abcg2 labels tissue-specific progenitor cell populations in multiple tissues, including marking of hematopoietic stem cells, intestinal stem cells, and interstitial cells in cardiac and skeletal muscle [13]. Labeled cells in cardiac and skeletal muscle are predominantly vascular and coexpress the endothelial gene CD31 [13][14][15]. Upon introduction of systemic oxidative stress, the contribution of the Abcg2 lineage to vascular cells increased [15].…”

“…Labeled cells in cardiac and skeletal muscle are predominantly vascular and coexpress the endothelial gene CD31 [13][14][15]. Upon introduction of systemic oxidative stress, the contribution of the Abcg2 lineage to vascular cells increased [15]. Following either chemical injury in skeletal muscle or response to cardiac oxidative stress, Abcg2-labeled cells contribute to microvascular cells but contribute only minimally to regenerated skeletal muscle fibers and do not contribute to cardiomyocytes [14,15].…”

“…Upon introduction of systemic oxidative stress, the contribution of the Abcg2 lineage to vascular cells increased [15]. Following either chemical injury in skeletal muscle or response to cardiac oxidative stress, Abcg2-labeled cells contribute to microvascular cells but contribute only minimally to regenerated skeletal muscle fibers and do not contribute to cardiomyocytes [14,15]. Furthermore, when cardiac injury is performed on Abcg2-null mice, they exhibit decreased cardiac function resulting in increased mortality contributing to impaired angiogenesis and antioxidant responses [9,10].…”