ArticleJournal of cellular and molecular medicine2008
Role of endogenous bone marrow cells in long-term repair mechanisms after myocardial infarction.
Article in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Thioredoxin 1 is upregulated in the bone and bone marrow following experimental myocardial infarction: evidence for a remote organ response.Histochemistry and cell biology · 2021Article
- Knockdown of Long Non-Coding RNA AFAP1-AS1 Promoted Viability and Suppressed Death of Cardiomyocytes in Response to I/R In Vitro and In Vivo.Journal of cardiovascular translational research · 2020Article
- Tracking mesenchymal stem cell contributions to regeneration in an immunocompetent cartilage regeneration model.JCI insight · 2017Article
- Implantation of a Poly-L-Lactide GCSF-Functionalized Scaffold in a Model of Chronic Myocardial Infarction.Journal of cardiovascular translational research · 2017Article
- Role of Circulating Fibrocytes in Cardiac Fibrosis.Chinese medical journal · 2016Review
- Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor-23.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- Targeting cardiac fibroblasts to treat fibrosis of the heart: focus on HDACs.Journal of molecular and cellular cardiology · 2014Review
- The origin and arrhythmogenic potential of fibroblasts in cardiac disease.Journal of cardiovascular translational research · 2012Review
- Mechanisms for progenitor cell-mediated repair for ischemic heart injury.Current stem cell research & therapy · 2012Review
- Experimental acute myocardial infarction: telocytes involvement in neo-angiogenesis.Journal of cellular and molecular medicine · 2011Article
- Hematopoietic bone marrow cells participate in endothelial, but not epithelial or mesenchymal cell renewal in adult rats.Journal of cellular and molecular medicine · 2011Article
- Classically and alternatively activated macrophages contribute to tissue remodelling after myocardial infarction.Journal of cellular and molecular medicine · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homing and regenerative potential of endogenous bone marrow cells (BMC) in myocardial infarction (MI) is a controversial issue. Using human placental alkaline phosphatase (hPLAP) as genetic marker for cell tracking, we examined the influx of bone marrow-derived cells during tissue repair after the induction of MI over a study period of 17 weeks in wild-type inbred Fischer 344 rats, lethally irradiated and reconstituted with bone marrow (BM) from transgenic F344 rats expressing hPLAP under the control of the ubiquitous R26 promoter. During the early phases of tissue repair, hPLAP-positive macrophages, endothelial cells, fibroblasts and also myofibroblast-like cells were recruited from BM. However, only some hPLAP-positive endothelial cells, fibroblasts and myofibroblast-like cells persisted until 17 weeks after MI. With the exception of a single cell, there was no evidence of BM-derived cardiomyocytes throughout the study. Rather, some local cardiac progenitor cells appeared to differentiate into cardiomyocytes in the peri-infarct regions. In conclusion, our data show that the inflammation-induced influx of BM-derived cells into the infarction area is restricted to leukocytes, endothelial cells, fibroblasts and myofibroblast-like cells. Our long-term analysis casts doubt on the hypothesis that circulating BM-derived mesenchymal precursor cells participate in cardiomyogenesis after MI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.