ArticleThe American journal of pathology2001
Vascular smooth muscle cells of recipient origin mediate intimal expansion after aortic allotransplantation in mice.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 110 citations in OpenAlex.
- PLX3397, a CSF1 receptor inhibitor, limits allotransplantation-induced vascular remodelling.Cardiovascular research · 2022Article
- Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function.Journal of visualized experiments : JoVE · 2017Article
- DNA Methylation Signature of Post-injury Neointimal Cells During Vascular Remodeling in the Rat Balloon Injury Model.Molecular biology (Los Angeles, Calif.) · 2016Article
- Histone deacetylases and cardiovascular cell lineage commitment.World journal of stem cells · 2015Review
- Endothelial dysfunction and cardiac allograft vasculopathy.Journal of cardiovascular translational research · 2013Review
- Acute regeneration and chronic acellular transformation of rabbit cryopreserved aortic allografts.Acta histochemica et cytochemica · 2012Article
- Bioengineered vascular graft grown in the mouse peritoneal cavity.Journal of vascular surgery · 2010Article
- Neutrophil mediated smooth muscle cell loss precedes allograft vasculopathy.Journal of cardiothoracic surgery · 2010Article
- Smooth muscle progenitor cells: friend or foe in vascular disease?Current stem cell research & therapy · 2009Review
- Mesenchymal stem cells-derived vascular smooth muscle cells release abundant levels of osteoprotegerin.European journal of histochemistry : EJH · 2009Review
- Progenitor cells and vascular disease.Cell proliferation · 2008Review
- Mouse models of arteriosclerosis: from arterial injuries to vascular grafts.The American journal of pathology · 2004Review
- Abundant progenitor cells in the adventitia contribute to atherosclerosis of vein grafts in ApoE-deficient mice.The Journal of clinical investigation · 2004Article
- Stem cell origins of intimal cells in graft arterial disease.Current atherosclerosis reports · 2003Review
- Progenitor cells in vascular disease.Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intimal expansion by vascular smooth muscle cells (SMCs) is a characteristic feature of graft vascular disease. Whether graft intimal SMCs arise from donor or recipient tissue is not well established but has important pathogenetic implications. We examined for the presence of male cells in the expanded intima of sex-mismatched mouse aortic allografts (C57BL/6-to-BALB/c) at 30 or 60 days after transplant by in situ hybridization using a Y-chromosome probe. Study groups included male-to-female allografts, female-to-male allografts, and female-to-female allografts in recipients previously engrafted with male bone marrow. Although intimal expansion developed in all allografts, male-to-female allografts lacked Y-chromosome-positive intimal cells. In contrast, such cells were abundant in female-to-male allografts and most of these cells co-labeled for smooth muscle alpha-actin by immunostain. Female-to-female allografts in recipients with male bone marrow showed a limited number of intimal Y-chromosome-positive cells. However, none of these clearly co-labeled for smooth muscle alpha-actin and their numbers declined throughout time, consistent with graft-infiltrating inflammatory cells. We conclude that intimal expansion of mouse aortic allografts is mediated by SMCs that originated from the recipient. There was little evidence of their derivation from the bone marrow, suggesting instead the adjacent host aorta as the primary source of intimal SMCs.
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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.