Abstract
Atherosclerosis is a chronic inflammatory process and progresses through characteristic morphologic stages. We have shown previously that chronically injecting bone-marrow-derived vascular progenitor cells can effect arterial repair. This repair capacity depends on the age of the injected marrow cells, suggesting a progressive decline in progenitor cell function. We hypothesized that the progression of atherosclerosis coincides with the deteriorating repair capacity of the bone marrow. Here, we ascribe patterns of gene expression that accurately and reproducibly identify specific disease states in murine atherosclerosis. We then use these expression patterns to determine the point in the disease process at which the repair of arteries by competent bone marrow cells ceases to be efficient. We show that the loss of the molecular signature for competent repair is concurrent with the initiation of atherosclerotic lesions. This work provides a previously unreported comprehensive molecular data set using broad-based analysis that links the loss of successful repair with the progression of a chronic illness.
| Original language | English |
|---|---|
| Pages (from-to) | 16789-16794 |
| Number of pages | 6 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 102 |
| Issue number | 46 |
| DOIs | |
| State | Published - Nov 15 2005 |
| Externally published | Yes |
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Keywords
- Aging
- Bone marrow obsolescence
- Genomic
- Inflammation
- Vascular progenitor cell
ASJC Scopus subject areas
- Genetics
- General
Cite this
Molecular evidence for arterial repair in atherosclerosis. / Karra, Ravi; Vemullapalli, Sreekanth; Dong, Chunming; Herderick, Edward E.; Song, Xiaohua; Slosek, Kathy; Nevins, Joseph R.; West, Mike; Goldschmidt-Clermont, Pascal; Seo, David M.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 102, No. 46, 15.11.2005, p. 16789-16794.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Molecular evidence for arterial repair in atherosclerosis
AU - Karra, Ravi
AU - Vemullapalli, Sreekanth
AU - Dong, Chunming
AU - Herderick, Edward E.
AU - Song, Xiaohua
AU - Slosek, Kathy
AU - Nevins, Joseph R.
AU - West, Mike
AU - Goldschmidt-Clermont, Pascal
AU - Seo, David M
PY - 2005/11/15
Y1 - 2005/11/15
N2 - Atherosclerosis is a chronic inflammatory process and progresses through characteristic morphologic stages. We have shown previously that chronically injecting bone-marrow-derived vascular progenitor cells can effect arterial repair. This repair capacity depends on the age of the injected marrow cells, suggesting a progressive decline in progenitor cell function. We hypothesized that the progression of atherosclerosis coincides with the deteriorating repair capacity of the bone marrow. Here, we ascribe patterns of gene expression that accurately and reproducibly identify specific disease states in murine atherosclerosis. We then use these expression patterns to determine the point in the disease process at which the repair of arteries by competent bone marrow cells ceases to be efficient. We show that the loss of the molecular signature for competent repair is concurrent with the initiation of atherosclerotic lesions. This work provides a previously unreported comprehensive molecular data set using broad-based analysis that links the loss of successful repair with the progression of a chronic illness.
AB - Atherosclerosis is a chronic inflammatory process and progresses through characteristic morphologic stages. We have shown previously that chronically injecting bone-marrow-derived vascular progenitor cells can effect arterial repair. This repair capacity depends on the age of the injected marrow cells, suggesting a progressive decline in progenitor cell function. We hypothesized that the progression of atherosclerosis coincides with the deteriorating repair capacity of the bone marrow. Here, we ascribe patterns of gene expression that accurately and reproducibly identify specific disease states in murine atherosclerosis. We then use these expression patterns to determine the point in the disease process at which the repair of arteries by competent bone marrow cells ceases to be efficient. We show that the loss of the molecular signature for competent repair is concurrent with the initiation of atherosclerotic lesions. This work provides a previously unreported comprehensive molecular data set using broad-based analysis that links the loss of successful repair with the progression of a chronic illness.
KW - Aging
KW - Bone marrow obsolescence
KW - Genomic
KW - Inflammation
KW - Vascular progenitor cell
UR - http://www.scopus.com/inward/record.url?scp=28044441350&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=28044441350&partnerID=8YFLogxK
U2 - 10.1073/pnas.0507718102
DO - 10.1073/pnas.0507718102
M3 - Article
C2 - 16275914
AN - SCOPUS:28044441350
VL - 102
SP - 16789
EP - 16794
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 46
ER -