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Bone marrow rejuvenation accelerates re-endothelialization and attenuates intimal hyperplasia after vascular injury in aging mice.

AbstractBACKGROUND:
Aging-associated functional impairment of endothelial progenitor cells (EPCs) contributes to delayed re-endothelialization after vascular injury and exaggerated intimal hyperplasia (IH). This study tested if bone marrow (BM) rejuvenation accelerates post-injury re-endothelialization in aging mice.
METHODS AND RESULTS:
Using BM transplantation (BMT(Gfp→Wild)), young(Gfp) to young(Wild) (YTY), old(Gfp) to old(Wild) (OTO), young(Gfp) to old(Wild) (YTO), and old(Gfp) to young(Wild) (OTY) groups were created. After vascular injury, IH was significantly greater in the old group than the young group (P<0.001). BM rejuvenation (YTO) significantly accelerated re-endothelialization and attenuated IH. Compared with the OTO group, the YTY and YTO groups had earlier and greater EPC-derived re-endothelialization (P<0.001). The number of Sca-1(+)KDR(+) EPCs mobilized in the circulation induced by vascular injury was higher in young, YTO, and YTY mice than in old mice (P<0.05). Sca-1(+) BM cells from the young, YTO, and YTY groups had better migration and adhesion capacities than those from the old group (P<0.05). The increase in blood vascular endothelial growth factor (VEGF) levels after vascular injury was higher in young than in old mice. PI3K, Akt, and FAK pathways played a pivotal role in VEGF-associated EPC migration. Specifically, EPCs from young and YTO mice, compared with old mice, demonstrated stronger FAK phosphorylation after VEGF stimulation.
CONCLUSIONS:
EPCs play a critical role in vascular repair in aging mice. BM rejuvenation accelerates re-endothelialization by improving EPC function.
AuthorsChao-Hung Wang, Ming-Feng Lee, Ning-I Yang, Hsiu-Fu Mei, Sheng-Yuan Lin, Wen-Chin Cherng
JournalCirculation journal : official journal of the Japanese Circulation Society (Circ J) Vol. 77 Issue 12 Pg. 3045-53 ( 2013) ISSN: 1347-4820 [Electronic] Japan
PMID24042255 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Phosphatidylinositol 3-Kinases
  • Focal Adhesion Kinase 1
  • Ptk2 protein, mouse
  • Proto-Oncogene Proteins c-akt
Topics
  • Aging (genetics, metabolism, pathology)
  • Allografts
  • Animals
  • Bone Marrow Transplantation
  • Cell Movement (genetics)
  • Endothelial Cells (metabolism, pathology)
  • Focal Adhesion Kinase 1 (genetics, metabolism)
  • Hyperplasia
  • Male
  • Mice
  • Mice, Transgenic
  • Phosphatidylinositol 3-Kinases (genetics, metabolism)
  • Proto-Oncogene Proteins c-akt (genetics, metabolism)
  • Signal Transduction (genetics)
  • Stem Cells (metabolism, pathology)
  • Tunica Intima (metabolism, pathology)
  • Vascular Endothelial Growth Factor A (genetics, metabolism)
  • Vascular System Injuries (genetics, metabolism, pathology)

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