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Am J Physiol Lung Cell Mol Physiol (November 2, 2007). doi:10.1152/ajplung.00316.2007
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Submitted on August 6, 2007
Accepted on October 31, 2007

Regulatory role for nucleosome assembly protein-1 in the proliferative and vasculogenic phenotype of pulmonary endothelium

Jennifer Clark1, Diego F. Alvarez1, Mikhail F. Alexeyev2, Judy A. C. King3, Lan Huang4, Mervin C. Yoder4, and Troy Stevens5*

1 Center for Lung Biology, University of South Alabama, Mobile, Alabama, United States
2 Cell Biology and Neuroscience, University of South Alabama, Mobile, Alabama, United States
3 Departments of Pharmacology and Pathology, University of South Alabama, Mobile, Alabama, United States
4 Pediatrics, University of Indiana, Indianapolis, Indiana, United States
5 Department of Pharmacology, University of South Alabama College of Medicine, Mobile, Alabama, United States

* To whom correspondence should be addressed. E-mail: tstevens{at}jaguar1.usouthal.edu.

Pulmonary microvascular endothelial cells (PMVECs) are enriched with progenitor cells that underlie their rapid proliferation and vasculogenic capacity. However, the molecular basis for such an enhanced growth potential is unknown. Nucleosome assembly protein-1 (NAP1), and its related family of proteins, has been incriminated in control of cell growth in a range of species. We therefore sought to determine whether NAP1 contributes to the rapid proliferation and vasculogenesis that is observed in PMVECs. NAP1 was expressed at a high level in two fast growing cell types, including PMVECs and resident microvascular endothelial progenitor cells that were selected from PMVECs, whereas it was expressed at a low level in slow growing pulmonary artery endothelial cells (PAECs). Heterologous NAP1 expression increased the growth potential of PAECs, whereas inhibiting NAP1 expression reduced the growth potential of PMVECs. To examine whether the growth promoting actions of NAP1 influence blood vessel formation, endothelial cells were mixed into Matrigel and subcutaneously implanted. PMVECs generated 8-fold more blood vessels than did PAECs over a 10-day time course. Heterologous NAP1 expression in PAECs increased the number of blood vessels formed by this cell type, where blood vessel growth approached that seen with PMVECs. Thus, our findings indicate that NAP1 functions as an important regulator of the proliferative and vasculogenic endothelial cell phenotype, without globally impacting endothelial cell phenotype specification.




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