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Ornithine decarboxylase (ODC) regulates the proliferative phenotype of rat pulmonary microvascular endothelial progenitor cells
Author(s) -
Olson Jack W.,
Koloteva Anna,
Parra Glenda,
Alvarez Diego F.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.771.6
Subject(s) - ornithine decarboxylase , progenitor cell , microbiology and biotechnology , progenitor , biology , endothelial progenitor cell , population , phenotype , cell growth , cancer research , angiogenesis , chemistry , immunology , stem cell , medicine , biochemistry , enzyme , gene , environmental health
Nucleosome Assembly Protein1 Like 1 (NAP1‐L1) enforces the progenitor phenotype of a population of rat pulmonary microvascular endothelial cells (PMVECs). These lung resident progenitor cells are characterized by their high proliferative potential (HPP), self‐renewal capability and vasculogenic behavior. PMVECs also are populated with non‐progenitor cells distinguished by their minimal NAP1‐L1 protein content, low proliferative potential (LPP) and inability to self‐renew and undergo vasculogenesis. Since polyamines are essential for cell survival and proliferation, we began to test whether ODC, the rate‐limiting enzyme in polyamine synthesis, regulates the NAP1‐L1 engendered phenotype of HPPs. LPPs have very low ODC activity compared to HPPs. Heterologous NAP1‐L1 expression switched LPPs to a HPP phenotype ‐ cells with high proliferative potential and ODC activity. DFMO (alpha‐difluoromethylornithine), a highly specific irreversible inhibitor of ODC, reduced the proliferation of HPPs by about 80%. These data support the concept that the HPP status of rat PMVEC progenitor cells requires NAP1‐L1‐increased ODC activity.