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C‐kit cardiac precursor cells exhibit a unique Nox isoform profile which may influence their survival, proliferation, and differentiation in the infarcted heart
Author(s) -
Spealman Alyson Korry,
Poor Daniel A.,
Sharma Ram V.,
Kotlikoff Michael I.,
Davisson Robin L.
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.1030.5
Subject(s) - nox1 , downregulation and upregulation , biology , stem cell , transcriptome , microbiology and biotechnology , progenitor cell , nox4 , gene isoform , cellular differentiation , andrology , gene expression , nadph oxidase , medicine , genetics , gene , reactive oxygen species
Compelling evidence now confirms the presence of small but distinct populations of stem cells residing in niche areas of the adult heart. Evidence from our laboratory demonstrates that c‐kit‐positive cells isolated from the hearts of c‐kit BAC ‐EGFP neonatal mice can be expanded and differentiated in vitro into all three cell lineages of the heart. Since N ADPH ox idases (Nox) play critical roles in cardiomyogenesis and stem cell survival, and also have distinct roles in cell signaling and death, we hypothesized that c‐kit cells exhibit a unique Nox profile compared to control neonatal cardiomyocytes. Utilizing real‐time RT‐PCR and expressing the data relative to β‐actin, our results indicate that Nox1 is markedly upregulated in c‐kit cells compared to control cardiomyocytes (13.40±4.34 fold, n=3, p<0.05). Nox4 is also upregulated, but to a lesser extent than Nox1 (1.73±0.45 fold, n=3). On the other hand, Nox2 is significantly downregulated compared to control cardiomyocytes (.37±.16 fold, n=3, p<0.05). These data reveal a highly unique Nox profile in c‐kit‐positive progenitors, and may provide genetic targets for improving cell survival, proliferation, and/or differentiation following cardiac damage. Supported by HL063887, HL084624, AHA 0540114N.