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Overexpression of stem cell niche factor fibroblast growth factor‐2 transgene in the renal medulla attenuated sodium retention in Dahl S rats
Author(s) -
ZHU QING,
Hu Junping,
Han WeiQing,
Li PinLan,
Li Ningjun
Publication year - 2013
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.27.1_supplement.1182.9
Subject(s) - renal medulla , endocrinology , medicine , stem cell , fibroblast growth factor , medullary cavity , biology , chemistry , microbiology and biotechnology , receptor
Adult stem cells play important roles in maintaining normal organ functions. Fibroblast growth factor‐2 (FGF2) is a fundamental stem cell niche factor that stimulates the proliferation and differentiation of stem cells. We showed before that there were defects in FGF2 and stem cells in the renal medulla in Dahl S (DS) rats, suggesting that the impairment of FGF2 and consequent stem cell deficiency may contribute to the renal medullary dysfunction in DS rats. The present study determined whether improvement of stem cell population by overexpression of FGF2 transgene in the renal medulla would recover the renal medullary dysfunction and attenuate the Na + retention in DS rats. FGF2 overexpression plasmid was transfected into the renal medulla in uninephrectomized DS rats for 10 days. FGF2 transfection significantly increased stem cell marker CD133+ cell numbers (0.89±0.29% in FGF2 rats vs. 0.21±0.02% in control) in the renal medulla and enhanced urinary Na + excretion by 16% compared with control after acute IV Na + loading. Furthermore, chronic high salt‐induced Na+ retention was remarkably attenuated in FGF2‐treated rats (10.55± 2.86 mmoles/day vs. 18.56± 1 in control). It is suggested that correction of the impairment in FGF2‐mediated regulation of stem cell function in the renal medulla improves the renal medullary dysfunction in DS rats. (support: NIH grants HL89563, HL106042 and DK54927).