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Inactivation of GATA3 in Principal Cells Leads to a Concentrating Defect
Author(s) -
Riemondy Kent,
Lucero Olivia,
Baumgartner Brett,
Mauch Teri Jo,
Miller Lance,
Nelson Raoul
Publication year - 2008
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.22.1_supplement.934.27
Subject(s) - gata3 , aquaporin 2 , biology , kidney , transcription factor , microbiology and biotechnology , reabsorption , medicine , endocrinology , chemistry , gene , genetics , mechanical engineering , water channel , engineering , inlet
GATA3, a member of the GATA zinc‐finger family of transcription factors, plays an important role in renal development; haploinsufficiency leads to Hypoparathyroidism, Deafness, and Renal agenesis. GATA3 has been shown to be expressed in the ureteric bud (UB) and collecting duct (CD) of the embryonic and adult kidneys, respectively. Its role in the developing UB is currently being explored; however, its role in the CD is completely unknown. The purpose of this study was to determine the role of GATA3 in renal principal cells of the adult mouse. We inactivated GATA3 using the AQP2‐Cre transgenic mouse (AQP2‐Cre) and the floxed GATA3 mouse (GATA3floxed). Inactivation of GATA3 in principal cells lead to a moderate concentrating defect, i.e., mice could only concentrate their urine ~60% of control; however, inactivation of GATA3 did not affect the ability to excrete an acute water load. Furthermore, other than the concentrating defect mice appear normal and healthy. We hypothesize that GATA3 transcriptionally regulates AQP2 or other collecting duct‐specific transporters involved in water reabsorption or maintaining the osmotic gradient. This study explores this hypothesis.