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Necrotizing enterocolitis leads to renal abnormality mediated through tight junction proteins (60.8)
Author(s) -
Garg Parvesh Mohan,
Tatum Rodney,
Ravisankar Srikant,
HewanLowe Karlene,
Shekhawat Prem,
Chen YanHua
Publication year - 2014
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.28.1_supplement.60.8
Subject(s) - necrotizing enterocolitis , kidney , medicine , hyponatremia , western blot , abnormality , pathology , necrosis , immunofluorescence , tight junction , gastroenterology , endocrinology , biology , immunology , antibody , biochemistry , psychiatry , gene , microbiology and biotechnology
. Necrotizing enterocolitis (NEC) is the most common intestinal disease of premature infants. Clinically, it is associated with hyponatremia & fluid imbalance. NEC is associated with changes in the intestinal tight junction (TJ) proteins, but its effect on kidney TJ proteins is unknown. We investigated the expression of TJ proteins in kidney using a mouse NEC model. Four day old C57BL/6 pups were divided into 2 groups: the control group was dam‐fed; the experimental group was fed 50 µl 33% Esbilac formula every 3 h and subjected to asphyxia ( 100% N 2 x 60 s) and cold stress (4°C for 10 min) twice a day to develop NEC. After 4 days of treatment, kidneys and intestines were collected. NEC was confirmed in intestines by histological exam. We found that the kidneys from the NEC group displayed interstitial edema. On western blot analysis, claudin‐1, ‐2, ‐3, and ‐7 were increased in the NEC kidney group compared to dam‐fed controls while the claudin‐5 expression remained unchanged. These findings were also confirmed on immunofluorescence. The levels of NF‐κB and p‐ERK1/2 in kidneys were elevated in the NEC group. No obvious apoptotic bodies and necrosis was seen in NEC group compared to controls. In conclusion, expression of several TJ proteins in kidneys was increased in the NEC group which may explain the reason behind kidney abnormality. Grant Funding Source : Supported by NIH grant number HL085752