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Sublethal Versus Lethal Hydrogen Peroxide‐Induced Injury To Renal Epithelial Cells: Roles Of Tight Junction Proteins
Author(s) -
Janosevic Danielle,
Singh Nancy,
AalamiHarandi Pegah,
Rohring Victoria,
Axis Josephine,
Amsler Kurt
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.954.8
Subject(s) - occludin , tight junction , paracellular transport , microbiology and biotechnology , gene knockdown , hydrogen peroxide , chemistry , biology , biochemistry , permeability (electromagnetism) , membrane , apoptosis
Hydrogen peroxide (H 2 O 2 ) treatment of renal epithelial cells is a model for renal ischemia‐reperfusion injury. Lethal, but not sublethal H 2 O 2 caused collapse of domes in confluent MDCK cell populations. H 2 O 2 produced a concentration‐dependent increase in paracellular calcein movement across confluent MDCK cell populations. In contrast, TransEpithelial Resistance was only decreased by lethal concentrations of H 2 O 2 . The cellular contents of tight junction proteins, occludin, ZO‐1 and ZO‐2, were not altered by treatment with either sublethal or lethal H 2 O 2 concentrations. H 2 O 2 produced a concentration‐dependent decrease in basal F‐actin stress fibers. Sublethal H 2 O 2 did not alter the localization of occludin, ZO‐1 or ZO‐2 but localization was affected modestly by lethal H 2 O 2 . Knockdown of either occludin or ZO‐2 increased the sensitivity of MDCK cells to H 2 O 2 ‐induced injury. In contrast, knockdown of ZO‐1 or overexpression of occludin decreased MDCK cell sensitivity to H 2 O 2 . These results indicate that occludin, ZO‐1 and ZO‐2 have different functional roles in mediating the effects of sublethal and lethal H 2 O 2 .