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Arachidonic acid‐induced apoptosis in human renal proximal tubular epithelial cells
Author(s) -
Alexander Larry D,
Hamzeh Mona T
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.727.12
Subject(s) - arachidonic acid , apoptosis , mapk/erk pathway , microbiology and biotechnology , kinase , programmed cell death , p38 mitogen activated protein kinases , signal transduction , reactive oxygen species , protein kinase a , chemistry , biology , biochemistry , enzyme
Arachidonic acid can induced several injury effects on renal tubular cells. The present study was aimed to investigate the effects of arachidonic acid on cellular apoptosis in human proximal tubular epithelial cells (HK‐2) and its signaling mechanisms. Treatment with various doses of arachidonic acid resulted in dose‐dependent decreases of cell viability and increases of reactive oxygen species (ROS). Arachidonic acid induced the phosphorylation of p38 MAPK, extracellular signal‐regulated kinase (ERK1/2), and c‐Jun N‐terminal kinase (JNK), the nuclear translocation of NF‐κB, and IκB‐degradation. Cell death detection assay revealed arachidonic acid induced apoptotic cell death of HK‐2 cells. Arachidonic acid‐induced apoptosis was significantly attenuated by inhibition of the NF‐κB and mitogen‐activated protein kinase (MAPK) signaling pathways. Moreover, the antioxidant N‐acetyl‐L‐cysteine (NAC), significantly inhibited arachidonic acid‐induced apoptosis and NF‐κB and MAPK activation. Taken together, these results indicate that arachidonic acid induced apoptosis mainly by stimulating ROS production and through NF‐κB and MAPK signaling pathways in human renal proximal tubular cells.