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Oscillatory and pulsatile shear stress differentially regulate mitochondrial redox state via JNK activation
Author(s) -
Ai Lisong,
Hamilton Ryan T,
Khalsa Bhavraj,
Darbandi Farhad,
Bressler Steven,
Hsiai Tzung K
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.964.37
Subject(s) - colocalization , phosphorylation , microbiology and biotechnology , mitochondrion , pulsatile flow , oxidative stress , reactive oxygen species , shear stress , chemistry , mitochondrial ros , biophysics , biology , materials science , endocrinology , biochemistry , composite material
Oscillatory shear stress (OSS) induces oxidative stress in regions of arterial bifurcations or curvatures, whereas pulsatile shear stress (PSS) confers an opposite effect in the straight regions. Shear stress is known to activate JNK that plays an important role in up‐regulation of adhesion molecules. It remains unknown whether OSS and PSS differentially induce mitochondrial reactive oxygen species (ROS) via JNK in BAEC. Confluent BAEC were subjected to the flow conditions that simulated carotid bifurcation: (1) Control under static conditions (2)PSS; and (3)OSS. In response to OSS, JNK‐2 phosphorylation peaked at 30 minutes. In response to PSS, JNK‐2 phosphorylation peaked at 3 hours. Both OSS‐ and PSS‐induced JNK activation was significantly attenuated in the presence of a JNK inhibitor. Confocal microscope revealed that phosphorylated JNK‐2 colocalized with mitochondria in response to OSS at 30 minutes and to PSS at 2 hours. An increased mitochondrial O 2 − production was demonstrated. This merged intensity was significantly attenuated in the presence of a JNK inhibitor. We demonstrate that PSS and OSS differentially modulate mitochondrial ROS generation via JNK activation and its colocalization with mitochondria. Shear stress‐induced JNK may play a role in the metabolic regulation of mitochondria with relevance to endothelial dysfunction.