Role of hydroxyl radical in the stimulation of arachidonic acid release caused by H2O2 in pulmonary smooth muscle cells: Protective effect of anion channel blocker

1995 ◽  
Vol 146 (2) ◽  
pp. 91-98 ◽  
Author(s):  
Sajal Chakraborti ◽  
Sandip K Batabyal ◽  
Tapati Chakraborti
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Protective Effect ◽  
Channel Blocker ◽  
Anion Channel ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
Anion Channel Blocker ◽  
Stimulation Of

Role of hydroxyl radical in superoxide induced microsomal lipid peroxidation: Protective effect of anion channel blocker

1996 ◽  
Vol 21 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Salil K. Ghosh ◽  
Tapati Chakraborti ◽  
Arun B. Banerjee ◽  
Sujata Roychoudhury ◽  
Sajal Chakraborti
Keyword(s):  
Lipid Peroxidation ◽  
Protective Effect ◽  
Hydroxyl Radical ◽  
Channel Blocker ◽  
Anion Channel ◽  
Microsomal Lipid Peroxidation ◽  
Anion Channel Blocker

Involvement of the mitogen-activated protein kinase cascade in peroxynitrite-mediated arachidonic acid release in vascular smooth muscle cells

2004 ◽  
Vol 286 (6) ◽  
pp. C1271-C1280 ◽  
Author(s):  
Rita K. Upmacis ◽  
Ruba S. Deeb ◽  
Matthew J. Resnick ◽  
Rochelle Lindenbaum ◽  
Caryn Gamss ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Reactive Nitrogen Species ◽  
Arachidonic Acid Release ◽  
Nitrogen Species ◽  
Eicosanoid Production ◽  
Mitogen Activated Protein ◽  
Acid Release

Eicosanoid production is reduced when the nitric oxide (NO·) pathway is inhibited or when the inducible NO synthase gene is deleted, indicating that the NO· and arachidonic acid pathways are linked. We hypothesized that peroxynitrite, formed by the reaction of NO· and superoxide anion, may cause signaling events leading to arachidonic acid release and subsequent eicosanoid generation. Western blot analysis of rat arterial smooth muscle cells demonstrated that peroxynitrite (100–500 μM) and 3-morpholinosydnonimine (SIN-1; 200 μM) stimulate phosphorylation of extracellular signal-regulated kinase (ERK), p38, and cytosolic phospholipase A2 (cPLA2). We found that peroxynitrite-induced arachidonic acid release was completely abrogated by the mitogen-activated protein/ERK kinase (MEK) inhibitor U0126 and by calcium chelators. With the p38 inhibitor SB-20219, we demonstrated that peroxynitrite-induced p38 phosphorylation led to minor arachidonic acid release, whereas U0126 completely blocked p38 phosphorylation. Addition of arachidonic acid caused p38 phosphorylation, suggesting that arachidonic acid or its metabolites are responsible for p38 activation. KN-93, a specific inhibitor of Ca2+/calmodulin-dependent kinase II (CaMKII), revealed no role for this kinase in peroxynitrite-induced arachidonic acid release in our cell system. Together, these results show that in response to peroxynitrite the cell initiates the MEK/ERK cascade leading to cPLA2 activation and arachidonic acid release. Thus studies investigating the role of the NO· pathway on eicosanoid production must consider the contribution of signaling pathways initiated by reactive nitrogen species. These findings may provide evidence for a new role of peroxynitrite as an important reactive nitrogen species in vascular disease.

PGE2 release by bradykinin in human airway smooth muscle cells: involvement of cyclooxygenase-2 induction

1997 ◽  
Vol 273 (6) ◽  
pp. L1132-L1140 ◽  
Author(s):  
Linhua Pang ◽  
Alan J. Knox
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Arachidonic Acid Release ◽  
Human Airway Smooth Muscle ◽  
Short Term ◽  
Human Airway ◽  
Acid Release ◽  
Cox 2

Prostanoids may be involved in bradykinin (BK)-induced bronchoconstriction in asthma. We investigated whether cyclooxygenase (COX)-2 induction was involved in prostaglandin (PG) E2 release by BK in cultured human airway smooth muscle (ASM) cells and analyzed the BK receptor subtypes responsible. BK stimulated PGE2release, COX activity, and COX-2 induction in a concentration- and time-dependent manner. It also time dependently enhanced arachidonic acid release. In short-term (15-min) experiments, BK stimulated PGE2 generation but did not increase COX activity or induce COX-2. In long-term (4-h) experiments, BK enhanced PGE2 release and COX activity and induced COX-2. The long-term responses were inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and the steroid dexamethasone. The effects of BK were mimicked by the B2-receptor agonist [Tyr(Me)8]BK, whereas the B1 agonist des-Arg9-BK was weakly effective at high concentrations. The B2antagonist HOE-140 potently inhibited all the effects, but the B1 antagonist des-Arg9,(Leu8)-BK was inactive. This study is the first to demonstrate that BK can induce COX-2. Conversion of increased arachidonic acid release to PGE2 by COX-1 is mainly involved in the short-term effect, whereas B2 receptor-related COX-2 induction is important in the long-term PGE2 release.

Sign in / Sign up

Export Citation Format

Share Document