Shear flow increases S-nitrosylation of proteins in endothelial cells

Huang, Bin; Chen, Shih Chung; Wang, Danny Ling

doi:10.1093/cvr/cvp154

Cited by 78 publications

(76 citation statements)

References 47 publications

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“…NO might affect signal transduction in many ways, through either changes in the redox balance or posttranslational modifications of proteins, such as S-nitrosylation. Interestingly, SS has been shown to increase S-nitrosylation of multiple proteins in endothelial cells, 43 particularly, caspase-3. 2 This mechanism likely contributes to the NO-mediated protection of endothelial cells from programmed cell death.…”

Section: Discussionmentioning

confidence: 99%

Shear Stress Regulates Endothelial Microparticle Release

Vion

Ramkhelawon

Loyer

et al. 2013

Circulation Research

150

117

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Rationale: Endothelial activation and apoptosis release membrane-shed microparticles (EMP) that emerge as important biological effectors. Objective: Because laminar shear stress (SS) is a major physiological regulator of endothelial survival, we tested the hypothesis that SS regulates EMP release. Methods and Results: EMP levels were quantified by flow cytometry in medium of endothelial cells subjected to low or high SS (2 and 20 dyne/cm 2 ). EMP levels augmented with time in low SS conditions compared with high SS conditions. This effect was sensitive to extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and Rho kinases inhibitors but unaffected by caspase inhibitors. Low SS-stimulated EMP release was associated with increased endothelial Rho kinases and ERK1/2 activities and cytoskeletal reorganization. Overexpression of constitutively active RhoA stimulated EMP release under high SS. We also examined the effect of nitric oxide (NO) in mediating SS effects. L-NG-nitroarginine methyl ester (L-NAME), but not D-NG-nitroarginine methyl ester, increased high SS-induced EMP levels by 3-fold, whereas the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) decreased it. L-NAME and SNAP did not affect Rho kinases and ERK1/2 activities. Then, we investigated NO effect on membrane remodeling because microparticle release is abolished in ABCA1-deficient cells. ABCA1 expression, which was greater under low SS than under high SS, was augmented by L-NAME under high SS and decreased by SNAP under low SS conditions. Conclusions: Altogether, these results demonstrate that sustained atheroprone low SS stimulates EMP release through activation of Rho kinases and ERK1/2 pathways, whereas atheroprotective high SS limits EMP release in a NO-dependent regulation of ABCA1 expression and of cytoskeletal reorganization. These findings, therefore, identify endothelial SS as a physiological regulator of microparticle release.

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Section: Discussionmentioning

confidence: 99%

Shear Stress Regulates Endothelial Microparticle Release

Vion

Ramkhelawon

Loyer

et al. 2013

Circulation Research

150

117

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“…HUVECs were cultured in M199 medium (Gibco, Thermo Fisher Scientific, Carlsbad, CA, USA) supplemented with 100 U/ml penicillin/streptomycin, 2.5 mg/ml amphotericin B, 20% fetal bovine serum (FBS), and 20% endothelial cell growth medium (Lonza, MD, USA). HUVECs from passages 3e4 were cultured on glass slides and exposed to shear flow (12 dyn/cm 2 ) for 30 min in a well-defined parallel plate flow chamber system [10].…”

Section: Cell Culture and Shear Flow Treatmentmentioning

confidence: 99%

Laminar shear flow increases hydrogen sulfide and activates a nitric oxide producing signaling cascade in endothelial cells

Huang

Chen

et al. 2015

Biochemical and Biophysical Research Communications

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“…57,58 Finally, endothelial cells exposed to shear flow were shown to have more than 12 proteins that had significantly increased S-nitrosylation among them Tm at Cys 170 located in the hydrophobic motif. 59 The authors suggest that such modification may allow for the remodelling together with maintaining the integrity of the endothelial cells under flow conditions. myosin activity.…”

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confidence: 99%