Ambient pressure upregulates nitric oxide synthase in a phosphorylated-extracellular regulated kinase– and protein kinase C–dependent manner Angela G.

Slides:

Advertisements

Similar presentations

Volume 68, Issue 4, Pages (October 2005)

Advertisements

Chung S. Lim, MRCS, PhD, Serafim Kiriakidis, PhD, Ewa M

The effects of doxycycline and micronized purified flavonoid fraction on human vein wall remodeling are not hypoxia-inducible factor pathway-dependent

Ellagic acid inhibits oxidized LDL-mediated LOX-1 expression, ROS generation, and inflammation in human endothelial cells Wen-Jane Lee, PhD, Hsiu-Chung.

Pressure activates colon cancer cell adhesion by inside-out focal adhesion complex and actin cytoskeletal signaling Vijayalakshmi Thamilselvan, Marc.

Regulation of vascular smooth muscle cell expression and function of matrix metalloproteinases is mediated by estrogen and progesterone exposure Oscar.

Chung S. Lim, MRCS, PhD, Serafim Kiriakidis, PhD, Ewa M

Reduced hind limb ischemia-reperfusion injury in Toll-like receptor-4 mutant mice is associated with decreased neutrophil extracellular traps Rahmi Oklu,

Ginkgo biloba extract inhibits oxidized low-density lipoprotein (oxLDL)-induced matrix metalloproteinase activation by the modulation of the lectin-like.

Regulation of vascular smooth muscle cell differentiation

Wei Zhou, MD, Hong Chai, MD, PhD, Andy Courson, BS, Peter H

Sustained orbital shear stress stimulates smooth muscle cell proliferation via the extracellular signal-regulated protein kinase 1/2 pathway Hidenori.

Early hypercholesterolemia contributes to vasomotor dysfunction and injury associated atherogenesis that can be inhibited by nitric oxide Kathleen G.

Growth hormone–releasing peptide ghrelin inhibits homocysteine-induced endothelial dysfunction in porcine coronary arteries and human endothelial cells

Ellagic acid inhibits oxidized LDL-mediated LOX-1 expression, ROS generation, and inflammation in human endothelial cells Wen-Jane Lee, PhD, Hsiu-Chung.

Shear stress-stimulated endothelial cells induce smooth muscle cell chemotaxis via platelet-derived growth factor-BB and interleukin-1α Alan Dardik,

Bertrand Poussier, MD, Alfredo C

Role of redox signaling and poly (adenosine diphosphate-ribose) polymerase activation in vascular smooth muscle cell growth inhibition by nitric oxide.

Domain-dependent action of urokinase on smooth muscle cell responses

Urokinase-induced smooth muscle cell responses require distinct signaling pathways: A role for the epidermal growth factor receptor Suzanne M. Nicholl,

Pharmacologic inhibition of nitric oxide synthases and cyclooxygenases enhances intimal hyperplasia in balloon-injured rat carotid arteries Jens W Fischer,

Tissue engineering applications to vascular bypass graft development: The use of adipose-derived stem cells Paul DiMuzio, MD, Thomas Tulenko, PhD Journal.

Sphingosine-1-phosphate inhibits H2O2-induced granulosa cell apoptosis via the PI3K/Akt signaling pathway Tatsuo Nakahara, M.D., Akira Iwase, M.D., Ph.D.,

Tetrandrine prevents monocrotaline-induced pulmonary arterial hypertension in rats through regulation of the protein expression of inducible nitric oxide.

Repetitive progressive thermal preconditioning hinders thrombosis by reinforcing phosphatidylinositol 3-kinase/Akt-dependent heat-shock protein/endothelial.

The cyclolignan picropodophyllin attenuates intimal hyperplasia after rat carotid balloon injury by blocking insulin-like growth factor-1 receptor signaling

Aspirin prevents resistin-induced endothelial dysfunction by modulating AMPK, ROS, and Akt/eNOS signaling Hsiu-Chung Ou, PhD, Wen-Jane Lee, PhD, Ching-Mei.

Transforming growth factor-β increases vascular smooth muscle cell proliferation through the Smad3 and extracellular signal-regulated kinase mitogen-activated.

Postmortem and ex vivo carbon monoxide ventilation reduces injury in rat lungs transplanted from non–heart-beating donors Boming Dong, MD, PhD, Paul.

Iodinated contrast induced renal vasoconstriction is due in part to the downregulation of renal cortical and medullary nitric oxide synthesis Stuart.

Α1-Adrenergic receptors mediate combined signals initiated by mechanical stretch stress and norepinephrine leading to accelerated mouse vein graft atherosclerosis

Wai-ki Yiu, MBBS, MRCS, Stephen W. K. Cheng, MS, FRCS, Bauer E

Metformin stimulates ischemia-induced revascularization through an eNOS dependent pathway in the ischemic hindlimb mice model Noriko Takahashi, MD, Rei.

Translocation of protein kinase C isoforms is involved in propofol-induced endothelial nitric oxide synthase activation L. Wang, B. Wu, Y. Sun, T. Xu,

Tetrandrine prevents monocrotaline-induced pulmonary arterial hypertension in rats through regulation of the protein expression of inducible nitric oxide.

Theresa A. Reno, PhD, Jae Y. Kim, MD, Dan J. Raz, MD

Toluene downregulates filaggrin expression via the extracellular signal-regulated kinase and signal transducer and activator of transcription–dependent.

Overexpression of transforming growth factor–β1 correlates with increased synthesis of nitric oxide synthase in varicose veins Theresa Jacob, PhD, Anil.

The essential role of endothelial nitric oxide synthase activation in insulin-mediated neuroprotection against ischemic stroke in diabetes Shiang-Suo.

Tissue factor pathway inhibitor-2 is induced by fluid shear stress in vascular smooth muscle cells and affects cell proliferation and survival Johan.

Pressure activates colon cancer cell adhesion by inside-out focal adhesion complex and actin cytoskeletal signaling Vijayalakshmi Thamilselvan, Marc.

Transforming growth factor (TGF)-β1-induced human endometrial stromal cell decidualization through extracellular signal-regulated kinase and Smad activation.

Hao G. Nguyen, MD, PhD, Amit Korach, MD, Chey Collura, MA, Benjamin R

Matrix metalloproteinases modulated by protein kinase Cε mediate resistin-induced migration of human coronary artery smooth muscle cells Qinxue Ding,

Polyphenols modulate calcium-independent mechanisms in human arterial tissue- engineered vascular media Myriam Diebolt, PhD, Karina Laflamme, PhD, Raymond.

Stuart I. Myers, MD, Li Wang, BS, Fang Liu, BS, Lori L. Bartula, BS

Volume 68, Issue 4, Pages (October 2005)

Sphingosine-1-phosphate–induced smooth muscle cell migration involves the mammalian target of rapamycin William J. Tanski, MD, Suzanne M. Nicholl, PhD,

Platelet-derived growth factor is a cofactor in the induction of 1α(I) procollagen expression by transforming growth factor β1 in smooth muscle cells

The effects of doxycycline and micronized purified flavonoid fraction on human vein wall remodeling are not hypoxia-inducible factor pathway-dependent

Nitric oxide prevents p21 degradation with the ubiquitin-proteasome pathway in vascular smooth muscle cells Melina R. Kibbe, MD, Suhua Nie, MD, Dai-Wu.

Gabriele Di Luozzo, MD, Jaya Bhargava, PhD, Richard J. Powell, MD

Protein kinase C-δ regulates migration and proliferation of vascular smooth muscle cells through the extracellular signal-regulated kinase 1/2 Bo Liu,

Volume 70, Issue 10, Pages (November 2006)

Nitric oxide inhibition increases matrix metalloproteinase–9 expression by rat aortic smooth muscle cells in vitro Gilbert R. Upchurch, MD, John W. Ford,

Akihiro Tada Journal of Investigative Dermatology

Endothelial cell activation of the smooth muscle cell phosphoinositide 3-kinase/Akt pathway promotes differentiation David J. Brown, MD, Eva M. Rzucidlo,

Chi-Hyun Park, Youngji Moon, Chung Min Shin, Jin Ho Chung

Pharmacologic relaxation of vein grafts is beneficial compared with pressure distention caused by upregulation of endothelial nitric oxide synthase and.

Nicotine and cotinine stimulate secretion of basic fibroblast growth factor and affect expression of matrix metalloproteinases in cultured human smooth.

Volume 75, Issue 7, Pages (April 2009)

Matthew A. Will, M. D. , Murugesan Palaniappan, Ph. D

Iodinated contrast induced renal vasoconstriction is due in part to the downregulation of renal cortical and medullary nitric oxide synthesis Stuart.

Suprarenal aortic clamping and reperfusion decreases medullary and cortical blood flow by decreased endogenous renal nitric oxide and PGE2 synthesis

Deon G. Uffort, Elizabeth A. Grimm, Julie A. Ellerhorst

IGF-1 regulation of type II collagen and MMP-13 expression in rat endplate chondrocytes via distinct signaling pathways M. Zhang, Ph.D., Q. Zhou, M.D.,

Effects of somatostatin, somatostatin analogs, and endothelial cell somatostatin gene transfer on smooth muscle cell proliferation in vitro Rajabrata.

Resveratrol neuroprotective effects during focal cerebral ischemia injury via nitric oxide mechanism in rats Shen-Kou Tsai, MD, PhD, Li-Man Hung, PhD,

Volume 114, Issue 1, Pages (January 1998)

Panagiotis Kougias, MD, Hong Chai, MD, PhD, Peter H. Lin, MD, Alan B

Presentation transcript:

Ambient pressure upregulates nitric oxide synthase in a phosphorylated-extracellular regulated kinase– and protein kinase C–dependent manner Angela G. Vouyouka, MD, Yan Jiang, MS, Ruchi Rastogi, MSc, Marc D. Basson, MD, PhD Journal of Vascular Surgery Volume 44, Issue 5, Pages 1076-1084 (November 2006) DOI: 10.1016/j.jvs.2006.06.033 Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 1 Conditioned media from pressurized endothelial cells (EC-P) decreased the cell counts of recipient smooth muscle cell (SMC) cultures compared with conditioned media from ambient endothelial cells (EC) (P ≤ .001). Media from atmospheric (SMC) and pressurized (SMC-P) had similar effect (a). This reversed trophic effect of conditioned medium from EC-P was abolished when the donor cells were pretreated with 2.5 to 5 mM of N-nitro-L-arginine-methyl ester (L-NAME) a nitric oxide inhibitor (b). The addition of L-NAME to pressurized endothelial media after its removal from the recipient cells had no effect on the properties of the pressurized media (c). Data are expressed as ± SEM. Journal of Vascular Surgery 2006 44, 1076-1084DOI: (10.1016/j.jvs.2006.06.033) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 2 Endothelial cell (EC) protein exposed to ambient (NP) and 135 mm Hg pressure (P) was analyzed for endothelial nitric oxide synthase (eNOS). Endothelial cells were treated with dimethylsulfoxide (DMSO) (vehicle control), calphostin C (CalC) to block protein kinase C, PD98059 (PD) to block extracellular signal-regulated kinase, or N-nitro-L-arginine-methyl ester (L-NAME) to inhibit nitric oxide. A, Shows typical western blot for eNOS from EC protein from ambient and high-pressure conditions. B, Pressure increased eNOS in the control and L-NAME group (*P = .04 and **P = .02, n =12). Calphostin C and PD98509 blocked this effect, suggesting that pressurized EC exhibit increased levels of eNOS via a PKC and ERK dependent pathways. Data are expressed as ± SEM. Journal of Vascular Surgery 2006 44, 1076-1084DOI: (10.1016/j.jvs.2006.06.033) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 3 Smooth muscle cell (SMC) protein was analyzed for inducible nitric oxide synthase (iNOS). Endothelial cell (EC) coculture and pressure increased to a similar degree iNOS levels. However, the combination of the two conditions in the form of pressurized coculture had no additive effect on iNOS (*P < .01 bars 2, 3, and 4 vs first bar, n = 3 experiments). SMC/0, SMCs grown in control conditions; SMC/EC, SMCs in coculture with ECs; SMC/0P control SMCs exposed to pressure; SMC/EC-P, SMCs in pressure coculture with ECs. Data are expressed as ± SEM. Journal of Vascular Surgery 2006 44, 1076-1084DOI: (10.1016/j.jvs.2006.06.033) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 4 A, Typical Western blot analysis and summary of four such Western blots of endothelial protein exposed for 2, 4, and 6 hours to control pressure (NP) and high pressure at 130 to 135 mm Hg (P). B, Pressure in each time-point increased activated phosphorylated extracellular signal-regulated kinase (p-ERK) 1/2 content over total ERK1/2 compared with control conditions (*P < .02, analysis of variance, n = 4). Data are expressed as ± SEM. Journal of Vascular Surgery 2006 44, 1076-1084DOI: (10.1016/j.jvs.2006.06.033) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 5 Summary of 4 similar Western blot analyses for phosphorylated extracellular signal-regulated kinase (p-ERK) from endothelial cells exposed to ambient (np) and 130 to 135 mm Hg pressure (p) for 4 hours. Cells were treated with 100 nm calphostin C (Cal-C) to block protein kinase C activation. Control cells were treated with dimethylsulfoxide. Each Western blot demonstrated a similar effect: endothelial cell treatment with calphostin C does not attenuate the increase in ERK activation by pressure. Indeed, there is a fivefold increase in p-ERK in pressurized endothelial cells treated with calphostin C compared with levels of ERK activation in endothelial cells treated with calphostin C at ambient pressure (P < .05 by analysis of variance). These findings suggest that pressure-induced ERK activation is independent of protein kinase C. Journal of Vascular Surgery 2006 44, 1076-1084DOI: (10.1016/j.jvs.2006.06.033) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions