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

Slides:



Advertisements
Similar presentations
Proinflammatory cytokine–induced and chemical mediator–induced IL-8 expression in human bronchial epithelial cells through p38 mitogen-activated protein.
Advertisements

Graft smooth muscle cells specifically synthesize increased collagen
Synthetic smooth muscle cell phenotype is associated with increased nicotinamide adenine dinucleotide phosphate oxidase activity: Effect on collagen secretion 
MicroRNA-30b is a multifunctional regulator of aortic valve interstitial cells  Mi Zhang, MD, Xiaohong Liu, MD, Xiwu Zhang, MD, Zhigang Song, MD, Lin Han,
Regulation of vascular smooth muscle cell expression and function of matrix metalloproteinases is mediated by estrogen and progesterone exposure  Oscar.
Ginkgo biloba extract inhibits oxidized low-density lipoprotein (oxLDL)-induced matrix metalloproteinase activation by the modulation of the lectin-like.
Mitogen-activated protein kinase activation: An alternate signaling pathway for sustained vascular smooth muscle contraction  Aaron M. Epstein, MD, Douglas.
Syk Mediates IL−17-Induced CCL20 Expression by Targeting Act1-Dependent K63- Linked Ubiquitination of TRAF6  Nan-Lin Wu, Duen-Yi Huang, Hsin-Ni Tsou, Ying-Cing.
M. -H. Moon, J. -K. Jeong, Y. -J. Lee, J. -W. Seol, C. J. Jackson, S
Shear stress-stimulated endothelial cells induce smooth muscle cell chemotaxis via platelet-derived growth factor-BB and interleukin-1α  Alan Dardik,
Prasad V. Gade, MD, José A. Andrades, PhD, Marcel E
Role of redox signaling and poly (adenosine diphosphate-ribose) polymerase activation in vascular smooth muscle cell growth inhibition by nitric oxide.
Nitric oxide may inhibit neointimal hyperplasia by decreasing isopeptidase T levels and activity in the vasculature  Nick D. Tsihlis, PhD, Muneera R.
Urokinase-induced smooth muscle cell responses require distinct signaling pathways: A role for the epidermal growth factor receptor  Suzanne M. Nicholl,
Histone deacetylase inhibitors suppress interleukin-1β-induced nitric oxide and prostaglandin E2 production in human chondrocytes  N. Chabane, M.Sc.,
Anti-apoptotic effect of transforming growth factor-β1 on human articular chondrocytes: role of protein phosphatase 2A  M. Lires-Deán, B.S., B. Caramés,
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.
Translocation of protein kinase C isoforms is involved in propofol-induced endothelial nitric oxide synthase activation  L. Wang, B. Wu, Y. Sun, T. Xu,
Thomas E. Arnold, MD, Dmitri Gnatenko, PhD, Wadie F. Bahou, MD 
J.A. Roman-Blas, M.D., D.G. Stokes, Ph.D., S.A. Jimenez, M.D. 
Daniel J. Wong, MD, Daniel Y. Lu, MD, Clinton D
Regulation of tissue factor expression in smooth muscle cells with nitric oxide  Melina R. Kibbe, MDa, Christopher Johnnides, MDa, Susan Gleixner, BSa,
Spleen Tyrosine Kinase Mediates EGFR Signaling to Regulate Keratinocyte Terminal Differentiation  Nan-Lin Wu, Duen-Yi Huang, Li-Fang Wang, Reiji Kannagi,
Ambient pressure upregulates nitric oxide synthase in a phosphorylated-extracellular regulated kinase– and protein kinase C–dependent manner  Angela G.
Freimut Schliess, Anna Kordelia Kurz, Dieter Häussinger 
Volume 131, Issue 4, Pages (October 2006)
Richard R. Keen, MD, Kevin D
Elastase-induced matrix degradation in arterial organ cultures: An in vitro model of aneurysmal disease  Andrew Wills, BSc, Matthew M. Thompson, MD, FRCS,
Inducible nitric oxide synthase (iNOS) expression upregulates p21 and inhibits vascular smooth muscle cell proliferation through p42/44 mitogen-activated.
IGF-II-Mediated COX-2 Gene Expression in Human Keratinocytes Through Extracellular Signal-Regulated Kinase Pathway  Hye Jung Kim, Tae-Yoon Kim  Journal.
Volume 120, Issue 5, Pages (April 2001)
Michael A. Golden, MD, Y. P. Tina Au, PhD, Richard D
Volume 7, Issue 5, Pages (May 2003)
Malcolm O. Perry, MD, Richard Kempczinski, MD 
Nick D. Tsihlis, PhD, Jozef Murar, BA, Muneera R. Kapadia, MD, Sadaf S
Vitiligo-Inducing Phenols Activate the Unfolded Protein Response in Melanocytes Resulting in Upregulation of IL6 and IL8  Siavash Toosi, Seth J. Orlow,
Platelet-derived growth factor is a cofactor in the induction of 1α(I) procollagen expression by transforming growth factor β1 in smooth muscle cells 
Profiling Motility Signal-Specific Genes in Primary Human Keratinocytes  Chieh-Fang Cheng, Jianhua Fan, Balaji Bandyopahdhay, Dennis Mock, Shengxi Guan,
A chemically modified dextran inhibits smooth muscle cell growth in vitro and intimal in stent hyperplasia in vivo  Jean-François Deux, MDa,b, Sandrine.
Gabriele Di Luozzo, MD, Jaya Bhargava, PhD, Richard J. Powell, MD 
Upregulation of Tenascin-C Expression by IL-13 in Human Dermal Fibroblasts via the Phosphoinositide 3-kinase/Akt and the Protein Kinase C Signaling Pathways 
Nitric oxide inhibits IFN regulatory factor 1 and nuclear factor-κB pathways in rhinovirus- infected epithelial cells  Rommy Koetzler, MD, MSc, Raza S.
Protein kinase C-δ regulates migration and proliferation of vascular smooth muscle cells through the extracellular signal-regulated kinase 1/2  Bo Liu,
Keratinocyte growth factor promotes goblet cell differentiation through regulation of goblet cell silencer inhibitor  Dai Iwakiri, Daniel K. Podolsky 
Nitric oxide inhibition increases matrix metalloproteinase–9 expression by rat aortic smooth muscle cells in vitro  Gilbert R. Upchurch, MD, John W. Ford,
Taeseung Lee, MD, Nowokere Esemuede, MD, Bauer E
Volume 61, Issue 5, Pages (May 2002)
Volume 61, Issue 6, Pages (June 2002)
Transforming growth factor-β1 increases lysyl oxidase enzyme activity and mRNA in rat aortic smooth muscle cells  Charles J. Shanley, MD, Mehrnaz Gharaee-Kermani,
Cavopulmonary anastomosis induces pulmonary expression of the angiotensin II receptor family  Sunil P. Malhotra, MD, V.Mohan Reddy, MD, Stephan Thelitz,
Nicotine and cotinine stimulate secretion of basic fibroblast growth factor and affect expression of matrix metalloproteinases in cultured human smooth.
Differential Regulation of Cyclooxygenase-2 Expression by Phytosphingosine Derivatives, NAPS and TAPS, and its Role in the NAPS or TAPS-Mediated Apoptosis 
Smooth muscle cell migration and proliferation are mediated by distinct phases of activation of the intracellular messenger mitogen-activated protein.
Vivian Gahtan, MD, Xiu-Jie Wang, MD, Masataka Ikeda, MD, Alliric I
Calvin B. Ernst, MD  Journal of Vascular Surgery 
Mechanism of inhibition of matrix metalloproteinase-2 expression by doxycycline in human aortic smooth muscle cells  Jian Liu, MD, Wanfen Xiong, PhD,
Overexpression of endothelial nitric oxide synthase increases skeletal muscle blood flow and oxygenation in severe rat hind limb ischemia  Lucy S Brevetti,
Nick D. Tsihlis, PhD, Jozef Murar, BA, Muneera R. Kapadia, MD, Sadaf S
Activation of integrin receptors is required for growth factor–induced smooth muscle cell dysfunction  Kyotaro Mawatari, MD, Bo Liu, PhD, K.Craig Kent,
Volume 15, Issue 7, Pages (July 2007)
Alex Limanni, M. D. , Timothy Fleming, Ph. D. , Rodolfo Molina, M. D
Adenovirus-mediated gene transfer of human inducible nitric oxide synthase in porcine vein grafts inhibits intimal hyperplasia  Melina R. Kibbe, MDa,
The effects of endothelial injury on smooth muscle cell proliferation
Deon G. Uffort, Elizabeth A. Grimm, Julie A. Ellerhorst 
Adenoviral-mediated uteroglobin gene transfer inhibits neointimal hyperplasia after balloon injury in the rat carotid artery  Robert A. Larson, MD, Mina.
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.,
Ultraviolet-B-Induced G1 Arrest is Mediated by Downregulation of Cyclin-Dependent Kinase 4 in Transformed Keratinocytes Lacking Functional p53  Arianna.
Effects of somatostatin, somatostatin analogs, and endothelial cell somatostatin gene transfer on smooth muscle cell proliferation in vitro  Rajabrata.
Volume 21, Issue 2, Pages (January 2006)
Presentation transcript:

Nitric oxide prevents p21 degradation with the ubiquitin-proteasome pathway in vascular smooth muscle cells  Melina R. Kibbe, MD, Suhua Nie, MD, Dai-Wu Seol, PhD, Imre Kovesdi, PhD, Alena Lizonova, PhD, Michel Makaroun, MD, FACS, Timothy R. Billiar, MD, FACS, Edith Tzeng, MD  Journal of Vascular Surgery  Volume 31, Issue 2, Pages 364-374 (February 2000) DOI: 10.1016/S0741-5214(00)90166-6 Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 1 The nitric oxide-donor, S-nitroso-N-acetylpenicillamine (SNAP ), induced a time- and concentration-dependent increase in the expression of p21 protein in cultured rat aortic smooth muscle cells by means of Western blot analysis. A, SNAP 0.5 mmol/L. B, Time = 6 hours. Data are representative of four similar experiments. Journal of Vascular Surgery 2000 31, 364-374DOI: (10.1016/S0741-5214(00)90166-6) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 2 Nitric oxide increases p21 messenger RNA (mRNA ) levels in rat aortic smooth muscle cells after exposure to S-nitroso-N-acetylpenicillamine (SNAP ) at an early point. A, Rat aortic smooth muscle cells were exposed to media or media containing SNAP (0.5 mmol/L) for the indicated times. The cells were collected, and the mRNA was subjected to Northern blot analysis. SNAP increased the steady-state levels of p21 mRNA after exposure to SNAP for 6 hours (*P <.001 vs control). There was no statistically significant difference at 24 hours. B, Cultured rat aortic smooth muscle cells were infected with adenoviral vectors encoding either β-galactosidase (AdlacZ) or human inducible nitric oxide synthase complementary DNA (AdiNOS ; multiplicity of infection = 10). After 24 hours of nitric oxide production, the cells were collected, and the mRNA was subjected to Northern blot analysis. AdiNOS-infected cells displayed a trend toward increased p21 mRNA levels, but this was not statistically significant. Densitometry data for p21 were normalized by 18S. Photomicrographs represent one of three independent experiments. Graphs represent the data from all three independent experiments. Journal of Vascular Surgery 2000 31, 364-374DOI: (10.1016/S0741-5214(00)90166-6) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 3 Transcription inhibitors prevent nitric oxide-induced upregulation of p21 messenger RNA (mRNA ) levels, but not p21 protein expression. Rat aortic smooth muscle cells were pretreated with the transcription inhibitors α-amanitin or actinomycin D, followed by exposure to S-nitroso-N-acetylpenicillamine (SNAP ) for 6 hours. It was revealed by means of Northern blot analysis that both α-amanitin and actinomycin D prevented the SNAP-induced upregulation of p21 mRNA levels; however, the upregulation of p21 protein expression by SNAP was not affected by either transcription inhibitor. Northern and Western blot analyses were performed on parallel experiments. Data are representative of two independent experiments. Journal of Vascular Surgery 2000 31, 364-374DOI: (10.1016/S0741-5214(00)90166-6) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 4 Nitric oxide decreases the level of ubiquinated p21 in rat aortic smooth muscle cells at both early and late points. Rat aortic smooth muscle cells were immunoprecipitated with an anti-p21 polyclonal antibody and subjected to Western blot analysis for both p21 and ubiquitin. A, S-nitroso-N-acetylpenicillamine (SNAP ; 0.5 mmol/L) treatment was associated with a marked upregulation of p21 expression, compared with control treated cells at both 6 and 24 hours. This was associated with a statistically significant decrease in the level of ubiquinated p21 (*P = 0.017 vs control at 6 hours; **P =.011 vs control at 24 hours). B, Rat aortic smooth muscle cells infected with adenoviral vectors encoding either β-galactosidase (AdlacZ) or human inducible nitric oxide synthase complementary DNA (AdiNOS ; multiplicity of infection = 10) were collected after exposure to nitric oxide for 24 hours. iNOS gene transfer resulted in a significant decrease in the expression of ubiquinated p21 (*P =.010 vs control). Photomicrographs represent one of four independent experiments. Graphs represent the densitometry data from all four independent experiments. Levels of ubiquinated p21 were normalized to total p21 signal. Journal of Vascular Surgery 2000 31, 364-374DOI: (10.1016/S0741-5214(00)90166-6) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 5 Nitric oxide increases protein serine/threonine and protein tyrosine phosphatase activity. Rat aortic smooth muscle cells were exposed to increasing concentrations of S-nitroso-N-acetylpenicillamine (SNAP ) for 2 or 6 hours. Cell lysate was collected and assayed for phosphatase activity by using phosphorylated myelin basic protein as the substrate. SNAP induced a concentration-dependent increase in A, protein serine/threonine phosphatase activity at both 2 (*P =.046 vs control) and 6 hours (*P <.001 vs control), and in B, protein tyrosine phosphatase activity at both 2 (*P =.008 and **P =.014 vs control) and 6 hours (*P =.026 vs control). Data represent one of four independent experiments (n = 3 per group). Journal of Vascular Surgery 2000 31, 364-374DOI: (10.1016/S0741-5214(00)90166-6) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 6 Phosphatase inhibitors prevent the upregulation of p21 by nitric oxide. Rat aortic smooth muscle cells were treated with S-nitroso-N-acetylpenicillamine (SNAP ; 0.5 mmol/L) with or without calyculin A (CaA ) and with or without cantharidin (Canth ). Whole cell lysate was collected after treatment for 6 hours. A, Both calyculin A (upper panel; *P <.001 vs control; #P <.001 vs SNAP) and cantharidin (lower panel; *P <.001 vs control; **P =.02; #P <.001 vs SNAP) inhibited basal and SNAP-induced protein serine/threonine phosphatase activity. B, It was revealed by means of Western blot analysis that calyculin A and cantharidin prevented the SNAP-induced upregulation of p21 in a concentration-dependent manner. Data are representative of four identical experiments; n = 3 per group for the phosphatase assay. Journal of Vascular Surgery 2000 31, 364-374DOI: (10.1016/S0741-5214(00)90166-6) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 7 Schematic illustration of the regulation of p21 expression by nitric oxide. We provide data demonstrating that nitric oxide increases phosphatase activity and that this may lead to the release of the phosphate from p21 that normally targets it for destruction by the ubiquitin-proteasome pathway. A non-ubiquinated form of p21 may then accumulate in the cell and induce cell cycle arrest. Journal of Vascular Surgery 2000 31, 364-374DOI: (10.1016/S0741-5214(00)90166-6) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions