Synthetic smooth muscle cell phenotype is associated with increased nicotinamide adenine dinucleotide phosphate oxidase activity: Effect on collagen secretion

Slides:

Advertisements

Similar presentations

Graft smooth muscle cells specifically synthesize increased collagen

Advertisements

The Fumagillin Analogue TNP-470 Inhibits DNA Synthesis of Vascular Smooth Muscle Cells Stimulated by Platelet-Derived Growth Factor and Insulin-like Growth.

Heparin inhibits thrombin-induced mitogen-activated protein kinase signaling in arterial smooth muscle cells Ulf Hedin, MD, PhD, Günter Daum, PhD, Alexander.

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

Patrick C. H. Hsieh, MD, Richard D. Kenagy, PhD, Eileen R

Accelerated aneurysmal dilation associated with apoptosis and inflammation in a newly developed calcium phosphate rodent abdominal aortic aneurysm model

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

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

Role of reactive oxygen species in inhibition of endothelial cell migration by oxidized low-density lipoprotein John A. van Aalst, MD, Dong-Mei Zhang,

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

Effect of tissue plasminogen activator on vascular smooth muscle cells

Reactive oxygen species amplify protein kinase C signaling in high glucose-induced fibronectin expression by human peritoneal mesothelial cells Hi Bahl.

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.

Cell migration in response to the amino-terminal fragment of urokinase requires epidermal growth factor receptor activation through an ADAM-mediated mechanism

Use of Brilliant Blue FCF during vein graft preparation inhibits intimal hyperplasia Michael J. Osgood, MD, Kevin Sexton, MD, Igor Voskresensky, MD, Kyle.

Arterial heparan sulfate proteoglycans inhibit vascular smooth muscle cell proliferation and phenotype change in vitro and neointimal formation in vivo

The antifibrotic drug halofuginone inhibits proliferation and collagen production by human leiomyoma and myometrial smooth muscle cells Meagan M. Grudzien,

Omar Araim, MD, James Ballantyne, Andrew L. Waterhouse, PhD, Bauer E

Andreea M. Bujor, Jaspreet Pannu, Shizhong Bu, Edwin A. Smith, Robin C

Β-Adrenergic regulation of the eosinophil respiratory burst as detected by lucigenin- dependent luminescence Nicholas E. Hadjokas, PhD a,b, Joseph J.

Howard P. Greisler, MD, Joan Ellinger, Scott C. Henderson, Anne M

Sphingosine-1-phosphate–induced oxygen free radical generation in smooth muscle cell migration requires Gα12/13 protein-mediated phospholipase C activation

Neal X. Chen, Kalisha D. O'Neill, Danxia Duan, Sharon M. Moe

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

Richard R. Keen, MD, Kevin D

Smooth muscle cells cultured from human saphenous vein exhibit increased proliferation, invasion, and mitogen-activated protein kinase activation in vitro.

Volume 59, Issue 5, Pages (May 2001)

Modulation of vascular smooth muscle cell alignment by cyclic strain is dependent on reactive oxygen species and P38 mitogen-activated protein kinase

Volume 117, Issue 3, Pages (September 1999)

The proliferative response to platelet-derived growth factor of smooth muscle cells isolated from synthetic vascular grafts in a canine model David J.

Hsueh Yang, Gabrielle Curinga, Cecilia M. Giachelli

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

Angiotensin II-mediated expression of p27Kip1 and induction of cellular hypertrophy in renal tubular cells depend on the generation of oxygen radicals[1]

Cellular stress inhibits vascular smooth muscle relaxation

IL-6 Secreted from Cancer-Associated Fibroblasts Mediates Chemoresistance in NSCLC by Increasing Epithelial-Mesenchymal Transition Signaling Yasushi.

Reduction in postsurgical adhesion formation after cardiac surgery in a rabbit model using N,O-carboxymethyl chitosan to block cell adherence Juan Zhou,

Volume 64, Issue 1, Pages (July 2003)

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

Volume 62, Issue 1, Pages (July 2002)

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

Yunge Zhao, MD, PhD, Mark Turlington, BS, Damien J. LaPar, MD, David R

Taeseung Lee, MD, Nowokere Esemuede, MD, Bauer E

Volume 61, Issue 5, Pages (May 2002)

Proliferative capacity of vein graft smooth muscle cells and fibroblasts in vitro correlates with graft stenosis Richard D. Kenagy, PhD, Nozomi Fukai,

Γ-irradiation modulates vascular smooth muscle cell and extracellular matrix function: implications for neointimal development Joerg Heckenkamp, MD,

David K.W. Chew, MD, Michael S. Conte, MD, Raouf A. Khalil, MD, PhD

In vitro differences between smooth muscle cells derived from varicose veins and normal veins Ying Xiao, PhD, Zhibin Huang, MD, Henghui Yin, PhD, Ying.

Regional differences in phorbol 12-myristate 13-acetate stimulation of PDGF production in the normal canine aorta John A. van Aalst, MDa, James A. Madura,

Transforming growth factor-β1 increases lysyl oxidase enzyme activity and mRNA in rat aortic smooth muscle cells Charles J. Shanley, MD, Mehrnaz Gharaee-Kermani,

Cathepsin G deficiency reduces periaortic calcium chloride injury-induced abdominal aortic aneurysms in mice Jing Wang, MD, PhD, Galina K. Sukhova, PhD,

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

Volume 60, Issue 5, Pages (November 2001)

Smooth muscle cell migration and proliferation are mediated by distinct phases of activation of the intracellular messenger mitogen-activated protein.

Reply Journal of Vascular Surgery

STAT proteins mediate angiotensin II–induced production of TIMP-1 in human proximal tubular epithelial cells Xiangmei Chen, Jianzhong Wang, Feng Zhou,

The effect of growth factors, cytokines, and extracellular matrix proteins on fibronectin production in human vascular smooth muscle cells Terry L. Kaiura,

Angiotensin II stimulates Pax-2 in rat kidney proximal tubular cells: Impact on proliferation and apoptosis Shao-Ling Zhang, Jun Guo, Babak Moini, Julie.

Lu-Cheng Cao, Thomas Honeyman, Julie Jonassen, Cheryl Scheid

Mechanism of inhibition of matrix metalloproteinase-2 expression by doxycycline in human aortic smooth muscle cells Jian Liu, MD, Wanfen Xiong, PhD,

Activation of integrin receptors is required for growth factor–induced smooth muscle cell dysfunction Kyotaro Mawatari, MD, Bo Liu, PhD, K.Craig Kent,

Interleukin-1β inhibits PDGF-BB−induced migration by cooperating with PDGF-BB to induce cyclooxygenase-2 expression in baboon aortic smooth muscle cells

Alex Limanni, M. D. , Timothy Fleming, Ph. D. , Rodolfo Molina, M. D

Androgen-Dependent Beard Dermal Papilla Cells Secrete Autocrine Growth Factor(s) in Response to Testosterone Unlike Scalp Cells M. Julie Thornton, Kazuto.

Α-tocopherol preserves endothelial cell migration in the presence of cell-oxidized low- density lipoprotein by inhibiting changes in cell membrane fluidity

Volume 77, Issue 5, Pages (March 2010)

The effects of endothelial injury on smooth muscle cell proliferation

Janet Powell, MD, Roger M. Greenhalgh, MD Journal of Vascular Surgery

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

Presentation transcript:

Synthetic smooth muscle cell phenotype is associated with increased nicotinamide adenine dinucleotide phosphate oxidase activity: Effect on collagen secretion Rajendra Patel, MD, Jeffry D. Cardneau, MD, Scott M. Colles, PhD, Linda M. Graham, MD Journal of Vascular Surgery Volume 43, Issue 2, Pages 364-371 (February 2006) DOI: 10.1016/j.jvs.2005.10.032 Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 1 Graft smooth muscle cells (SMCs) secrete more collagen type I than aortic SMCs under basal conditions and in response to LY83583 (LY). A, Graft and aortic SMCs (passage 2) were grown to near confluence in Dulbecco’s modified Eagle’s medium (DMEM) with 10% fetal bovine serum (FBS). Cells were made quiescent by placing them in DMEM with 5% FBS for 24 hours. Medium and cells were collected at 1, 2, 3, 6, 9, and 12 hours after the addition of 1 μmol/L LY83583. Collagen type I present in the medium was determined by enzyme-linked immunoabsorbent assay. DNA in the cell layer was quantitated by fluorometric assay. The collagen type I was standardized to μg of DNA. P < .01 for graft SMCs compared with aortic SMCs at all times, P < .01 for graft SMCs + LY compared with graft SMCs at all times after 2 hours, P < .01 for aortic SMCs + LY compared with aortic SMCs at all times after 2 hours. B, Graft and aortic SMCs (passage 2) were grown as above. At 12 hours after the addition of LY83583, collagen type I, and DNA were measured. *P < .01 compared with aortic SMCs at same LY83583 concentration (Student’s t test) #P < .01 for LY83583-treated aortic or graft SMCs compared to untreated aortic or graft SMCs. Representative graphs of five separate experiments are shown in A and B. Values are expressed as the mean ± SD. Journal of Vascular Surgery 2006 43, 364-371DOI: (10.1016/j.jvs.2005.10.032) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 2 Graft smooth muscle cells (SMCs) treated with LY83583 (LY) generate more O2.− than LY83583-treated aortic SMCs. LY83583 (3 μmol/L) and lucigenin (10 μmol/L) were added to aliquots of 200,000 aortic or graft SMCs (passage 3). Luminescence was measured every 2 minutes. The graph depicts mean ± SEM of counts obtained in four separate experiments. P < .01 for all points after t = 0 when comparing either graft SMCs + LY83583 or aortic SMCs + LY83583 with respective controls. Journal of Vascular Surgery 2006 43, 364-371DOI: (10.1016/j.jvs.2005.10.032) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 3 Scavenger of O2.− inhibits collagen type I secretion in smooth muscle cells (SMCs) treated with LY83583 (LY). A, Confluent aortic SMCs were placed in medium containing 5% fetal bovine serum (FBS) for 24 hours. SMCs (200,000) were suspended in phenol-free Roswell Park Memorial Institute medium and incubated with 3 μmol/L LY83583. In parallel wells, 1.5 mmol/L tiron was added for 30 minutes before and during LY83583 treatment. Luminescence was measured as described in Methods and depicted as the fold increase (mean ± SD) in counts per second compared with respective untreated SMCs at t = 0. B, Aortic SMCs (passage 3) were grown to near confluence and placed in media containing 5% FBS for 24 hours. Cells were treated with 1.5 mmol/L tiron for 30 minutes before and during incubation with 1 μmol/L LY83583 as indicated. After 9 hours, medium was collected and the cells were harvested to measure the DNA. Collagen type I was normalized to μg of DNA. C, Graft SMCs were incubated with 3 μmol/L LY83583 with or without 1.5 mmol/L tiron, and O2.− production was measured as described in A. D, Graft SMCs (passage 3) were grown to near confluence and treated in an identical fashion to aortic SMCs described in B. A and C are representative of 3 separate experiments, B and D are representative graphs of 5 separate experiments. In A and C, P < .01 at all time points after t = 0 comparing LY83583-treated SMCs with control SMCs or LY83583-treated SMCs with tiron. In B and D, *P < .01 when compared with control. Journal of Vascular Surgery 2006 43, 364-371DOI: (10.1016/j.jvs.2005.10.032) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 4 Nicotinamide adenine phosphate dinucleotide (NADPH) oxidase activity is higher in graft smooth muscle cells (SMCs) than in aortic SMCs. Graft and aortic SMCs (passage 3) were harvested and suspended in phenol-free Roswell Park Memorial Institute medium. Aliquots of 200,000 graft or aortic SMCs were incubated with 0.1 mmol/L NADPH or solvent control. In parallel wells, SMCs were treated with 2 μmol/L diphenylene iodonium (DPI) for 30 minutes before and during incubation with NADPH. Luminescence was measured as described in Methods, and depicted as fold increase (mean ± SD) in counts per second compared with respective untreated SMCs at t = 0 (n = 3 separate experiments). P < .01 at all times after t = 0 for NADPH-treated graft or aortic SMCs compared with respective controls or NADPH-treated SMCs pretreated with DPI. Journal of Vascular Surgery 2006 43, 364-371DOI: (10.1016/j.jvs.2005.10.032) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions

Fig 5 Inhibition of nicotinamide adenine (phosphate) dinucleotide (NAD[P]H) oxidase diminishes LY83583 (LY)-induced O2.− and collagen type I production by aortic and graft smooth muscle cells (SMCs). A, Diphenylene iodonium (DPI) (2 μmol/L) and 100 μmol/L hydralazine (H) were added to SMCs (passage 3) for 30 minutes before and during LY83583 (3 μmol/L) treatment. Production of O2.− was measured by lucigenin chemiluminescent assay as described in Methods and depicted as fold increase (mean ± SD) in counts per second compared with respective untreated SMCs at t = 0 (n = 3 separate experiments). P < .01 for all time points when comparing LY83583-treated SMCs with LY83583-treated SMCs pretreated with DPI and hydralazine. B, SMCs (passage 3) were grown to near confluence, made quiescent, then treated with 2 μmol/L DPI and/or 100 μmol/L hydralazine, as indicated, for 30 minutes before and during incubation with 1 μmol/L LY83583 for 9 hours. Conditioned medium was collected and collagen type I measured by enzyme-linked immunoabsorbent assay. SMCs were lysed and DNA measured by fluorometric assay. Collagen type I was standardized to micrograms of DNA. Representative graph of five separate experiments is shown. *P < .01 compared with aortic SMCs under the same conditions, #P < .01 compared with respective LY83583-treated graft or aortic SMCs. Journal of Vascular Surgery 2006 43, 364-371DOI: (10.1016/j.jvs.2005.10.032) Copyright © 2006 The Society for Vascular Surgery Terms and Conditions