Literature DB >> 15115983

Vein graft arterialization causes differential activation of mitogen-activated protein kinases.

Paul C Saunders1, Giuseppe Pintucci, Costas S Bizekis, Ram Sharony, Kevin M Hyman, Fiorella Saponara, F Gregory Baumann, Eugene A Grossi, Stephen B Colvin, Paolo Mignatti, Aubrey C Galloway.   

Abstract

OBJECTIVE: Vascular injury results in activation of the mitogen-activated protein kinases-extracellular-signal regulated kinases, c-jun N-terminal kinase, and p38(MAPK)-which have been implicated in cell proliferation, migration, and apoptosis. The goal of this study was to characterize mitogen-activated protein kinase activation in arterialized vein grafts.
METHODS: Carotid artery bypass using reversed external jugular vein was performed in 29 dogs. Vein grafts were harvested after 30 minutes and 3, 8, and 24 hours, and 4, 7, 14, and 28 days. Contralateral external jugular vein and external jugular vein interposition vein-to-vein grafts were used as controls. Vein graft extracts were analyzed for extracellular-signal regulated kinases, c-jun N-terminal kinase, and p38(MAPK) activation. Proliferating cell nuclear antigen expression was investigated as a parameter of cell proliferation. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick end labeling staining and intimal hyperplasia by morphometric examination of tissue sections.
RESULTS: Significant intimal hyperplasia was observed at 28 days. Over the time points studied, vein graft arterialization resulted in bimodal activation of both extracellular-signal regulated kinase and p38(MAPK) (30 minutes through 3 hours; 4 days) but did not induce activation of c-jun N-terminal kinase. Proliferating cell nuclear antigen expression increased from days 1 through 28, and apoptosis increased between 8 and 24 hours.
CONCLUSION: Vein graft arterialization induces bimodal activation of extracellular-signal regulated kinase and p38(MAPK); however, in contrast with what is described in arterial injury, it does not induce c-jun N-terminal kinase activation. These results provide the first comprehensive characterization of the mitogen-activated protein kinase signaling pathways activated in vein graft arterialization and identify mitogen-activated protein kinases as potential mediators of vein graft remodeling and subsequent intimal hyperplasia.

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Year:  2004        PMID: 15115983     DOI: 10.1016/j.jtcvs.2003.07.017

Source DB:  PubMed          Journal:  J Thorac Cardiovasc Surg        ISSN: 0022-5223            Impact factor:   5.209


  10 in total

1.  A novel cell permeant peptide inhibitor of MAPKAP kinase II inhibits intimal hyperplasia in a human saphenous vein organ culture model.

Authors:  Luciana B Lopes; Colleen M Brophy; Charles R Flynn; Zhengping Yi; Benjamin P Bowen; Christopher Smoke; Brandon Seal; Alyssa Panitch; Padmini Komalavilas
Journal:  J Vasc Surg       Date:  2010-09-22       Impact factor: 4.268

2.  MK2 inhibitory peptide delivered in nanopolyplexes prevents vascular graft intimal hyperplasia.

Authors:  Brian C Evans; Kyle M Hocking; Michael J Osgood; Igor Voskresensky; Julia Dmowska; Kameron V Kilchrist; Colleen M Brophy; Craig L Duvall
Journal:  Sci Transl Med       Date:  2015-06-10       Impact factor: 17.956

3.  Nitric oxide, endothelin-1, and superoxide production in arterial bypass grafts.

Authors:  Fehime Benli Aksungar; Hadi Moini; Mehmet Unal; Oguz Yilmaz; Bingur Sonmez; Serpil Bilsel
Journal:  Tex Heart Inst J       Date:  2006

Review 4.  Vein graft failure.

Authors:  Christopher D Owens; Warren J Gasper; Amreen S Rahman; Michael S Conte
Journal:  J Vasc Surg       Date:  2013-10-03       Impact factor: 4.268

Review 5.  Vein graft failure: from pathophysiology to clinical outcomes.

Authors:  Margreet R de Vries; Karin H Simons; J Wouter Jukema; Jerry Braun; Paul H A Quax
Journal:  Nat Rev Cardiol       Date:  2016-05-19       Impact factor: 32.419

6.  Arterialization of a vein graft promotes cell cycle progression through Akt and p38 mitogen-activated protein kinase pathways: impact of the preparation procedure.

Authors:  Ada W Y Chung; Jerry Wong; Honglin Luo; York N Hsiang; Cornelis van Breemen; Elena B Okon
Journal:  Can J Cardiol       Date:  2007-12       Impact factor: 5.223

7.  Modulating vascular intimal hyperplasia using HSV-1 mutant requires activated MEK.

Authors:  C L Skelly; Q He; L Spiguel; S McCormick; R Weichselbaum
Journal:  Gene Ther       Date:  2012-03-15       Impact factor: 5.250

8.  Therapeutic MK2 inhibition blocks pathological vascular smooth muscle cell phenotype switch.

Authors:  J William Tierney; Brian C Evans; Joyce Cheung-Flynn; Bo Wang; Juan M Colazo; Monica E Polcz; Rebecca S Cook; Colleen M Brophy; Craig L Duvall
Journal:  JCI Insight       Date:  2021-10-08

9.  Heterogeneous Maturation of Arterio-Venous Fistulas and Loop-Shaped Venous Interposition Grafts: A Histological and 3D Flow Simulation Comparison.

Authors:  Balazs Szabo; Balazs Gasz; Laszlo Adam Fazekas; Adam Varga; Levente Kiss-Papai; Orsolya Matolay; Zsofia Rezsabek; Mohammad W Al-Smadi; Norbert Nemeth
Journal:  Biomedicines       Date:  2022-06-25

Review 10.  The Role of Endothelial Cells in the Onset, Development and Modulation of Vein Graft Disease.

Authors:  Shameem S Ladak; Liam W McQueen; Georgia R Layton; Hardeep Aujla; Adewale Adebayo; Mustafa Zakkar
Journal:  Cells       Date:  2022-09-29       Impact factor: 7.666

  10 in total

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