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

Slides:

Advertisements

Similar presentations

Cyclic adenosine monophosphate response-element binding protein activation by mitogen-activated protein kinase-activated protein kinase 3 and four-and-a-half.

Advertisements

Local lentiviral short hairpin RNA silencing of CCR2 inhibits vein graft thickening in hypercholesterolemic apolipoprotein E3-Leiden mice Daniël Eefting,

Cyclic adenosine monophosphate response-element binding protein activation by mitogen-activated protein kinase-activated protein kinase 3 and four-and-a-half.

Upregulation of PD-L1 by EGFR Activation Mediates the Immune Escape in EGFR- Driven NSCLC: Implication for Optional Immune Targeted Therapy for NSCLC Patients.

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.

In vivo electroporation of constitutively expressed HIF-1α plasmid DNA improves neovascularization in a mouse model of limb ischemia Geoffrey O. Ouma,

Undifferentiated mesenchymal stem cells seeded on a vascular prosthesis contribute to the restoration of a physiologic vascular wall Alain Mirza, MD,

Twist-related protein 1 negatively regulated osteoblastic transdifferentiation of human aortic valve interstitial cells by directly inhibiting runt-related.

Yi-kuan Chen, MD, Xue-mei Jiang, MSc, Jian-ping Gong, MD

Differential expression of Hedgehog/Notch and transforming growth factor-β in human abdominal aortic aneurysms Adam J. Doyle, MD, Eileen M. Redmond,

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

Nicotine Induces Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor by α1 Nicotinic Acetylcholine Receptor–Mediated Activation in.

Perivascular innate immune events modulate early murine vein graft adaptations Binh T. Nguyen, MD, Peng Yu, MD, Ming Tao, MD, Shuai Hao, BS, Tianyu Jiang,

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

Low molecular weight (LMW) heparin inhibits injury-induced femoral artery remodeling in mouse via upregulating CD44 expression Gaofeng Zhao, MD, PhD,

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

Volume 88, Issue 4, Pages (October 2015)

Altered microRNA expression in stenoses of native arteriovenous fistulas in hemodialysis patients Lei Lv, MD, Weibin Huang, MD, Jiwei Zhang, MD, Yaxue.

The Protective Effects of Melittin on Propionibacterium acnes–Induced Inflammatory Responses In Vitro and In Vivo Woo-Ram Lee, Kyung-Hyun Kim, Hyun-Jin.

Gene transduction into aortic wall using plasmid-loaded cationized gelatin hydrogel- coated polyester stent graft Hongshan Zhong, MD, Osamu Matsui, MD,

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

Local lentiviral short hairpin RNA silencing of CCR2 inhibits vein graft thickening in hypercholesterolemic apolipoprotein E3-Leiden mice Daniël Eefting,

Gene transduction into aortic wall using plasmid-loaded cationized gelatin hydrogel- coated polyester stent graft Hongshan Zhong, MD, Osamu Matsui, MD,

Inflammation-related induction of absent in melanoma 2 (AIM2) in vascular cells and atherosclerotic lesions suggests a role in vascular pathogenesis

Vascular smooth muscle cell peroxisome proliferator-activated receptor-γ deletion promotes abdominal aortic aneurysms Milton Hamblin, PhD, Lin Chang,

Volume 69, Issue 8, Pages (April 2006)

Lipoplex gene transfer of inducible nitric oxide synthase inhibits the reactive intimal hyperplasia after expanded polytetrafluoroethylene bypass grafting

Combination of stromal-derived factor-1α and vascular endothelial growth factor gene- modified endothelial progenitor cells is more effective for ischemic.

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

A novel function for cadherin 11/osteoblast-cadherin in vascular smooth muscle cells: Modulation of cell migration and proliferation Thomas S. Monahan,

Adventitial delivery of platelet-derived endothelial cell growth factor gene prevented intimal hyperplasia of vein graft Mitsuteru Handa, MD, Wei Li,

Adenovirus-mediated intra-arterial delivery of cellular repressor of E1A-stimulated genes inhibits neointima formation in rabbits after balloon injury

Increased connexin43 expression in human saphenous veins in culture is associated with intimal hyperplasia Sébastien Déglise, MD, David Martin, MS, Hervé.

Afshin Ehsan, MD, Adam P. McGraw, PhD, Mark J

Thomas E. Arnold, MD, Dmitri Gnatenko, PhD, Wadie F. Bahou, MD

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

Hydrogen ameliorates pulmonary hypertension in rats by anti-inflammatory and antioxidant effects Yasuaki Kishimoto, MD, Taichi Kato, MD, PhD, Mikako.

Bone morphogenic protein 2 induces Runx2 and osteopontin expression in human aortic valve interstitial cells: Role of Smad1 and extracellular signal-regulated.

Daniel J. Wong, MD, Daniel Y. Lu, MD, Clinton D

Histamine Contributes to Tissue Remodeling via Periostin Expression

Nicotine Induces Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor by α1 Nicotinic Acetylcholine Receptor–Mediated Activation in.

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

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

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

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

Effect of microRNA-145 to prevent vein graft disease in rabbits by regulation of smooth muscle cell phenotype Motoaki Ohnaka, MD, Akira Marui, MD, PhD,

Galit Ankri-Eliahoo, PhD, Kevin Weitz, BS, Timothy C. Cox, PhD, Gale L

S-phase kinase-associated protein-2 (Skp2) promotes vascular smooth muscle cell proliferation and neointima formation in vivo Yih-Jer Wu, MD, PhD, Graciela.

Enhanced expression of glucose transporter-1 in vascular smooth muscle cells via the Akt/tuberous sclerosis complex subunit 2 (TSC2)/mammalian target.

In vivo suppression of vein graft disease by nonviral, electroporation-mediated, gene transfer of tissue inhibitor of metalloproteinase-1 linked to the.

Role of hemodynamic forces in the ex vivo arterialization of human saphenous veins Xavier Berard, MD, PhD, Sébastien Déglise, MD, Florian Alonso, PhD,

Adventitial delivery of platelet-derived endothelial cell growth factor gene prevented intimal hyperplasia of vein graft Mitsuteru Handa, MD, Wei Li,

Volume 82, Issue 7, Pages (October 2012)

Navin K. Kapur, MD, Ce Bian, MD, Edward Lin, MD, Clayton B

Prolonged increases in vein wall tension increase matrix metalloproteinases and decrease constriction in rat vena cava: Potential implications in varicose.

Volume 24, Issue 2, Pages (February 2016)

Gene expression changes evoked in a venous segment exposed to arterial flow Deborah Abeles, MD, Stephanie Kwei, MD, George Stavrakis, MS, Yuzhi Zhang,

Jin H. Li, Xiao R. Huang, Hong-Jian Zhu, Richard Johnson, Hui Y. Lan

Lisheng Zhang, MD, Leigh Brian, MS, Neil J. Freedman, MD

Loss of PTEN Expression by Dermal Fibroblasts Causes Skin Fibrosis

Volume 22, Issue 2, Pages (February 2014)

Development of a spontaneously beating vein by cardiomyocyte transplantation in the wall of the inferior vena cava in a rat: A pilot study Wangde Dai,

Temporal genomics of vein bypass grafting through oligonucleotide microarray analysis Jeffrey A Kalish, MD, David J Willis, MD, Cheng Li, PhD, Jeffrey.

IL-17A Upregulates Keratin 17 Expression in Keratinocytes through STAT1- and STAT3- Dependent Mechanisms Xiaowei Shi, Liang Jin, Erle Dang, Ting Chang,

Volume 22, Issue 6, Pages (June 2014)

Controlled release of small interfering RNA targeting midkine attenuates intimal hyperplasia in vein grafts Hiroshi Banno, MD, Yoshifumi Takei, PhD,

Differential transcriptional activation of matrix metalloproteinase-2 and membrane type-1 matrix metalloproteinase by experimental deep venous thrombosis.

Galit Ankri-Eliahoo, PhD, Kevin Weitz, BS, Timothy C. Cox, PhD, Gale L

Gene expression changes evoked in a venous segment exposed to arterial flow Deborah Abeles, MD, Stephanie Kwei, MD, George Stavrakis, MS, Yuzhi Zhang,

Presentation transcript:

α1-Adrenergic receptors mediate combined signals initiated by mechanical stretch stress and norepinephrine leading to accelerated mouse vein graft atherosclerosis Shuying Liu, MD, PhD, Yuhuang Li, MD, PhD, Zhengyu Zhang, MD, PhD, Fukang Xie, PhD, Qingbo Xu, MD, PhD, Xi Huang, MD, PhD, Jintao Huang, BS, Chaohong Li, PhD Journal of Vascular Surgery Volume 57, Issue 6, Pages 1645-1656.e3 (June 2013) DOI: 10.1016/j.jvs.2012.09.061 Copyright © 2013 Society for Vascular Surgery Terms and Conditions

Fig 1 A-E, Differential expression of α1-adrenergic receptor (α1-AR) subtypes and norepinephrine (NE)-induced extracellular signal-regulated kinase (ERK) activation in vascular smooth muscle cells (VSMCs). A, The expression level of mRNAs of α1A-ARs, α1B-ARs, α1D-ARs in VSMCs as detected by real-time quantitative polymerase chain reaction (qPCR). Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was served as an internal control. B, NE dose-dependently induces ERK activation in VSMCs, which is dose-dependently inhibited by prazosin (D). C and E, Statistical results of phosphorylated ERK (pERK) levels of B and D from three independent experiments. β-actin was served as internal control. *P < .05 vs negative control (NC); #P < .05 vs NE. Journal of Vascular Surgery 2013 57, 1645-1656.e3DOI: (10.1016/j.jvs.2012.09.061) Copyright © 2013 Society for Vascular Surgery Terms and Conditions

Fig 2 A-H, Mechanical stretch induces Gαq translocation from membrane to cytosol and extracellular signal-regulated kinase (ERK) phosphorylation in vascular smooth muscle cells (VSMCs) partially inhibited by prazosin. A, The cyclic stretch stress (SS)-induced VSMCs Gαq translocation from membrane to cytosol in a time-dependent manner. RAGE and β-actin were used as internal controls of membrane-Gαq and cytosol-Gαq. C, Prazosin partially inhibited SS-induced Gαq translocation. E, SS-induced VSMCs ERK phosphorylation in an elongation-dependent manner, which can be dose-dependently inhibited by prazosin (G). B, D, F, and H show statistical results of A, C, E, and G from three independent experiments. Pan-ERKs or β-actin served as internal control. *P < .05 vs negative control (NC); #P < .05 vs SS without prazosin. Journal of Vascular Surgery 2013 57, 1645-1656.e3DOI: (10.1016/j.jvs.2012.09.061) Copyright © 2013 Society for Vascular Surgery Terms and Conditions

Fig 3 A and B, α1-Adrenergic receptors (α1-ARs) partially mediate additive activation of extracellular signal-regulated kinases (ERKs) in vascular smooth muscle cells (VSMCs) initiated by combined treatment of cyclic stretch stress (SS) and norepinephrine (NE). A, The additive activation of ERKs in VSMCs stimulated by combined treatment with cyclic SS (10% elongation for 10 minutes) and NE (10−7 M, 10 minutes) with or without prazosin (Praz) (10−7 M). B, Statistical results of phosphorylated ERK (pERK) levels of A from three independent experiments. β-actin served as internal control. *P < .05 vs negative control (NC); aP < .05 vs NE; bP < .05 vs SS; cP < .05 vs SS+NE; $P < .05 vs SS+NE. Journal of Vascular Surgery 2013 57, 1645-1656.e3DOI: (10.1016/j.jvs.2012.09.061) Copyright © 2013 Society for Vascular Surgery Terms and Conditions

Fig 4 A-D, α1-Adrenergic receptors α1B-AR and α1D-AR partially mediate stretch-induced extracellular signal-regulated kinase (ERK) phosphorylation in vascular smooth muscle cells (VSMCs). A, Mechanical stretch (10% elongation for 1 hour, continually cultured for 6 hours) upregulates the expression of α1B-AR and α1D-AR mRNAs but not α1A-AR. B and C, α1B-AR and α1D-AR siRNAs (50 nM) significantly suppress the expression of VSMC α1B-AR and α1D-AR mRNAs. D, A graph of statistical results from three independent experiments that stretch stress (SS)-induced (10% elongation for 10 minutes) ERK phosphorylation in VSMCs can be partially inhibited by α1B-AR and α1D-AR siRNAs (50 nM). NC, Negative control; LIP, Lipofectamine 2000 control; SiC, nontargeting siRNA control; Siα1B, α1B-AR siRNA; Siα1D, α1D-AR siRNA; *P < .05 vs NC; #P < .05 vs SS. Journal of Vascular Surgery 2013 57, 1645-1656.e3DOI: (10.1016/j.jvs.2012.09.061) Copyright © 2013 Society for Vascular Surgery Terms and Conditions

Fig 5 A-I, α1-Adrenergic receptors (α1-ARs) partially mediate the additive effects of vascular smooth muscle cell (VSMC) proliferation (Ki67 expression) induced by combined treatment of cyclic stretch stress (SS) and norepinephrine (NE). Serum-starved VSMCs were pretreated with or without prazosin (Praz) for 1 hour and then subjected to cyclic SS or NE or NE plus cyclic SS for 1 hour and continually cultured 23 hours. The red-colored end products indicate the Ki67 antigens, and blue-colored end products indicate the nuclei of VSMCs. (Bar = 20 μm.) I, shows a graph of statistical results of A through H from three independent experiments. *P < .05 vs NC; aP < .05 vs NE; bP < .05 vs SS; cP < .05 vs SS+NE; $P < .05 vs SS+NE. Journal of Vascular Surgery 2013 57, 1645-1656.e3DOI: (10.1016/j.jvs.2012.09.061) Copyright © 2013 Society for Vascular Surgery Terms and Conditions

Fig 6 A-K, α1-Adrenergic receptors (α1-ARs) partially mediate the vein graft remodeling in vivo. Under anesthesia, the vena cava segments of mice were grafted into the carotid arteries of the recipient mice. The recipient mice postoperatively accepted prazosin (1.0 mg/kg/d) (E and I) or equal value of saline (C and G) via intraperitoneal injections for 2 weeks (C and E) or 4 weeks (G and I) and were sacrificed, and the vein grafts were fixed, embedded, sectioned, and stained with hematoxylin and eosin. The recipient mouse vena cava itself served as negative control (NC) (A and B). Arrow and stars indicate the wall thickness between vessel lumen and adventitia (arrows) and vessel lumens (stars) of the control vein (A and B) and vein grafts (C-J). B, D, F, H, and J, High-magnification areas of regions enclosed by a box (A, C, E, G, and I) (Bar = 50 μm). K, Statistical graphs of wall thickness of vein grafts from different groups (0, 2, and 4 weeks postoperatively). VG, Vein graft; VGP, vein graft plus prazosin. aP < .05 vs NC; bP < .05 vs VG2W; cP < .05 vs VG4W. Journal of Vascular Surgery 2013 57, 1645-1656.e3DOI: (10.1016/j.jvs.2012.09.061) Copyright © 2013 Society for Vascular Surgery Terms and Conditions

Fig 7 Potential signal pathway by which α1-adrenergic receptors (α1-ARs) partially mediate the additive effects of combined treatment of cyclic stretch stress (SS) and norepinephrine (NE) on vascular smooth muscle cell (VSMC) extracellular signal-regulated kinase (ERK) activation and proliferation. Hyperactivation of the sympathetic system results in increased catecholamine (eg, NE) in circulation. NE specifically binds to α1-ARs and initiates intracellular signaling including increased VSMC Gαq translocation, ERK phosphorylation, gene expression, and cell contraction and proliferation leading to the eventual development of hypertension. When hypertension occurs, hypertension-induced mechanical SS results in deformation of VSMCs and activates α1-ARs and downstream signaling, which further amplifies previous NE-induced signaling leading to additive effects of accelerated vascular remodeling. The effect can be partially inhibited by prasozin. The α1-ARs play a linker role between hypertension-induced SS and sympathetic system overdrive-increased NE in plasma. Journal of Vascular Surgery 2013 57, 1645-1656.e3DOI: (10.1016/j.jvs.2012.09.061) Copyright © 2013 Society for Vascular Surgery Terms and Conditions