Repetitive progressive thermal preconditioning hinders thrombosis by reinforcing phosphatidylinositol 3-kinase/Akt-dependent heat-shock protein/endothelial nitric oxide synthase signaling

Ping Chia Li, Chih Ching Yang, Shih Ping Hsu, Chiang-Ting Chien

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11 Citations (Scopus)

Abstract

Objective: We compared the effects of modified progressive thermal preconditioning (PTP) and whole-body thermal preconditioning (TP) on stress responses, oxidative stress biomarkers, and arterial thrombosis formation, and explored their possible actions through phosphatidylinositol 3-kinase (PI3K)/Akt-dependent heat-shock protein (Hsp)/endothelial nitric oxide synthase (eNOS) pathways. Methods: We divided four groups of 249 male Wistar rats into nonimmersed controls, TP, and one (1-PTP) and three consecutive cycles (3-PTP) of PTP in a 42°C water bath. We evaluated the stress responses, including hemodynamics, total energy transfer, endoplasmic reticulum (ER) stress marker glucose-regulated protein (GRP78), and blood reactive oxygen species level during TP or PTP treatment. We compared 1-PTP, 3-PTP, or TP effects on oxidative stress, intercellular adhesion molecule 1 (ICAM-1), Hsp70, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) activity, and vascular phosphorylated Akt (p-Akt) and eNOS (p-eNOS) expressions in a model of topical ferric chloride (FeCl3)-induced carotid artery thrombosis. Results: PTP significantly (P <.05) induced less hemodynamic fluctuations, total energy transfer, ER, and oxidative stress than TP did. After 24 or 72 hours of treatment, 1-PTP, 3-PTP, and TP significantly (P <.05) elevated carotid arterial Hsp70, p-Akt, and p-eNOS expression, significantly (P <.05) depressed FeCl3-enhanced vascular 2′,7′- dichlorodihydrofluorescein diacetate, chemokine (C-X3-C motif) ligand 1 (CX3CL1), 3-nitrotyrosine, 4-hydroxynonenal, and ICAM-1 stain, PAI-1, and t-PA activity, leukocyte infiltration and thrombus size, and significantly (P <.05) delayed thrombus formation compared with controls. 3-PTP and TP had a higher (P <.05) protection than 1-PTP. PI3K/Akt, Hsp70, or N(G)-nitro-l-arginine methyl ester hydrochloride (L-NAME) inhibitors significantly (P <.05) depressed 3-PTP and TP-induced vascular protection. Conclusions: Repetitive PTP is better than single PTP to hinder thrombosis formation via reinforcing PI3K/Akt-dependent Hsp70/eNOS signaling.

Original languageEnglish
Pages (from-to)159-170
Number of pages12
JournalJournal of Vascular Surgery
Volume56
Issue number1
DOIs
Publication statusPublished - 2012 Jul 1

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Phosphatidylinositol 3-Kinase
Nitric Oxide Synthase Type III
Heat-Shock Proteins
Thrombosis
Hot Temperature
Blood Vessels
Oxidative Stress
Endoplasmic Reticulum Stress
Energy Transfer
Tissue Plasminogen Activator
Intercellular Adhesion Molecule-1

ASJC Scopus subject areas

  • Surgery
  • Cardiology and Cardiovascular Medicine

Cite this

@article{2fffc0a503a349bf83bec27947a1e927,
title = "Repetitive progressive thermal preconditioning hinders thrombosis by reinforcing phosphatidylinositol 3-kinase/Akt-dependent heat-shock protein/endothelial nitric oxide synthase signaling",
abstract = "Objective: We compared the effects of modified progressive thermal preconditioning (PTP) and whole-body thermal preconditioning (TP) on stress responses, oxidative stress biomarkers, and arterial thrombosis formation, and explored their possible actions through phosphatidylinositol 3-kinase (PI3K)/Akt-dependent heat-shock protein (Hsp)/endothelial nitric oxide synthase (eNOS) pathways. Methods: We divided four groups of 249 male Wistar rats into nonimmersed controls, TP, and one (1-PTP) and three consecutive cycles (3-PTP) of PTP in a 42°C water bath. We evaluated the stress responses, including hemodynamics, total energy transfer, endoplasmic reticulum (ER) stress marker glucose-regulated protein (GRP78), and blood reactive oxygen species level during TP or PTP treatment. We compared 1-PTP, 3-PTP, or TP effects on oxidative stress, intercellular adhesion molecule 1 (ICAM-1), Hsp70, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) activity, and vascular phosphorylated Akt (p-Akt) and eNOS (p-eNOS) expressions in a model of topical ferric chloride (FeCl3)-induced carotid artery thrombosis. Results: PTP significantly (P <.05) induced less hemodynamic fluctuations, total energy transfer, ER, and oxidative stress than TP did. After 24 or 72 hours of treatment, 1-PTP, 3-PTP, and TP significantly (P <.05) elevated carotid arterial Hsp70, p-Akt, and p-eNOS expression, significantly (P <.05) depressed FeCl3-enhanced vascular 2′,7′- dichlorodihydrofluorescein diacetate, chemokine (C-X3-C motif) ligand 1 (CX3CL1), 3-nitrotyrosine, 4-hydroxynonenal, and ICAM-1 stain, PAI-1, and t-PA activity, leukocyte infiltration and thrombus size, and significantly (P <.05) delayed thrombus formation compared with controls. 3-PTP and TP had a higher (P <.05) protection than 1-PTP. PI3K/Akt, Hsp70, or N(G)-nitro-l-arginine methyl ester hydrochloride (L-NAME) inhibitors significantly (P <.05) depressed 3-PTP and TP-induced vascular protection. Conclusions: Repetitive PTP is better than single PTP to hinder thrombosis formation via reinforcing PI3K/Akt-dependent Hsp70/eNOS signaling.",
author = "Li, {Ping Chia} and Yang, {Chih Ching} and Hsu, {Shih Ping} and Chiang-Ting Chien",
year = "2012",
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doi = "10.1016/j.jvs.2011.11.062",
language = "English",
volume = "56",
pages = "159--170",
journal = "Journal of Vascular Surgery",
issn = "0741-5214",
publisher = "Mosby Inc.",
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TY - JOUR

T1 - Repetitive progressive thermal preconditioning hinders thrombosis by reinforcing phosphatidylinositol 3-kinase/Akt-dependent heat-shock protein/endothelial nitric oxide synthase signaling

AU - Li, Ping Chia

AU - Yang, Chih Ching

AU - Hsu, Shih Ping

AU - Chien, Chiang-Ting

PY - 2012/7/1

Y1 - 2012/7/1

N2 - Objective: We compared the effects of modified progressive thermal preconditioning (PTP) and whole-body thermal preconditioning (TP) on stress responses, oxidative stress biomarkers, and arterial thrombosis formation, and explored their possible actions through phosphatidylinositol 3-kinase (PI3K)/Akt-dependent heat-shock protein (Hsp)/endothelial nitric oxide synthase (eNOS) pathways. Methods: We divided four groups of 249 male Wistar rats into nonimmersed controls, TP, and one (1-PTP) and three consecutive cycles (3-PTP) of PTP in a 42°C water bath. We evaluated the stress responses, including hemodynamics, total energy transfer, endoplasmic reticulum (ER) stress marker glucose-regulated protein (GRP78), and blood reactive oxygen species level during TP or PTP treatment. We compared 1-PTP, 3-PTP, or TP effects on oxidative stress, intercellular adhesion molecule 1 (ICAM-1), Hsp70, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) activity, and vascular phosphorylated Akt (p-Akt) and eNOS (p-eNOS) expressions in a model of topical ferric chloride (FeCl3)-induced carotid artery thrombosis. Results: PTP significantly (P <.05) induced less hemodynamic fluctuations, total energy transfer, ER, and oxidative stress than TP did. After 24 or 72 hours of treatment, 1-PTP, 3-PTP, and TP significantly (P <.05) elevated carotid arterial Hsp70, p-Akt, and p-eNOS expression, significantly (P <.05) depressed FeCl3-enhanced vascular 2′,7′- dichlorodihydrofluorescein diacetate, chemokine (C-X3-C motif) ligand 1 (CX3CL1), 3-nitrotyrosine, 4-hydroxynonenal, and ICAM-1 stain, PAI-1, and t-PA activity, leukocyte infiltration and thrombus size, and significantly (P <.05) delayed thrombus formation compared with controls. 3-PTP and TP had a higher (P <.05) protection than 1-PTP. PI3K/Akt, Hsp70, or N(G)-nitro-l-arginine methyl ester hydrochloride (L-NAME) inhibitors significantly (P <.05) depressed 3-PTP and TP-induced vascular protection. Conclusions: Repetitive PTP is better than single PTP to hinder thrombosis formation via reinforcing PI3K/Akt-dependent Hsp70/eNOS signaling.

AB - Objective: We compared the effects of modified progressive thermal preconditioning (PTP) and whole-body thermal preconditioning (TP) on stress responses, oxidative stress biomarkers, and arterial thrombosis formation, and explored their possible actions through phosphatidylinositol 3-kinase (PI3K)/Akt-dependent heat-shock protein (Hsp)/endothelial nitric oxide synthase (eNOS) pathways. Methods: We divided four groups of 249 male Wistar rats into nonimmersed controls, TP, and one (1-PTP) and three consecutive cycles (3-PTP) of PTP in a 42°C water bath. We evaluated the stress responses, including hemodynamics, total energy transfer, endoplasmic reticulum (ER) stress marker glucose-regulated protein (GRP78), and blood reactive oxygen species level during TP or PTP treatment. We compared 1-PTP, 3-PTP, or TP effects on oxidative stress, intercellular adhesion molecule 1 (ICAM-1), Hsp70, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) activity, and vascular phosphorylated Akt (p-Akt) and eNOS (p-eNOS) expressions in a model of topical ferric chloride (FeCl3)-induced carotid artery thrombosis. Results: PTP significantly (P <.05) induced less hemodynamic fluctuations, total energy transfer, ER, and oxidative stress than TP did. After 24 or 72 hours of treatment, 1-PTP, 3-PTP, and TP significantly (P <.05) elevated carotid arterial Hsp70, p-Akt, and p-eNOS expression, significantly (P <.05) depressed FeCl3-enhanced vascular 2′,7′- dichlorodihydrofluorescein diacetate, chemokine (C-X3-C motif) ligand 1 (CX3CL1), 3-nitrotyrosine, 4-hydroxynonenal, and ICAM-1 stain, PAI-1, and t-PA activity, leukocyte infiltration and thrombus size, and significantly (P <.05) delayed thrombus formation compared with controls. 3-PTP and TP had a higher (P <.05) protection than 1-PTP. PI3K/Akt, Hsp70, or N(G)-nitro-l-arginine methyl ester hydrochloride (L-NAME) inhibitors significantly (P <.05) depressed 3-PTP and TP-induced vascular protection. Conclusions: Repetitive PTP is better than single PTP to hinder thrombosis formation via reinforcing PI3K/Akt-dependent Hsp70/eNOS signaling.

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U2 - 10.1016/j.jvs.2011.11.062

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