دورية أكاديمية

Chronic whole-body heat treatment relieves atherosclerotic lesions, cardiovascular and metabolic abnormalities, and enhances survival time restoring the anti-inflammatory and anti-senescent heat shock response in mice.

التفاصيل البيبلوغرافية
العنوان: Chronic whole-body heat treatment relieves atherosclerotic lesions, cardiovascular and metabolic abnormalities, and enhances survival time restoring the anti-inflammatory and anti-senescent heat shock response in mice.
المؤلفون: Bruxel MA; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., Tavares AMV; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., Zavarize Neto LD; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., de Souza Borges V; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., Schroeder HT; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., Bock PM; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., Rodrigues MIL; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., Belló-Klein A; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil., Homem de Bittencourt PI Jr; Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil. Electronic address: pauloivo@ufrgs.br.
المصدر: Biochimie [Biochimie] 2019 Jan; Vol. 156, pp. 33-46. Date of Electronic Publication: 2018 Sep 28.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Editions Scientifiques Elsevier Country of Publication: France NLM ID: 1264604 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1638-6183 (Electronic) Linking ISSN: 03009084 NLM ISO Abbreviation: Biochimie Subsets: MEDLINE
أسماء مطبوعة: Publication: Paris : Editions Scientifiques Elsevier
Original Publication: Paris.
مواضيع طبية MeSH: Heat-Shock Response* , Hyperthermia, Induced*, Aorta/*metabolism , Atherosclerosis/*therapy, Animals ; Atherosclerosis/chemically induced ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Cholesterol/adverse effects ; Cholesterol/pharmacology ; Dietary Fats/adverse effects ; Dietary Fats/pharmacology ; Gene Expression Regulation ; Heat-Shock Proteins/biosynthesis ; Hot Temperature ; Male ; Mice ; Mice, Knockout ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Sirtuin 1/biosynthesis
مستخلص: Unhealthy lifestyle persistently feeds forward inflammation in metabolic organs thus imposing senescence-associated secretory phenotype (SASP), as observed in obesity and type 2 diabetes. However, SASP blocks physiological resolution of inflammation by suppressing the anti-inflammatory and anti-senescent heat shock (HS) response, i.e., the gene program centered in heat shock factor-1 (HSF1)-dependent expression heat shock proteins (HSPs). As SASP-inducing factors are not removed, leading to the perpetuation of inflammation, we argued that SIRT1-HSF1-HSP axis might also be suppressed in atherosclerosis, which could be reversible by heat treatment (HT), the most powerful HS response trigger. LDLr -/- adult mice were fed on high-fat/high-cholesterol diet from the age of 90 days until the end of study (age of 270 days). After 120 days under atherosclerotic diet, the animals were submitted to either whole-body HT (n = 42; 40 °C) or sham (n = 59; 37 °C) treatment (15 min/session), under anesthesia, once a week, for 8 weeks, being echographically and metabolically monitored. Aortic expressions of SIRT1, HSF1, HSP27, HSP72 and HSP73 were progressively depressed in atherosclerotic animals, as compared to normal (LDLr +/+ ; n = 25) healthy counterparts, which was paralleled by increased expression of NF-κB-dependent VCAM1 adhesion molecule. Conversely, HT completely reversed suppression of the above HS response proteins, while markedly inhibiting both VCAM1 expression and NF-κB DNA-binding activity. Also, HT dramatically reduced plasma levels of TG, total cholesterol, LDL-cholesterol, oxidative stress, fasting glucose and insulin resistance while rising HDL-cholesterol levels. HT also decreased body weight gain, visceral fat, cellular infiltration and aortic fatty streaks, and heart ventricular congestive hypertrophy, thereby improving aortic blood flow and myocardial performance (Tei) indices. Remarkably, heat-treated mice stopped dying after the third HT session (= 8 human years), suggesting a curative effect. Therefore, evolution of atherosclerosis is associated with suppression of the anti-inflammatory and anti-senescent SIRT1-HSF1-HSP molecular axis, which is refreshed by chronic heat treatment.
(Copyright © 2018 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.)
فهرسة مساهمة: Keywords: Atherosclerosis; HSF1; HSP27; HSP70; Heat shock response; Sirtuin-1
المشرفين على المادة: 0 (Dietary Fats)
0 (Heat-Shock Proteins)
0 (Receptors, LDL)
97C5T2UQ7J (Cholesterol)
EC 3.5.1.- (Sirt1 protein, mouse)
EC 3.5.1.- (Sirtuin 1)
تواريخ الأحداث: Date Created: 20181002 Date Completed: 20190109 Latest Revision: 20190109
رمز التحديث: 20221213
DOI: 10.1016/j.biochi.2018.09.011
PMID: 30273616
قاعدة البيانات: MEDLINE
الوصف
تدمد:1638-6183
DOI:10.1016/j.biochi.2018.09.011