Multiple Progressive Thermopreconditioning Improves Cardiac Ischemia/Reperfusion-induced Left Ventricular Contractile Dysfunction and Structural Abnormality in Rat.
Adaptor Proteins, Signal Transducing
/ physiology
Animals
Apoptosis
Apoptosis Regulatory Proteins
/ physiology
Granulocyte Colony-Stimulating Factor
/ pharmacology
Heart Ventricles
/ pathology
Ischemic Preconditioning, Myocardial
Male
Microcirculation
Myocardial Contraction
/ physiology
Myocardial Reperfusion Injury
/ pathology
Proto-Oncogene Proteins c-bcl-2
/ analysis
Rats
Rats, Wistar
Ventricular Dysfunction, Left
/ prevention & control
Journal
Transplantation
ISSN: 1534-6080
Titre abrégé: Transplantation
Pays: United States
ID NLM: 0132144
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
pubmed:
15
2
2020
medline:
7
10
2020
entrez:
15
2
2020
Statut:
ppublish
Résumé
Triple progressive thermopreconditioning (3PTP) may induce high Hsp-70 expression to maintain cardiac function. We suggest that 3PTP may reduce myocardial ischemia/reperfusion (I/R) injury during organ transplantation through Bag3/Hsp-70 mediated defense mechanisms. Male Wistar rats were divided into sham control group and 72 h after 3PTP in a 42°C water bath (3PTP) group. Rats underwent 60 min of ischemia by occlusion of the left anterior descending coronary artery followed by 240 min reperfusion. Hemodynamic parameters, including the electrocardiogram, microcirculation, heart rate, left ventricular end-diastolic pressure, maximal rate of rise (+dp/dt), and fall (-dp/dt) in the left ventricular pressure for index of contraction and relaxation were determined. Myocardial infarct size was evaluated by the Evans blue-2,3,5-triphenyltetrazolium chloride method. 3PTP-induced protective mechanisms were determined by Western blot and immunohistochemistry. Cardiac I/R depressed cardiac microcirculation, induced S-T segment elevation, and R-R and P-R interval elongation increased infarct size associated with erythrocyte extravasation, leukocytes and macrophage/monocyte infiltration, granulocyte colony-stimulating factor, poly(ADP-ribose) polymerase 1 stain, and transferase-mediated dUTP-biotin nick end labeling positive cells. However, 3PTP evoked significant cardioprotection against I/R injury, characterized by the increased +dp/dt value and the decreased elevated left ventricular end-diastolic pressure, erythrocyte extravasation, leukocyte and macrophage/monocyte infiltration, granulocyte colony-stimulating factor expression, poly(ADP-ribose) polymerase 1 expression, transferase-mediated dUTP-biotin nick end labeling positive cells, and fragmentation and infarct area. In addition, 3PTP increased Hsp-70 and Bag3 expression and decreased Bax/Bcl-2 ratio, but did not affect the Beclin-1 and LC3-II/LC3-I ratio in the heart with I/R injury. 3PTP therapies may through Bag3 upregulation alleviate I/R injury-induced left ventricular structural deterioration and dysfunction.
Sections du résumé
BACKGROUND
Triple progressive thermopreconditioning (3PTP) may induce high Hsp-70 expression to maintain cardiac function. We suggest that 3PTP may reduce myocardial ischemia/reperfusion (I/R) injury during organ transplantation through Bag3/Hsp-70 mediated defense mechanisms.
METHODS
Male Wistar rats were divided into sham control group and 72 h after 3PTP in a 42°C water bath (3PTP) group. Rats underwent 60 min of ischemia by occlusion of the left anterior descending coronary artery followed by 240 min reperfusion. Hemodynamic parameters, including the electrocardiogram, microcirculation, heart rate, left ventricular end-diastolic pressure, maximal rate of rise (+dp/dt), and fall (-dp/dt) in the left ventricular pressure for index of contraction and relaxation were determined. Myocardial infarct size was evaluated by the Evans blue-2,3,5-triphenyltetrazolium chloride method. 3PTP-induced protective mechanisms were determined by Western blot and immunohistochemistry.
RESULTS
Cardiac I/R depressed cardiac microcirculation, induced S-T segment elevation, and R-R and P-R interval elongation increased infarct size associated with erythrocyte extravasation, leukocytes and macrophage/monocyte infiltration, granulocyte colony-stimulating factor, poly(ADP-ribose) polymerase 1 stain, and transferase-mediated dUTP-biotin nick end labeling positive cells. However, 3PTP evoked significant cardioprotection against I/R injury, characterized by the increased +dp/dt value and the decreased elevated left ventricular end-diastolic pressure, erythrocyte extravasation, leukocyte and macrophage/monocyte infiltration, granulocyte colony-stimulating factor expression, poly(ADP-ribose) polymerase 1 expression, transferase-mediated dUTP-biotin nick end labeling positive cells, and fragmentation and infarct area. In addition, 3PTP increased Hsp-70 and Bag3 expression and decreased Bax/Bcl-2 ratio, but did not affect the Beclin-1 and LC3-II/LC3-I ratio in the heart with I/R injury.
CONCLUSIONS
3PTP therapies may through Bag3 upregulation alleviate I/R injury-induced left ventricular structural deterioration and dysfunction.
Identifiants
pubmed: 32058468
doi: 10.1097/TP.0000000000003176
pii: 00007890-202009000-00021
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
Apoptosis Regulatory Proteins
0
BAG3 protein, rat
0
Proto-Oncogene Proteins c-bcl-2
0
Granulocyte Colony-Stimulating Factor
143011-72-7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1869-1878Références
Niccoli G, Scalone G, Lerman A, et al. Coronary microvascular obstruction in acute myocardial infarction. Eur Heart J. 2016; 37:1024–1033. doi:10.1093/eurheartj/ehv484
doi: 10.1093/eurheartj/ehv484
Thiele H, Akin I, Sandri M, et al.; CULPRIT-SHOCK Investigators. PCI strategies in patients with acute myocardial infarction and cardiogenic shock. N Engl J Med. 2017; 377:2419–2432. doi:10.1056/NEJMoa1710261
doi: 10.1056/NEJMoa1710261
Chien CY, Chien CT, Wang SS. Progressive thermopreconditioning attenuates rat cardiac ischemia/reperfusion injury by mitochondria-mediated antioxidant and antiapoptotic mechanisms. J Thorac Cardiovasc Surg. 2014; 148:705–713. doi:10.1016/j.jtcvs.2013.12.065
doi: 10.1016/j.jtcvs.2013.12.065
Lian WS, Lin H, Cheng WT, et al. Granulocyte-CSF induced inflammation-associated cardiac thrombosis in iron loading mouse heart and can be attenuated by statin therapy. J Biomed Sci. 2011; 18:26. doi:10.1186/1423-0127-18-26
doi: 10.1186/1423-0127-18-26
Song H, Yan C, Tian X, et al. CREG protects from myocardial ischemia/reperfusion injury by regulating myocardial autophagy and apoptosis. Biochim Biophys Acta Mol Basis Dis. 2017; 1863:1893–1903. doi:10.1016/j.bbadis.2016.11.015
doi: 10.1016/j.bbadis.2016.11.015
Li PC, Yang CC, Hsu SP, et al. Repetitive progressive thermal preconditioning hinders thrombosis by reinforcing phosphatidylinositol 3-kinase/Akt-dependent heat-shock protein/endothelial nitric oxide synthase signaling. J Vasc Surg. 2012; 56:159–170. doi:10.1016/j.jvs.2011.11.062
doi: 10.1016/j.jvs.2011.11.062
Schreckenberg R, Bencsik P, Weber M, et al. Adverse effects on β-adrenergic receptor coupling: ischemic postconditioning failed to preserve long-term cardiac function. J Am Heart Assoc. 2017; 6:e006809. doi:10.1161/JAHA.117.006809
doi: 10.1161/JAHA.117.006809
Ma H, Gong H, Chen Z, et al. Association of stat3 with HSF1 plays a critical role in G-CSF-induced cardio-protection against ischemia/reperfusion injury. J Mol Cell Cardiol. 2012; 52:1282–1290. doi:10.1016/j.yjmcc.2012.02.011
doi: 10.1016/j.yjmcc.2012.02.011
Katsaros KM, Speidl WS, Demyanets S, et al. G-CSF predicts cardiovascular events in patients with stable coronary artery disease. PLoS One. 2015; 10:e0142532. doi:10.1371/journal.pone.0142532
doi: 10.1371/journal.pone.0142532
McCormick PH, Chen G, Tlerney S, et al. Clinically relevant thermal preconditioning attenuates ischemia-reperfusion injury. J Surg Res. 2003; 109:24–30. doi:10.1016/s0022-4804(02)00035-5
doi: 10.1016/s0022-4804(02)00035-5
Yellon DM, Pasini E, Cargnoni A, et al. The protective role of heat stress in the ischaemic and reperfused rabbit myocardium. J Mol Cell Cardiol. 1992; 24:895–907. doi:10.1016/0022-2828(92)91102-b
doi: 10.1016/0022-2828(92)91102-b
Okada M, Hasebe N, Aizawa Y, et al. Thermal treatment attenuates neointimal thickening with enhanced expression of heat-shock protein 72 and suppression of oxidative stress. Circulation. 2004; 109:1763–1768. doi:10.1161/01.CIR.0000124226.88860.55
doi: 10.1161/01.CIR.0000124226.88860.55
Sobajima M, Nozawa T, Ihori H, et al. Repeated sauna therapy improves myocardial perfusion in patients with chronically occluded coronary artery-related ischemia. Int J Cardiol. 2013; 167:237–243. doi:10.1016/j.ijcard.2011.12.064
doi: 10.1016/j.ijcard.2011.12.064
Kubota K, Tamura K, Take H, et al. Acute myocardial infarction and cerebral infarction at Kusatsu-spa. Nihon Ronen Igakkai Zasshi. 1997; 34:23–29. doi:10.3143/geriatrics.34.23
doi: 10.3143/geriatrics.34.23
Meng X, Pei H, Lan C. Icariin exerts protective effect against myocardial ischemia/reperfusion injury in rats. Cell Biochem Biophys. 2015; 73:229–235. doi:10.1007/s12013-015-0669-6
doi: 10.1007/s12013-015-0669-6
Gavrieli Y, Sherman Y, Ben-Sasson SA. Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation. J Cell Biol. 1992; 119:493–501. doi:10.1083/jcb.119.3.493
doi: 10.1083/jcb.119.3.493
Tuuminen R, Dashkevich A, Keränen MA, et al. Platelet-derived growth factor-B protects rat cardiac allografts from ischemia-reperfusion injury. Transplantation. 2016; 100:303–313. doi:10.1097/TP.0000000000000909
doi: 10.1097/TP.0000000000000909
Cubedo J, Suades R, Padro T, et al. Erythrocyte-heme proteins and STEMI: implications in prognosis. Thromb Haemost. 2017; 117:1970–1980. doi:10.1160/TH17-05-0314
doi: 10.1160/TH17-05-0314
Maekawa Y, Anzai T, Yoshikawa T, et al. Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction. J Am Coll Cardiol. 2004; 44:1510–1520. doi:10.1016/j.jacc.2004.05.083
doi: 10.1016/j.jacc.2004.05.083
Huang SC, Tsai YF, Cheng YS, et al. Vascular protection with less activation evoked by progressive thermal preconditioning in adrenergic receptor-mediated hypertension and tachycardia. Chin J Physiol. 2009; 52:419–425. doi:10.4077/cjp.2009.amh048
doi: 10.4077/cjp.2009.amh048
Kevelaitis E, Patel AP, Oubenaissa A, et al. Backtable heat-enhanced preconditioning: a simple and effective means of improving function of heart transplants. Ann Thorac Surg. 2001; 72:107–112. Discussion 112–103. doi:10.1016/s0003-4975(01)02495-x
doi: 10.1016/s0003-4975(01)02495-x
Hishiya A, Kitazawa T, Takayama S. BAG3 and Hsc70 interact with actin capping protein CapZ to maintain myofibrillar integrity under mechanical stress. Circ Res. 2010; 107:1220–1231. doi:10.1161/CIRCRESAHA.110.225649
doi: 10.1161/CIRCRESAHA.110.225649
Cheung JY, Gordon J, Wang J, et al. Mitochondrial dysfunction in human immunodeficiency virus-1 transgenic mouse cardiac myocytes. J Cell Physiol. 2019; 234:4432–4444. doi:10.1002/jcp.27232
doi: 10.1002/jcp.27232
Su F, Myers VD, Knezevic T, et al. Bcl-2-associated athanogene 3 protects the heart from ischemia/reperfusion injury. JCI Insight. 2016; 1:e90931. doi:10.1172/jci.insight.90931
doi: 10.1172/jci.insight.90931
Frankenreiter S, Bednarczyk P, Kniess A, et al. cGMP-elevating compounds and ischemic conditioning provide cardioprotection against ischemia and reperfusion injury via cardiomyocyte-specific BK channels. Circulation. 2017; 136:2337–2355. doi:10.1161/CIRCULATIONAHA.117.028723
doi: 10.1161/CIRCULATIONAHA.117.028723
Cai S, Ichimaru N, Zhao M, et al. Prolonged mouse cardiac graft cold storage via attenuating ischemia-reperfusion injury using a new antioxidant-based preservation solution. Transplantation. 2016; 100:1032–1040. doi:10.1097/TP.0000000000001079
doi: 10.1097/TP.0000000000001079
Sugano Y, Anzai T, Yoshikawa T, et al. Granulocyte colony-stimulating factor attenuates early ventricular expansion after experimental myocardial infarction. Cardiovasc Res. 2005; 65:446–456. doi:10.1016/j.cardiores.2004.10.008
doi: 10.1016/j.cardiores.2004.10.008
Baldo MP, Davel AP, Damas-Souza DM, et al. The antiapoptotic effect of granulocyte colony-stimulating factor reduces infarct size and prevents heart failure development in rats. Cell Physiol Biochem. 2011; 28:33–40. doi:10.1159/000331711
doi: 10.1159/000331711
Han TH, Qamirani E, Nelson AG, et al. Regulation of nitric oxide consumption by hypoxic red blood cells. Proc Natl Acad Sci U S A. 2003; 100:12504–12509. doi:10.1073/pnas.2133409100
doi: 10.1073/pnas.2133409100
Wang X, Wang Q, Guo W, et al. Hydrogen sulfide attenuates cardiac dysfunction in a rat model of heart failure: a mechanism through cardiac mitochondrial protection. Biosci Rep. 2011; 31:87–98. doi:10.1042/BSR20100003
doi: 10.1042/BSR20100003
Chien CT, Chang TC, Tsai CY, et al. Adenovirus-mediated bcl-2gene transfer inhibits renal ischemia/reperfusion induced tubular oxidative stress and apoptosis. Am J Transplant. 2005; 5:1194–1203. doi:10.1111/j.1600-6143.2005.00826.x
doi: 10.1111/j.1600-6143.2005.00826.x
Tahrir FG, Knezevic T, Gupta MK, et al. Evidence for the role of BAG3 in mitochondrial quality control in cardiomyocytes. J Cell Physiol. 2017; 232:797–805. doi:10.1002/jcp.25476
doi: 10.1002/jcp.25476
Laukkanen T, Kunutsor SK, Khan H, et al. Sauna bathing is associated with reduced cardiovascular mortality and improves risk prediction in men and women: a prospective cohort study. BMC Med. 2018; 16:219. doi:10.1186/s12916-018-1198-0
doi: 10.1186/s12916-018-1198-0
Källström M, Soveri I, Oldgren J, et al. Effects of sauna bath on heart failure: a systematic review and meta-analysis. Clin Cardiol. 2018; 41:1491–1501. doi:10.1002/clc.23077
doi: 10.1002/clc.23077