scholarly journals Hypothermia preserves function and signaling for mitochondrial biogenesis during subsequent ischemia

1998 ◽  
Vol 274 (3) ◽  
pp. H786-H793 ◽  
Author(s):  
Xue-Han Ning ◽  
Cheng-Su Xu ◽  
Ying C. Song ◽  
Yun Xiao ◽  
Ying-Jia Hu ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Mitochondrial Biogenesis ◽  
Stress Responses ◽  
Adenine Nucleotide ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Ischemia And Reperfusion ◽  
Mrna Levels

Hypothermia is known to protect myocardium during ischemia, but its role in induction of a protective stress response before ischemia has not been evaluated. As cold incites stress responses in other tissues, including heat shock protein induction and signaling mitochondrial biogenesis, we postulated that hypothermia in perfused hearts would produce similar phenomena while reducing injury during subsequent ischemia. Studies were performed in isolated perfused rabbit hearts ( n = 77): a control group (C) and a hypothermic group (H) subjected to decreasing infusate temperature from 37 to 31°C over 20 min. Subsequent ischemia during cardioplegic arrest at 34°C for 120 min was followed by reperfusion. At 15 min of reperfusion, recovery of left ventricular developed pressure (LVDP), maximum first derivative of left ventricular pressure (LV dP/d tmax), LV −dP/d tmax, and the product of heart rate and LVDP was significantly increased in H ( P < 0.01) compared with C hearts. Ischemic contracture started later in H (97.5 ± 3.6 min) than in C (67.3 ± 3.3 min) hearts. Myocardial ATP preservation and repletion during ischemia and reperfusion were higher in H than in C hearts. mRNA levels of the nuclear-encoded mitochondrial proteins adenine nucleotide translocase isoform 1 (ANT1) and β-F1-adenosinetriphosphatase (β-F1-ATPase) normalized to 28S RNA decreased in C hearts but were preserved in H hearts after reperfusion. Inducible heat shock protein (HSP70–1) mRNA was elevated nearly 4-fold after ischemia in C hearts and 12-fold in H hearts. These data indicate that hypothermia preserves myocardial function and ATP stores during subsequent ischemia and reperfusion. Signaling for mitochondrial biogenesis indexed by ANT1and β-F1-ATPase mRNA levels is also preserved during a marked increase in HSP70–1 mRNA.

Assessment of placental and maternal stress responses in patients with pregnancy related complications via monitoring of heat shock protein mRNA levels

2014 ◽  
Vol 42 (3) ◽  
pp. 625-637 ◽  
Author(s):  
Ilona Hromadnikova ◽  
Lenka Dvorakova ◽  
Katerina Kotlabova ◽  
Andrea Kestlerova ◽  
Lucie Hympanova ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Stress Responses ◽  
Maternal Stress ◽  
Mrna Levels

4 IDENTIFICATION AND FUNCTIONAL CHARACTERIZATION OF HEAT SHOCK PROTEIN 40 IN PIG OVARY

2011 ◽  
Vol 23 (1) ◽  
pp. 108
Author(s):  
G. Pennarossa ◽  
S. Maffei ◽  
M. M. Rahman ◽  
A. Vanelli ◽  
G. Berruti ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Conformational Changes ◽  
Sequence Data ◽  
Functional Characterization ◽  
Pcr Amplification ◽  
Cumulus Cells ◽  
Control Group ◽  
Mrna Levels

Decreased fertility during the hot season is a common problem in pigs. Maternal hyperthermia reduces oocyte fertilizability and increases embryonic mortality. Cell biochemical thermoprotection mechanisms involve members of the heat shock protein (Hsp) family. Hsp40, also known as Mammalian Relative of DnaJ (MRJ) protein, plays a pivotal role as co-chaperone after heat shocks. This protein binds Hsp70 and, through ATP hydrolysis, induces the conformational changes needed by Hsp70 to bind and release heat unfolded proteins. However, no information is available on the role of Hsp40 in mammalian ovary. Here we investigate a) the expression and localization of Hsp40 in pig ovaries; b) its response to heat stress in oocytes and cumulus cells. To identify Hsp40 in pig, we extracted RNA from ovaries, granulosa cells and from pools of 5 oocytes. cDNA was amplified using primers specifically designed for Hsp40, based on sequence data available in other species. The amplified products were sequenced and aligned using ClustalW. The nucleotide sequence showed an homology of 95% with the human, 92% with the bovine and 84% with the mouse orthologs. A polyclonal antibody was raised against the mouse GST/MSJ1(145–242) homologue protein in New Zealand rabbits and serum was affinity-purified using a GST-coupled Affigel-10 column. Whole ovary proteins were separated by SDS PAGE, immunoblotted and stained with the Hsp40 antibody. The protein displayed a MW of 38 KDa, in agreement with results obtained in other species. Immunofluorescence studies showed that Hsp40 is found in oocytes, granulosa and theca cells of follicle at all developmental stages. Pig ovaries, collected at the slaughterhouse, were exposed to 42°C for 1 h, to verify whether Hsp40 has a functional response to heat stress in this specie. Transcript level was compared with the control group, maintained at 38.5°C. mRNA was extracted from cumulus cells and pools of 5 oocytes, isolated from follicles of 3 to 5 mm. Semi-quantitative analysis was performed in the exponential phase of PCR amplification, using 28S as endogenous control. Data were analyzed with Quantity One (Bio-Rad) and Student-t statistical analysis was performed. Exposure of porcine ovaries to 42°C for 1 h resulted in a significant increase (P ≤ 0.05) of Hsp40 mRNA levels (2.4 ± 0.35 fold) in oocytes, while no significant raise was detected in cumulus cells. To our knowledge, this is the first demonstration that Hsp40 is expressed and responds to a thermal stress in pig ovary. Since this co-chaperone acts upstream to other heat shock protein-such as Hsp70- and it is specifically up regulated in the oocytes, our findings suggest that it may play an important protective role against heat stress infertility.

Short-term exercise training can improve myocardial tolerance to I/R without elevation in heat shock proteins

2001 ◽  
Vol 281 (3) ◽  
pp. H1346-H1352 ◽  
Author(s):  
Karyn L. Hamilton ◽  
Scott K. Powers ◽  
Takao Sugiura ◽  
Sunjoo Kim ◽  
Shannon Lennon ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Antioxidant Defenses ◽  
Control Group ◽  
Shock Proteins ◽  
Mnsod Activity ◽  
Over Time

We examined the effects of 3 days of exercise in a cold environment on the expression of left ventricular (LV) heat shock proteins (HSPs) and contractile performance during in vivo ischemia-reperfusion (I/R). Sprague-Dawley rats were divided into the following three groups ( n = 12/group): 1) control, 2) exercise (60 min/day) at 4°C (E-Cold), and 3) exercise (60 min/day) at 25°C (E-Warm). Left anterior descending coronary occlusion was maintained for 20 min, followed by 30 min of reperfusion. Compared with the control group, both the E-Cold and E-Warm groups maintained higher ( P < 0.05) LV developed pressure, first derivative of pressure development over time (+dP/d t), and pressure relaxation over time (−dP/d t) throughout I/R. Relative levels of HSP90, HSP72, and HSP40 were higher ( P < 0.05) in E-Warm animals compared with both control and E-Cold. HSP10, HSP60, and HSP73 did not differ between groups. Exercise increased manganese superoxide dismutase (MnSOD) activity in both E-Warm and E-Cold hearts ( P < 0.05). Protection against I/R-induced lipid peroxidation in the LV paralleled the increase in MnSOD activity whereas lower levels of lipid peroxidation were observed in both E-Warm and E-Cold groups compared with control. We conclude that exercise-induced myocardial protection against a moderate duration I/R insult is not dependent on increases in myocardial HSPs. We postulate that exercise-associated cardioprotection may depend, in part, on increases in myocardial antioxidant defenses.

Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension

2006 ◽  
Vol 100 (2) ◽  
pp. 541-547 ◽  
Author(s):  
Patricia O. Reger ◽  
Mary F. Barbe ◽  
Mamta Amin ◽  
Brian F. Renna ◽  
Leigh Ann Hewston ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heat Shock ◽  
Exercise Training ◽  
Heat Shock Protein ◽  
Endurance Training ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Rate Pressure Product ◽  
Protein Abundance ◽  
Myocardial Hypoperfusion

The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (age: 4 mo; N = 40) were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 h/day, 5 days/wk for 16 wk). Four groups were studied: WKY-SED ( n = 10), WKY-TRD ( n = 10), SHR-SED ( n = 10), and SHR-TRD ( n = 10). Blood pressure and heart rate were determined, and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product was significantly elevated in SHR relative to WKY, training-induced bradycardia reduced the rate-pressure product in SHR-TRD ( P < 0.05) without an attenuation in systolic blood pressure. Heart-to-body weight ratio was greater in both groups of SHR vs. WKY-SED ( P < 0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Postreperfusion 72-kDa heat shock protein abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05) and was highly correlated with absolute left ventricular functional recovery during reperfusion ( R2= 0.86, P < 0.0001). These data suggest that both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased postreperfusion 72-kDa heat shock protein abundance was, in part, associated with the cardioprotective phenotype observed in this study.

scholarly journals PERUBAHAN EKSPRESI HEAT SHOCK PROTEIN 70 AKIBAT PAPARAN MEDAN ELEKTROMAGNETIK EXTREMELY LOW FREQUENCY PADA MAKROFAG PERITONEUM MENCIT YANG DIINFEKSI Toxoplasma gondii

Biomedika ◽  
2015 ◽  
Vol 7 (2) ◽  
Author(s):  
Mochammad Arief Taufiqurochman
Keyword(s):  
Heat Shock ◽  
Toxoplasma Gondii ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Low Frequency ◽  
T Test ◽  
Control Group ◽  
Hsp 70 ◽  
Extremely Low Frequency ◽  
Promotor Region

Penelitian dilakukan untuk mengetahui efek paparan medan elektromagnetik ELF sebesar 100 μT 8 jam/ hari selama 2 dan 4 minggu terhadap ekspresi HSP 70 makrofag peritoneum mencit yang diinfeksi dengan Toxoplasma gondii. Jenis penelitian ini adalah Eksperimen Biomedik menggunakan rancangan randomized separate posttest control group designdengan hewan coba mencit strain Balb/c, melalui pengamatan ekspresi HSP 70 , terdiri dari 3 kelompok kontrol dan 4 kelompok perlakuan, tiap kelompok terdiri dari 4 hewan coba. Pengamatan jaringan menggunakan metode imunohistokimia indirek, hasilnya dianalisis menggunakan uji statistik Independent t-test antar kelompok setelah dilakukan uji homogenitas dan normalitas data penelitian ( α=0.05). Hasil penelitian menunjukkan bahwa akibat paparanME ELF dengan itensitas 100 μT selama 2 minggu belum mampu melemahkan atau memutus rantai DNA gen HSP 70 promotor region tetapi menimbulkan stres seluler yang berakibat teraktifasinya HSF 1 melalui konversi menjadi trimer yang akan meregulasi secara cepat sintesis HSP 70 . Paparan medan elektromegnetik ME ELF selama 4 minggu dapat melemahkan bahkan memutus rantai DNA hsp 70 promotor region, sehingga sintesis HSP akan terhambat secara signifikan (p<0.05). Terdapat peningkatan secara signifikan ekspresi HSP 70 makrofag peritoneum mencit yang terpapar ME ELF dengan itensitas 100 μT selama 2 minggu pada kelompok yang terinfeksi toxoplasma gondii dan terjadi penurunan secara signifikan ekspresi HSP 70 pada kelompok terpapar ME ELF selama4 minggu pada kelompok yang terinfeksi Toxoplasma gondi dibandingkan dengan konrol.Kata Kunci: Medan Electromagnetik ELF, HSP 70, Makrofag, Toxoplasma gondii.

scholarly journals Pulmonary prophylactic impact of melatonin and/or quercetin: A novel therapy for inflammatory hypoxic stress in rats

2017 ◽  
Vol 67 (1) ◽  
pp. 125-135 ◽  
Author(s):  
Nouf M. Al-Rasheed ◽  
Laila Fadda ◽  
Hala A. Attia ◽  
Iman A. Sharaf ◽  
Azza M. Mohamed ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Lung Tissue ◽  
Inflammatory Mediators ◽  
Histopathological Examination ◽  
Serum Levels ◽  
Control Group ◽  
Novel Therapy ◽  
Protein Expressions ◽  
Pre Treatment

AbstractThe study aims to compare, through histological and biochemical studies, the effects of quercetin, melatonin and their combination in regulation of immuno-inflammatory mediators and heat shock protein expressions in sodium nitrite induced hypoxia in rat lungs. The results revealed that NaNO2injection caused a significant decrease in Hb in rats, while serum levels of TNF-α, IL-6 and CRP, VEGF and HSP70 were elevated compared to the control group. Administration of melatonin, quercetin or their combination before NaNO2injection markedly reduced these parameters. Histopathological examination of the lung tissue supported these biochemical findings. The study suggests that melatonin and/or quercetin are responsible for lung tissue protection in hypoxia by downregulation of immuno-inflammatory mediators and heat shock protein expressions. Pre-treatment of hypoxic animals with a combination of melatonin and quercetin was effective in modulating most of the studied parameters to near-normal levels.

Functional Evaluation of the Medtronic Stentless Porcine Xenograft Mitral Valve in Sheep

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Paul Dagum ◽  
G. Randall Green ◽  
Tomasz A. Timek ◽  
George T. Daughters ◽  
Linda E. Foppiano ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Lateral Displacement ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Attractive Alternative ◽  
Functional Evaluation ◽  
Mitral Valves ◽  
Hemodynamic Performance ◽  
Porcine Xenograft

Background —Recently, renewed interest in allograft and stentless “freehand” bileaflet xenograft mitral valve replacement has arisen. The variability of human papillary tip anatomy and scarcity of donors limit allograft availability, making xenograft mitral valves an attractive alternative; however, these valves require new surgical implantation techniques, and assessment of their hemodynamics and functional geometry is lacking. Methods —Seven sheep underwent implantation of a new stentless, glutaraldehyde-preserved porcine mitral valve (Physiological Mitral Valve [PMV], Medtronic) and were studied acutely under open-chest conditions. A new method of retrograde cardioplegia was developed. Hemodynamic valve function was assessed by epicardial Doppler echocardiography. 3D motion of miniature radiopaque markers sutured to the valve leaflets, annulus, and papillary tips was measured. Six other sheep with implanted markers served as controls. Results —Both papillary muscle tips avulsed in the first animal, leaving 6 other animals. Mitral regurgitation was not observed in any xenograft valve. The peak and mean transvalvular gradients were 4.6±1.8 mm Hg and 2.6±1.5 mm Hg, respectively. The average mitral valve area was 5.7±1.6 cm 2 . Valve closure in the xenograft group occurred later (30±11 ms, P <0.015) and at higher left-ventricular pressure (61±9 mm Hg, P <0.001) than in the control group; furthermore, leaflet coaptation was displaced more apically (5.6±2.2 mm, P <0.001) and septally (5.8±1.5 mm, P <0.001), and the anterolateral papillary tip underwent greater septal-lateral displacement (2.7±1.5 mm, P <0.001). Annular contraction during the cardiac cycle was similar in the 2 groups (xenograft 9.2±4.5% versus control 10.6±4.5% [mean±SD; 2-factor ANOVA model]). Conclusions —Successful freehand stentless porcine mitral valve implantation is feasible in sheep and was associated with excellent early postoperative hemodynamics. Physiological mitral valve annular contraction and functional leaflet closure mechanics were preserved. Long-term valve durability, calcification, and hemodynamic performance remain to be determined in models.

scholarly journals Melatonin protects mouse oocyte from heat stress damage

2020 ◽  
Vol 6 (3) ◽  
pp. 13
Author(s):  
Haiyan Du ◽  
Shouhong Wang ◽  
Weiwei Huang
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Spindle Assembly ◽  
Shock Group ◽  
Mouse Oocyte ◽  
Control Group ◽  
Mouse Oocytes ◽  
Early Apoptosis ◽  
Maturation Rate

Objective: To explore the potential effect of melatonin on the in-vitro maturation of mouse oocytes under heat shock condition.Methods: This study used a heat shock model of mouse oocyte maturation. The oocytes were randomly divided into three groups: control group, heat shock group and heat shock + melatonin group, in order to evaluate the effect of 1×10−9 mol/L melatonin on the quality of oocytes after heat shock.Results: In comparison with the control group, the maturation rate of mouse oocytes in heat shock group was significantly decreased [(33.00 ± 0.07)% vs. (85.00 ± 0.03)%, p < .01], with abnormal spindle assembly, and the early apoptosis rate was significantly increased [(59.7 ± 4.5)% vs. (22.0 ± 3.5)%, p < .01]. Compared with heat shock group, the maturation rate ofoocytes was significantly increased in heat shock + melatonin group [(70.00 ± 0.05)% vs. (33.00 ± 0.07)%, p < .01], meanwhile, the spindle abnormality rate and the early apoptosis rate were significantly decreased accordingly [(37.3 ± 6.1)% vs. (59.7 ± 4.5)%, p < .01]. The expression level of heat shock protein 70 was significantly up-regulated in heat shock + melatonin group in comparison with other two groups (p < .01).Conclusions: By regulating the over-expression of heat shock protein 70, melatonin can improve the declined maturation rate of oocytes and the increased rates of spindle assembly abnormality and early apoptosis caused by heat shock.

One-day cold perfusion of bimakalim and butanedione monoxime restores ex situ cardiac function

1996 ◽  
Vol 271 (5) ◽  
pp. H1884-H1892 ◽  
Author(s):  
D. F. Stowe ◽  
B. M. Graf ◽  
S. Fujita ◽  
G. J. Gross
Keyword(s):  
Cardiac Function ◽  
Myocardial Function ◽  
Left Ventricular Pressure ◽  
Katp Channels ◽  
Left Ventricular ◽  
Ex Situ ◽  
Control Group ◽  
Cardiac Efficiency ◽  
Time Control ◽  
Butanedione Monoxime

Bimakalim (Bim), an opener of ATP-sensitive K+ (KATP) channels, was given alone or with 2,3-butanedione monoxime (BDM), a reversible uncoupler of contractility, to protect myocardial function during 1 day of hypothermia. Left ventricular pressure (LVP), coronary flow (CF), percent O2 extraction (%O2E), and cardiac efficiency were measured in 96 isolated, perfused guinea pig hearts divided into seven groups: 1) cold control (no drugs); 2) BDM; 3) Bim; 4) BDM + Bim; 5) BDM + glibenclamide (Glib, a blocker of KATP channels); 6) BDM + Bim + Glib; and 7) time control (6 h warm perfusion only). Drugs were given before, during, and initially after 22 h of low CF at 3.8 degrees C. At 26 h (cold groups) or 4 h (warm group) LVP (mmHg; means +/- SE) was similar for time control (94 +/- 4) and BDM + Bim (92 +/- 4) groups, lower and equivalent in the BDM (65 +/- 7) and BDM + Bim + Glib (64 +/- 7) groups, but LVP was higher than in the Bim group (46 +/- 3), and lowest in the cold control (30 +/- 8) group. In addition, only in the BDM + Bim group were basal CF, %O2E, and cardiac efficiency returned to values obtained in the time control group. Epinephrine increased LVP to that of the time control (106 +/- 3) group only in the BDM + Bim group (106 +/- 3) after hypothermia, and CF increases with adenosine, 5-hydroxytryptamine, and nitroprusside were similar to that of the time control group only in the BDM + Bim group after hypothermia. All of the effects of Bim were reversed by Glib. These results indicate that Bim, given with BDM, effectively preserves myocardial function and metabolism as well as inotropic and vasodilatory reserve during long-term hypothermic preservation as if the 1-day hypothermic state had not been instituted. Because the beneficial effects of Bim are blocked by Glib, the protective effect of Bim likely results from maintained KATP channel opening. Treatment with exogenous KATP openers may prove useful in preserving cardiac function in the transplanted heart.

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