scholarly journals Consequences of heat shock protein 72 (Hsp72) expression and activity on stress-induced apoptosis in CD30+ NPM–ALK+ anaplastic large-cell lymphomas

Leukemia ◽  
2012 ◽  
Vol 26 (6) ◽  
pp. 1375-1382 ◽  
Author(s):  
P Bonvini ◽  
E Zorzi ◽  
L Mussolin ◽  
M Pillon ◽  
C Romualdi ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Large Cell ◽  
Heat Shock Protein 72 ◽  
Induced Apoptosis ◽  
Hsp72 Expression ◽  
Expression And Activity

scholarly journals Targeting heat shock protein 72 enhances Hsp90 inhibitor-induced apoptosis in myeloma

Leukemia ◽  
2010 ◽  
Vol 24 (10) ◽  
pp. 1804-1807 ◽  
Author(s):  
E L Davenport ◽  
A Zeisig ◽  
L I Aronson ◽  
H E Moore ◽  
S Hockley ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Hsp90 Inhibitor ◽  
Heat Shock Protein 72 ◽  
Induced Apoptosis

scholarly journals Regulated Overexpression of Heat Shock Protein 72 Protects Madin-Darby Canine Kidney Cells from the Detrimental Effects of High Urea Concentrations

2001 ◽  
Vol 12 (12) ◽  
pp. 2565-2571 ◽  
Author(s):  
Wolfgang Neuhofer ◽  
Karin Lugmayr ◽  
Maria-Luisa Fraek ◽  
Franz-X Beck
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Mdck Cells ◽  
Heat Shock Protein 72 ◽  
Madin Darby Canine Kidney ◽  
Lactate Dehydrogenase Activity ◽  
Hsp72 Expression ◽  
Darby Canine Kidney ◽  
Canine Kidney ◽  
Medullary Cells

ABSTRACT. Exposure of renal medullary cells to elevated extracellular NaCl concentrations is associated with increased heat shock protein 72 (HSP72) expression and improved resistance to subsequent exposure to a high urea concentration (600 mM). To establish a causal relationship between HSP72 expression and protection against high urea concentrations, HSP72 was inducibly overexpressed in Madin-Darby canine kidney (MDCK) cells, in the absence of hypertonic stress before urea exposure. For this purpose, the human stress-inducible HSP72 gene was cloned downstream from a dexamethasone (DEX)-inducible promoter in the eukaryotic expression vector pLKneo. This construct allowed robust induction of HSP72 by exposure of stably transfected MDCK cells (MDCK-LK72) to 0.1 μM DEX. Increased HSP72 abundance significantly improved survival rates after 24-h exposure of the cells to medium containing 600 mM urea (14 versus 43%). In mock-transfected or wild-type cells, DEX had no significant effect on HSP72 abundance or urea resistance. In accordance with those findings, lactate dehydrogenase activity in the supernatant was significantly reduced, compared with appropriate control samples, only in MDCK-LK72 cells overexpressing HSP72. Labeling with annexin V-FITC and propidium iodide, followed by flow cytometry, revealed that overexpression of HSP72 was associated with a reduction in the number of apoptotic-lysed cells, a concomitant retardation of apoptosis, and an increase in the number of viable cells. These data support the view that HSP72, which is very abundant in the renal inner medulla, is an important component of the defense mechanism of medullary cells against extreme concentrations of urea.

scholarly journals Impaired heat shock protein 72 expression in women with polycystic ovary syndrome following a supervised exercise programme

2019 ◽  
Vol 25 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Rebecca V Vince ◽  
Richard J Kirk ◽  
Myint M Aye ◽  
Stephen L Atkin ◽  
Leigh A Madden
Keyword(s):  
Heat Shock ◽  
Polycystic Ovary Syndrome ◽  
Heat Shock Protein ◽  
Polycystic Ovary ◽  
Exercise Programme ◽  
Control Group ◽  
Heat Shock Protein 72 ◽  
Ovary Syndrome ◽  
Baseline Values ◽  
Hsp72 Expression

AbstractInduction of heat shock protein expression and the heat shock (stress) response are seen in exercise. This exercise-induced response is thought protective against cellular stress through the expression of heat shock proteins. The highly inducible heat shock protein 72 (HSP72) has been shown to be expressed in a number of stress-related conditions, but not investigated in women with polycystic ovary syndrome (PCOS). Twenty-one women (10 controls, 11 with PCOS) concluded an 8-week supervised, moderate-intensity exercise programme. Monocytes and lymphocytes were analysed by flow cytometry for HSP72 expression from blood samples prior to, mid-way and at the completion of the programme. The monocyte HSP72 expression showed an increase from baseline values through mid-way (p = 0.025), and at the completion of the programme (p = 0.011) only in the control group, the PCOS group showed no significant change. This pattern was similar for lymphocyte HSP72 expression where a significant increase was found at the completion of the programme (p = 0.01) only in the control group. The magnitude of increased HSP72 expression following completion of the programme was linked to baseline values only in the control group. In conclusion, increased HSP72 expression to exercise over an 8-week period was seen in control but not in PCOS women, suggesting that there is an impairment of HSP72 expression in response to exercise in these women.

Extracellular heat shock protein 72 protects schwann cells from hydrogen peroxide-induced apoptosis

2012 ◽  
Vol 90 (6) ◽  
pp. 1261-1269 ◽  
Author(s):  
Xinjing Luo ◽  
Lingjian Tao ◽  
Peng Lin ◽  
Xuanrong Mo ◽  
Haixiao Chen
Keyword(s):  
Hydrogen Peroxide ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Schwann Cells ◽  
Heat Shock Protein 72 ◽  
Induced Apoptosis

scholarly journals Heat Shock Protein 72 Modulates Pathways of Stress-induced Apoptosis

1998 ◽  
Vol 273 (27) ◽  
pp. 17147-17153 ◽  
Author(s):  
Katherine A. Buzzard ◽  
Amato J. Giaccia ◽  
Marilyn Killender ◽  
Robin L. Anderson
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 72 ◽  
Induced Apoptosis

Correlation between Clinicopathology and Expression of Heat Shock Protein 72 in Human Hepatocellular Carcinoma

2014 ◽  
Vol 556-562 ◽  
pp. 23-26
Author(s):  
Yan Fang ◽  
Xiao Ping Wang ◽  
Huan Ping Lin ◽  
Bing Xu ◽  
Jing Gang Fang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Lymph Node ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Human Hepatocellular Carcinoma ◽  
Tumor Infiltration ◽  
Heat Shock Protein 72 ◽  
Hepatocellular Carcinomas ◽  
Cancer Tissues ◽  
Hsp72 Expression

Heat shock protein 72 (HSP72) is highly expressed in cancer tissues. Recent studies indicate the possible roles of HSP72 in the development and progression of hepatocellular carcinomas but detailed information is still ambiguous. The aim of the study is to investigate the correlation between clinicopathology and immunolocalization of HSP72 in human hepatocellular carcinoma. Immunohistochemistry demonstrated that HSP72 expression in hepatocellular carcinomas with metastasis was significantly higher than those with non-metastasis. HSP72 expression was significantly associated with the presence of tumor infiltration, lymph node and remote metastasis.

scholarly journals Receptor-Mediated Suppression of Cardiac Heat-Shock Protein 72 Expression by Testosterone in Male Rat Heart

Endocrinology ◽  
2007 ◽  
Vol 148 (7) ◽  
pp. 3148-3155 ◽  
Author(s):  
Hiroaki Kohno ◽  
Naohiko Takahashi ◽  
Tetsuji Shinohara ◽  
Tatsuhiko Ooie ◽  
Kunio Yufu ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Ischemia Reperfusion ◽  
Male Rat ◽  
Sprague Dawley ◽  
Heat Shock Protein 72 ◽  
Heat Shock Element ◽  
Sprague Dawley Rats ◽  
The Impact ◽  
Hsp72 Expression

The impact of testosterone on cardiac expression of heat-shock protein 72 (HSP72) remains to be elucidated. Male Sprague Dawley rats 10 wk of age (adult) were castrated. Four weeks later, testosterone (10 mg/kg, ip) was administered as a single dose, followed by the application of hyperthermia (HT) (43 C) at 6 h after testosterone administration. Twenty-four hours later, each heart was isolated. Cardiomyocytes were prepared from 3- to 5-d-old Wistar rats and male Sprague Dawley rats 10 wk of age. Testosterone (0.1–10 μm) was added to the medium, followed by the application of HT (42 C). Twenty-four hours later, cells were collected. We observed the following: 1) Exogenous testosterone suppressed HT-induced HSP72 expression, but castration alone had no influence. 2) HT resulted in better reperfusion-induced cardiac performance in castrated rats comparable with sham-operated rats, which was inhibited by testosterone. The number of apoptotic cells after ischemia/reperfusion was also increased by testosterone. 3) HT-induced HSP72 expression in cultured cardiomyocytes was suppressed by testosterone. 4) HT resulted in less damage to cells, including apoptosis, in response to hypoxia/reoxygenation, which was inhibited by testosterone. 5) Flutamide, a testosterone receptor blocker, cancelled the suppressive effects of testosterone on HSP72 expression. 6) The HT-induced increase in heat-shock factor 1 activity to bind to heat-shock element DNA was suppressed by testosterone, and this was reversed by flutamide. Our results indicate that testosterone potentially has inhibitory effects on cardiac HSP72 expression by modulating transcription, through testosterone receptor-mediated genomic mechanisms.

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