Heat Shock Proteins: Endogenous Modulators of Apoptotic Cell Death

2001 ◽  
Vol 286 (3) ◽  
pp. 433-442 ◽  
Author(s):  
Carmen Garrido ◽  
Sandeep Gurbuxani ◽  
Luigi Ravagnan ◽  
Guido Kroemer
Keyword(s):  
Cell Death ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Shock Proteins ◽  
Endogenous Modulators

scholarly journals Necrotic but not apoptotic cell death releases heat shock proteins, which deliver a partial maturation signal to dendritic cells and activate the NF-κB pathway

2000 ◽  
Vol 12 (11) ◽  
pp. 1539-1546 ◽  
Author(s):  
Sreyashi Basu ◽  
Robert J. Binder ◽  
Ryuichiro Suto ◽  
Kirstin M. Anderson ◽  
Pramod K. Srivastava
Keyword(s):  
Cell Death ◽  
Dendritic Cells ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Shock Proteins

Extracellular heat shock proteins protect U937 cells from H2O2-induced apoptotic cell death

2015 ◽  
Vol 412 (1-2) ◽  
pp. 19-26 ◽  
Author(s):  
Lourdes Franco ◽  
Jorge Terrinca ◽  
Ana B. Rodríguez ◽  
Javier Espino ◽  
José A. Pariente
Keyword(s):  
Cell Death ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
U937 Cells ◽  
Shock Proteins

scholarly journals SECOND ANOXIA-REOXYGENATION DOES NOT CAUSE THE APOPTOTIC CELL DEATH OF NEONATAL CARDIOMYOCYTES: POSSIBLE ROLE OF CHANGES OF mRNA EXPRESSION OF CYTOPROTECTIVE GENES

2009 ◽  
Vol 55 (1) ◽  
pp. 19-26
Author(s):  
O.V. Surova ◽  
◽  
V.E. Dosenko ◽  
V.S. Nagibin ◽  
L.V. Tumanovskaya ◽  
...  
Keyword(s):  
Cell Death ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Apoptotic Cell ◽  
First Episode ◽  
Mrna Levels ◽  
Neonatal Cardiomyocytes ◽  
Genes Expression ◽  
Shock Proteins

The cells death and genes expression in neonatal cardiomyocytes culture at two anoxia-reoxygenation modeling were investigated. The primary culture of neonatal cardiomyocytes was under­gone 30 min of anoxia followed by 24 h (A-R1) and the second anoxia-reoxygenation – 30 min and 60 min respectively (A-R2). The percentages of living, necrotic, apoptotic and autophagic cells were determined by staining with bis-benzimide, propidium iodide and monodansylcadaverine. Anoxia-reoxygenation sig­nificantly influenced the ratio of living, necrotic, apoptotic and autophagic cells both at its first A-R1 and second A-R2 epi­sodes. It was shown that the main mechanism of cell death after the both periods of anoxia-reoxygenation is necrosis. The changes of mRNA levels of genes of heat shock proteins HSP70 and HSP90, antiapoptotic protein Bcl2 and key regulator of au-tophagy FRAP in cardiomyocytes culture were established. The data obtained allow to make suggestion that in 24 h after the first episode of anoxia-reoxygenation A-R1 the overexpression of heat shock proteins starts the cascade of reactions that causes the necrotic cell death prevalent and the blocking of apoptotic program at second anoxia-reoxygenation A-R2.

scholarly journals In situ localization of heat-shock proteins and cell death labelling in the salivary gland of acaricide-treated honeybee larvae

Apidologie ◽  
2006 ◽  
Vol 37 (5) ◽  
pp. 507-516 ◽  
Author(s):  
Elaine C.M. Silva-Zacarin ◽  
Ales Gregorc ◽  
Regina L.M. Silva de Moraes
Keyword(s):  
Cell Death ◽  
Salivary Gland ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Shock Proteins

scholarly journals Immunomodulation of function of small heat shock proteins prevents their assembly into heat stress granules and results in cell death at sublethal temperatures

2004 ◽  
Vol 41 (2) ◽  
pp. 269-281 ◽  
Author(s):  
Sergey Miroshnichenko ◽  
Joanna Tripp ◽  
Uta zur Nieden ◽  
Dieter Neumann ◽  
Udo Conrad ◽  
...  
Keyword(s):  
Cell Death ◽  
Heat Stress ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Stress Granules ◽  
Small Heat Shock Proteins ◽  
Shock Proteins

scholarly journals Activation of the heat shock response in a primary cellular model of motoneuron neurodegeneration-evidence for neuroprotective and neurotoxic effects

2009 ◽  
Vol 14 (2) ◽  
Author(s):  
Bernadett Kalmar ◽  
Linda Greensmith
Keyword(s):  
Cell Death ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Apoptotic Cell ◽  
Experimental Conditions ◽  
Pharmacological Agents ◽  
Shock Response ◽  
Induced Apoptosis ◽  
Shock Proteins ◽  
The Relationship

AbstractPharmacological up-regulation of heat shock proteins (hsps) rescues motoneurons from cell death in a mouse model of amyotrophic lateral sclerosis. However, the relationship between increased hsp expression and neuronal survival is not straightforward. Here we examined the effects of two pharmacological agents that induce the heat shock response via activation of HSF-1, on stressed primary motoneurons in culture. Although both arimoclomol and celastrol induced the expression of Hsp70, their effects on primary motoneurons in culture were significantly different. Whereas arimoclomol had survival-promoting effects, rescuing motoneurons from staurosporin and H2O2 induced apoptosis, celastrol not only failed to protect stressed motoneurons from apoptosis under same experimental conditions, but was neurotoxic and induced neuronal death. Immunostaining of celastrol-treated cultures for hsp70 and activated caspase-3 revealed that celastrol treatment activates both the heat shock response and the apoptotic cell death cascade. These results indicate that not all agents that activate the heat shock response will necessarily be neuroprotective.

Heat shock protein synthesis over time in infective Trichinella spiralis larvae raised in suboptimal culture conditions

2004 ◽  
Vol 78 (3) ◽  
pp. 243-247 ◽  
Author(s):  
J. Martinez ◽  
J. Perez-Serrano ◽  
W.E. Bernadina ◽  
I. Rincon ◽  
F. Rodriguez-Caabeiro
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Heat Shock Protein ◽  
Trichinella Spiralis ◽  
Culture Conditions ◽  
Induce Stress ◽  
Shock Proteins ◽  
Over Time

AbstractChanges in the viability, infectivity and heat shock protein (Hsp) levels are reported in Trichinella spiralis first stage larvae (L1) stored in 199 medium for up to seven days at 37°C. These conditions induce stress that the larvae, eventually, cannot overcome. After three days of storage, the infectivity and viability were unchanged, although higher Hsp70 levels were observed. After this time, larvae gradually lost viability and infectivity, coinciding with a decrease in Hsp70 and Hsp90 and an increase in actin (a housekeeping protein). In addition, a possibly inducible heat shock protein, Hsp90i, appeared as constitutive Hsp90 disappeared. No significant changes in Hsp60 levels were detected at any time. These results suggest that heat shock proteins initially try to maintain homeostasis, but on failing, may be involved in cell death.

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