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

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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In situ localization of the 60 k protein of Helicobacter pylori, which belongs to the family of heat shock proteins, by immuno-electron microscopy

Zentralblatt für Bakteriologie ◽

10.1016/s0934-8840(11)80942-4 ◽

1993 ◽

Vol 280 (1-2) ◽

pp. 73-85 ◽

Cited By ~ 7

Author(s):

B. Eschweiler ◽

B. Bohrmann ◽

B. Gerstenecker ◽

E. Schiltz ◽

M. Kist

Keyword(s):

Electron Microscopy ◽

Helicobacter Pylori ◽

Heat Shock ◽

Heat Shock Proteins ◽

The Family ◽

Immuno Electron Microscopy ◽

Shock Proteins

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In situ cell-based ELISA for determination of multiple heat shock proteins

Toxicology ◽

10.1016/j.tox.2006.05.095 ◽

2006 ◽

Vol 226 (1) ◽

pp. 71 ◽

Cited By ~ 1

Author(s):

Mudafara Bengleil ◽

Jeffrey R. Fry

Keyword(s):

Heat Shock ◽

Heat Shock Proteins ◽

Shock Proteins

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

Fiziolohichnyĭ zhurnal ◽

10.15407/fz55.01.019 ◽

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.

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