Stress protein response in two sibling species of Marenzelleria (Polychaeta: Spionidae): Is there an influence of acclimation salinity?

2006 ◽  
Vol 144 (4) ◽  
pp. 451-462 ◽  
Author(s):  
M. Blank ◽  
R. Bastrop ◽  
K. Jürss
Keyword(s):  
Sibling Species ◽  
Stress Protein ◽  
Protein Response

The stress protein response in cultured neurons: Characterization and evidence for a protective role in excitotoxicity

Neuron ◽  
1991 ◽  
Vol 7 (6) ◽  
pp. 1053-1060 ◽  
Author(s):  
Daniel H. Lowenstein ◽  
Pak H. Chan ◽  
Michael F. Miles
Keyword(s):  
Stress Protein ◽  
Protective Role ◽  
Cultured Neurons ◽  
Protein Response

Alpha-lipoic acid does not alter stress protein response to acute exercise in diabetic brain

2010 ◽  
Vol 28 (8) ◽  
pp. 644-650 ◽  
Author(s):  
Jani Lappalainen ◽  
Zekine Lappalainen ◽  
Niku K. J. Oksala ◽  
David E. Laaksonen ◽  
Savita Khanna ◽  
...  
Keyword(s):  
Lipoic Acid ◽  
Acute Exercise ◽  
Stress Protein ◽  
Alpha Lipoic Acid ◽  
Diabetic Brain ◽  
Protein Response

scholarly journals Oxidation of Bilirubin Produces Compounds that Cause Prolonged Vasospasm of Rat Cerebral Vessels: A Contributor to Subarachnoid Hemorrhage–Induced Vasospasm

2002 ◽  
Vol 22 (4) ◽  
pp. 472-478 ◽  
Author(s):  
Joseph F. Clark ◽  
Melinda Reilly ◽  
Frank R. Sharp
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Stress Protein ◽  
Cerebral Vessels ◽  
Oxidation Products ◽  
Adult Rats ◽  
Cranial Window ◽  
Related Stress ◽  
Protein Response

The authors have previously shown that bilirubin-oxidation products (BOXes) are present in CSF of subarachnoid hemorrhage patients with vasospasm, and that BOXes cause vasoconstriction in vitro. This study determined whether BOXes cause vasospasm in vivo. Identical volumes of either lysed blood or standardized amounts of BOXes were injected into the cisterna magna of adult rats. BOX injections caused 6 of 10 rats to die within 10 minutes, whereas 12 of 12 rats survived for 24 hours after blood injections. The mechanism for this significant ( P ⩽ 0.01) increase in mortality was unclear. To directly test whether BOXes produced vasospasm, a cranial window technique was used. Application of 20 μL of 10-μmol/L bilirubin had little effect on the vessels. However, application of BOXes produced marked, dose-dependent small artery and arteriole vasospasm that approached a 90% decrease in diameter by 40 minutes after application in some vessels, and persisted for at least 24 hours. To determine if BOX-mediated vasospasm led to cortical injury, histology and immunocytochemistry were performed on animals that survived for 24 hours. There was a BOX-related stress protein response for HSP25 and HSP32 (HO-1) without evidence of infarction. The finding that the BOXes produce vasospasm of cerebral vessels in vivo, in conjunction with BOXes being found in CSF of vasospasm patients, supports our hypothesis that BOXes contribute to or cause cerebral vasospasm after subarachnoid hemorrhage.

Stress protein response and catalase activity in freshwater planarian Dugesia (Girardia) schubarti exposed to copper

2003 ◽  
Vol 56 (3) ◽  
pp. 351-357 ◽  
Author(s):  
Temenouga N. Guecheva ◽  
Bernardo Erdtmann ◽  
Mara S. Benfato ◽  
João A.P. Henriques
Keyword(s):  
Catalase Activity ◽  
Stress Protein ◽  
Freshwater Planarian ◽  
Protein Response

scholarly journals The stress protein response transiently inhibits STAT1 signaling via inhibition of Hsp90 binding

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Marybeth Howard ◽  
Jeremie Roux ◽  
Jean‐Francois Pittet
Keyword(s):  
Stress Protein ◽  
Stat1 Signaling ◽  
Protein Response

scholarly journals Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury

2006 ◽  
Vol 291 (3) ◽  
pp. L354-L361 ◽  
Author(s):  
Michael T. Ganter ◽  
Lorraine B. Ware ◽  
Marybeth Howard ◽  
Jérémie Roux ◽  
Brandi Gartland ◽  
...  
Keyword(s):  
Heat Shock ◽  
Pulmonary Edema ◽  
Stress Protein ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial ◽  
Edema Fluid ◽  
Protein Response ◽  
Alveolar Edema

Previous studies have shown that heat shock protein 72 (Hsp72) is found in the extracellular space (eHsp72) and that eHsp72 has potent immunomodulatory effects. However, whether eHsp72 is present in the distal air spaces and whether eHsp72 could modulate removal of alveolar edema is unknown. The first objective was to determine whether Hsp72 is released within air spaces and whether Hsp72 levels in pulmonary edema fluid would correlate with the capacity of the alveolar epithelium to remove alveolar edema fluid in patients with ALI/ARDS. Patients with hydrostatic edema served as controls. The second objective was to determine whether activation of the stress protein response (SPR) caused the release of Hsp72 into the extracellular space in vivo and in vitro and to determine whether SPR activation and/or eHsp72 itself would prevent the IL-1β-mediated inhibition of the vectorial fluid transport across alveolar type II cells. We found that eHsp72 was present in plasma and pulmonary edema fluid of ALI patients and that eHsp72 was significantly higher in pulmonary edema fluid from patients with preserved alveolar epithelial fluid clearance. Furthermore, SPR activation in vivo in mice and in vitro in lung endothelial, epithelial, and macrophage cells caused intracellular expression and extracellular release of Hsp72. Finally, SPR activation, but not eHsp72 itself, prevented the decrease in alveolar epithelial ion transport induced by exposure to IL-1β. Thus SPR may protect the alveolar epithelium against oxidative stress associated with experimental ALI, and eHsp72 may serve as a marker of SPR activation in the distal air spaces of patients with ALI.

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