scholarly journals A novel kinase function of a nucleoside-diphosphate-kinase homologue in Porphyromonas gingivalis is critical in subversion of host cell apoptosis by targeting heat-shock protein 27

2018 ◽  
Vol 20 (5) ◽  
pp. e12825 ◽  
Author(s):  
Jungnam Lee ◽  
JoAnn S. Roberts ◽  
Kalina R. Atanasova ◽  
Nityananda Chowdhury ◽  
Özlem Yilmaz
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Host Cell ◽  
Porphyromonas Gingivalis ◽  
Cell Apoptosis ◽  
Nucleoside Diphosphate Kinase ◽  
Heat Shock Protein 27 ◽  
Host Cell Apoptosis ◽  
Kinase Homologue

scholarly journals ATP scavenging by the intracellular pathogen Porphyromonas gingivalis inhibits P2X7-mediated host-cell apoptosis

2008 ◽  
Vol 10 (4) ◽  
pp. 863-875 ◽  
Author(s):  
Özlem Yilmaz ◽  
Luyu Yao ◽  
Kazuhiko Maeda ◽  
Timothy M. Rose ◽  
Emma L. Lewis ◽  
...  
Keyword(s):  
Host Cell ◽  
Porphyromonas Gingivalis ◽  
Cell Apoptosis ◽  
Intracellular Pathogen ◽  
Host Cell Apoptosis

scholarly journals Human heat shock protein 27-overexpressing mice are protected against acute kidney injury after hepatic ischemia and reperfusion

2009 ◽  
Vol 297 (4) ◽  
pp. F885-F894 ◽  
Author(s):  
Sang Won Park ◽  
Sean W. C. Chen ◽  
Mihwa Kim ◽  
Vivette D. D'Agati ◽  
H. Thomas Lee
Keyword(s):  
Acute Kidney Injury ◽  
Endothelial Cell ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cell Apoptosis ◽  
Kidney Injury ◽  
Heat Shock Protein 27 ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Endothelial Cell Apoptosis ◽  
Liver And Kidney

Liver ischemia-reperfusion injury (IRI) causes acute kidney injury (AKI) in mice characterized by renal endothelial cell apoptosis, renal tubular necrosis, inflammation, and filamentous (F)-actin disruption. Since heat shock protein 27 (HSP27) protects against apoptosis, necrosis, and stabilizes F-actin, we questioned whether overexpression of human HSP27 (huHSP27 OE) in mice would attenuate AKI after liver IRI. Twenty-four hours after hepatic IRI, HSP27 wild-type (WT) mice developed acute liver and kidney injury with elevated plasma alanine aminotransferase and creatinine, a reduced glomerular filtration rate, and histological evidence of renal endothelial cell apoptosis and tubular injury (necrosis, vacuolization, and F-actin disruption). The huHSP27 OE mice, however, were significantly protected against both liver and kidney injury after hepatic IRI. The huHSP27 OE mice also showed less induction of several proinflammatory mRNAs (TNF-α, MIP-2, and keratinocyte-derived cytokine), neutrophil infiltration, and reduction in apoptosis (terminal deoxynucleotidyl transferase biotin-dUTP nick end-labeling assay and DNA laddering) in the kidney compared with the HSP27 WT mice. Moreover, the huHSP27 OE mice showed significantly less disruption of F-actin in renal proximal tubules and better preserved vascular endothelial cell integrity compared with the huHSP27 OE mice. Finally, the kidney plays a major role in the hepatoprotective effects of huHSP27 overexpression as the hepatoprotection was reduced or abolished in mice subjected to unilateral or bilateral nephrectomy, respectively. Our results show that overexpression of huHSP27 protects against hepatic injury and AKI associated with liver IRI in vivo. Harnessing the mechanisms of cytoprotection with renal HSP27 may lead to new therapies for the perioperative AKI and liver injury associated with liver IRI.

765: Modified Expression of Heat Shock Protein 27 in Renal Cell Carcinoma

2004 ◽  
Vol 171 (4S) ◽  
pp. 203-203
Author(s):  
Cecilia Sarto ◽  
Paolo Favini ◽  
Cristina Valsecchi ◽  
Stefano Casellato ◽  
Fulvio Magni ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Heat Shock Protein 27

Protektive Wirkung von Heat Shock Protein 27 in der Magenmukosa

2005 ◽  
Vol 43 (05) ◽  
Author(s):  
M Ebert ◽  
C Schäfer ◽  
J Hoffmann ◽  
C Kubisch ◽  
G Treiber ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 27 ◽  
Protektive Wirkung
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