Vascular reactivity in old spontaneously hypertensive stroke-prone rats- effects of in vitro ischemia/reperfusion injury

2021 ◽  
Vol 04 (03) ◽  
Author(s):  
Sevil Korkmaz-Icöz ◽  
Mona Isabella Benker ◽  
Shiliang Li ◽  
Sivakkanan Loganathan ◽  
Patricia Kraft ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Vascular Reactivity ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spontaneously Hypertensive ◽  
In Vitro Ischemia

Vascular reactivity in old spontaneously hypertensive stroke-prone rats- effects of in vitro ischemia/reperfusion injury

2021 ◽  
Vol 04 (03) ◽  
Author(s):  
Sevil Korkmaz-Icöz ◽  
Mona Isabella Benker ◽  
Shiliang Li ◽  
Sivakkanan Loganathan ◽  
Patricia Kraft ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Vascular Reactivity ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spontaneously Hypertensive ◽  
In Vitro Ischemia

A novel in vitro ischemia/reperfusion injury model

2009 ◽  
Vol 32 (3) ◽  
pp. 421-429 ◽  
Author(s):  
Won Hee Lee ◽  
Sungkwon Kang ◽  
Pavlos P. Vlachos ◽  
Yong Woo Lee
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
In Vitro Ischemia ◽  
Injury Model

The Ste20-like kinase SLK promotes p53 transactivation and apoptosis

2009 ◽  
Vol 297 (4) ◽  
pp. F971-F980 ◽  
Author(s):  
Andrey V. Cybulsky ◽  
Tomoko Takano ◽  
Julie Guillemette ◽  
Joan Papillon ◽  
Rildo A. Volpini ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Kidney Development ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter ◽  
Enhancer Element ◽  
Double Mutation ◽  
Reporter Activity ◽  
In Vitro Ischemia

Expression and activity of the germinal center SLK are increased during kidney development and recovery from renal ischemia-reperfusion injury. SLK promotes apoptosis, in part, via pathway(s) involving apoptosis signal-regulating kinase-1 and p38 mitogen-activated protein kinase. This study addresses the role of p53 as a potential effector of SLK. p53 transactivation was measured after transient transfection of a luciferase reporter plasmid that contains a p53 cis-acting enhancer element. Overexpression of SLK in COS-1 cells and cotransfection of SLK and p53-wild type (wt) cDNAs in glomerular epithelial cells (GECs) stimulated p53 transactivational activity, as measured by a p53 response element-driven luciferase reporter. In GECs, chemical anoxia followed by glucose reexposure (in vitro ischemia-reperfusion) increased p53 reporter activity, and this increase was amplified by overexpression of SLK. Expression of SLK induced p53 phosphorylation on serine (S)-33 and S315. In GECs, cotransfection of SLK with p53-wt, p53-S33A, p53-S315A, or p53-S33A+S315A mutants showed that only the double mutation abolished the SLK-induced increase in p53 reporter activity. SLK-induced stimulation of p53 reporter activity was attenuated by inhibition of JNK. Overexpression of SLK amplified apoptosis induced by subjecting cells to in vitro ischemia-reperfusion injury, while ectopic expression of a dominant negative SLK mutant attenuated the ischemia-reperfusion-induced apoptosis. The p53 transactivation inhibitor pifithrin-α significantly attenuated the amount of apoptosis after ischemia-reperfusion and SLK overexpression. Thus SLK induces p53 phosphorylation and transactivation, which enhances apoptosis after in vitro ischemia-reperfusion injury.

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