scholarly journals Potent cardioprotection from ischemia-reperfusion injury by a two-domain fusion protein comprising annexin V and Kunitz protease inhibitor

2013 ◽  
Vol 11 (8) ◽  
pp. 1454-1463 ◽  
Author(s):  
C.-H. Yeh ◽  
T.-P. Chen ◽  
Y.-C. Wang ◽  
S.-W. Fang ◽  
T.-C. Wun
Keyword(s):  
Fusion Protein ◽  
Protease Inhibitor ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Domain Fusion ◽  
Kunitz Protease Inhibitor

scholarly journals Investigation of a Potential Scintigraphic Tracer for Imaging Apoptosis: Radioiodinated Annexin V-Kunitz Protease Inhibitor Fusion Protein

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Mei-Hsiu Liao ◽  
Tong-Rong Jan ◽  
Chao-Chih Chiang ◽  
Kuo-Chen Yen ◽  
Tse-Zung Liao ◽  
...  
Keyword(s):  
Fusion Protein ◽  
Protease Inhibitor ◽  
Annexin V ◽  
High Yield ◽  
Apoptotic Cells ◽  
Erythrocyte Ghosts ◽  
Kunitz Protease Inhibitor ◽  
Apoptosis Detection ◽  
Iodine 123 ◽  
Iodine 125

Radiolabeled annexin V (ANV) has been widely used for imaging cell apoptosis. Recently, a novel ANV-Kunitz-type protease inhibitor fusion protein, ANV-6L15, was found to be a promising probe for improved apoptosis detection based on its higher affinity to phosphatidylserine (PS) compared to native ANV. The present paper investigates the feasibility of apoptosis detection using radioiodinated ANV-6L15. Native ANV and ANV-6L15 were labeled with iodine-123 and iodine-125 using Iodogen method. The binding between the radioiodinated proteins and erythrocyte ghosts or chemical-induced apoptotic cells was examined. ANV-6L15 can be radioiodinated with high yield (40%−60%) and excellent radiochemical purity (>95%).123I-ANV-6L15 exhibited a higher binding ratio to erythrocyte ghosts and apoptotic cells compared to123I-ANV. The biodistribution of123I-ANV-6L15 in mice was also characterized.123I-ANV-6L15 was rapidly cleared from the blood. High uptake in the liver and the kidneys may limit the evaluation of apoptosis in abdominal regions. Our data suggest that radiolabled ANV-6L15 may be a better scintigraphic tracer than native ANV for apoptosis detection.

scholarly journals Follistatin-Like 1 Attenuates Ischemia/Reperfusion Injury in Cardiomyocytes via Regulation of Autophagy

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Weijun Yang ◽  
Qunjun Duan ◽  
Xian Zhu ◽  
Kaiyu Tao ◽  
Aiqiang Dong
Keyword(s):  
Cell Viability ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Protective Role ◽  
Autophagic Flux ◽  
Rat Cardiomyocytes ◽  
Hypoxia Ischemia ◽  
Myocardial Ischemia Reperfusion

Background. The cardioprotective effect of FSTL1 has been extensively studied in recent years, but its role in myocardial ischemia/reperfusion injury (IRI) is unclear. In this study, we investigated the effect of FSTL1 pretreatment on myocardial IRI as well as the possible involvement of autophagic pathways in its effects. Methods. The effects of FSTL1 on the viability and apoptosis of rat cardiomyocytes were investigated after exposure of cardiomyocytes to hypoxia/ischemia by using the CCK-8 assay and Annexin V/PI staining. Further, western blot analysis was used to detect the effects of FSTL1 pretreatment on autophagy-associated proteins, and confocal microscopy was used to observe autophagic flux. To confirm the role of autophagy, the cells were treated with the autophagy promoter rapamycin or the autophagy inhibitor 3-methyladenine, and cell viability and apoptosis during IRI were observed. These effects were also observed after treatment with rapamycin or 3-methyladenine followed by FSTL1 administration and IRI. Results. FSTL1 pretreatment significantly increased viability and reduced apoptosis in cardiomyocytes exposed to hypoxia/ischemia conditions. Further, FSTL1 pretreatment affected the levels of the autophagy-related proteins and enhanced autophagic flux during IRI. In addition, cell viability was enhanced and apoptosis was decreased by rapamycin treatment, while these effects were reversed by 3-MA treatment. However, when the myocardial cells were pretreated with rapamycin or 3-methyladenine, there was no significant change in their viability or apoptosis with FSTL1 treatment during IRI. Conclusions. FSTL1 plays a protective role in myocardial IRI by regulating autophagy.

Diannexin, a Novel Annexin V Homodimer, Provides Prolonged Protection Against Hepatic Ischemia-Reperfusion Injury in Mice

2007 ◽  
Vol 133 (2) ◽  
pp. 632-646 ◽  
Author(s):  
Narci C. Teoh ◽  
Yoshiya Ito ◽  
Jacqueline Field ◽  
Nancy W. Bethea ◽  
Deama Amr ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion
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