Gene Therapy for Heart Transplantation-Associated Acute Rejection, Ischemia / Reperfusion Injury and Coronary Arteriosclerosis

2004 ◽  
Vol 4 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Mitsuaki Isobe ◽  
Hisanori Kosuge ◽  
Noritaka Koga ◽  
Hideki Futamatsu ◽  
Jun-ichi Suzuki
Keyword(s):  
Gene Therapy ◽  
Acute Rejection ◽  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Arteriosclerosis

Phosphodiesterase-5-inhibition reduces ischemia/reperfusion injury after heart transplantation

2009 ◽  
Vol 56 (S 01) ◽  
Author(s):  
S Loganathan ◽  
T Radovits ◽  
K Hirschberg ◽  
S Korkmaz ◽  
E Barnucz ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Phosphodiesterase 5

scholarly journals Use of peroxiredoxin for preconditioning of heterotopic heart transplantation in a rat

2020 ◽  
Vol 22 (2) ◽  
pp. 158-164
Author(s):  
N. V. Grudinin ◽  
V. K. Bogdanov ◽  
M. G. Sharapov ◽  
N. S. Bunenkov ◽  
N. P. Mozheiko ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Mammalian Cells ◽  
Ischemia Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Signal Transmission ◽  
Redox Homeostasis ◽  
Heterotopic Heart Transplantation ◽  
Wide Range

Peroxiredoxin 6 (Prdx6) is an antioxidant enzyme in the human body that performs a number of important functions in the cell. Prdx6 restores a wide range of peroxide substrates, thus playing a leading role in maintaining redox homeostasis in mammalian cells. In addition to peroxidase activity, Prdx6 has an activity of phospholipase A2, thus taking part in membrane phospholipid metabolism. Due to its peroxidase and phospholipase activity, Prdx6 participates in intracellular and intercellular signal transmission, thereby facilitating the initiation of regenerative processes in the cell, suppression of apoptosis and activation of cell proliferation. Given the functions performed, Prdx6 can effectively deal with oxidative stress caused by various factors, including ischemia-reperfusion injury. On an animal model of rat heterotopic heart transplantation, we showed the cardioprotective potential of exogenous recombinant Prdx6, introduced before transplantation and subsequent reperfusion injury of the heart. It has been demonstrated that exogenous Prdx6 effectively alleviates the severity of ischemia-reperfusion injury of the heart by 2–3 times, providing normalization of its structural and functional state during heterotopic transplantation. The use of recombinant Prdx6 can be an effective approach in preventing/alleviating ischemia-reperfusion injury of the heart, as well as in maintaining an isolated heart during transplantation.

scholarly journals Effects of Thyroid Hormone Analogue and a Leukotrienes Pathway-Blocker on Reperfusion Injury Attenuation after Heart Transplantation

2013 ◽  
Vol 2013 ◽  
pp. 1-8
Author(s):  
Fadhil G. Al-Amran ◽  
Najah R. Hadi ◽  
Haider S. H. Al-Qassam
Keyword(s):  
Myocardial Ischemia ◽  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Control Group ◽  
Group I ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Background. Global myocardial ischemia reperfusion injury after heart transplantation is believed to impair graft function and aggravate both acute and chronic rejection episodes. Objectives. To assess the possible protective potential of MK-886 and 3,5-diiodothyropropionic acid DITPA against global myocardial ischemia reperfusion injury after heart transplantation. Materials and Methods. Adult albino rats were randomized into 6 groups as follows: group I sham group; group II, control group; groups III and IV, control vehicles (1,2); group V, MK-886 treated group. Donor rats received MK-886 30 min before transplantation, and the same dose was repeated for recipients upon reperfusion; in group VI, DITPA treated group, donors and recipients rats were pretreated with DITPA for 7 days before transplantation. Results. Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF-α, IL-1β, and ICAM-1 and plasma level of cTnI (). Morphologic analysis showed that both MK-886 and DITPA markedly improved () the severity of cardiac injury in the heterotopically transplanted rats. Conclusions. The results of our study reveal that both MK-886 and DITPA may ameliorate global myocardial ischemia reperfusion injury after heart transplantation via interfering with inflammatory pathway.

Reduction of cold ischemia–reperfusion injury by graft-expressing clusterin in heart transplantation

2011 ◽  
Vol 30 (7) ◽  
pp. 819-826 ◽  
Author(s):  
Shuyuan Li ◽  
Qiunong Guan ◽  
Zhishui Chen ◽  
Martin E. Gleave ◽  
Christopher Y.C. Nguan ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cold Ischemia

Ischemia-Reperfusion Injury During Experimental Heart Transplantation. Evaluation of Trimetazidine's Cytoprotective Effect

2005 ◽  
Vol 58 (8) ◽  
pp. 941-950
Author(s):  
Evaristo Castedo ◽  
Javier Segovia ◽  
Cristina Escudero ◽  
Begoña Olmedilla ◽  
Fernando Granado ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cytoprotective Effect

scholarly journals Systemic gene therapy with interleukin-13 attenuates renal ischemia–reperfusion injury

2008 ◽  
Vol 73 (12) ◽  
pp. 1364-1373 ◽  
Author(s):  
M. Sandovici ◽  
R.H. Henning ◽  
H. van Goor ◽  
W. Helfrich ◽  
D. de Zeeuw ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Interleukin 13 ◽  
Renal Ischemia Reperfusion Injury

Cardiomyocyte-specific Bcl-2 overexpression attenuates ischemia-reperfusion injury, immune response during acute rejection, and graft coronary artery disease

Blood ◽  
2004 ◽  
Vol 104 (12) ◽  
pp. 3789-3796 ◽  
Author(s):  
Masashi Tanaka ◽  
Susumu Nakae ◽  
Raya D. Terry ◽  
Golnaz K. Mokhtari ◽  
Feny Gunawan ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Acute Rejection ◽  
Immune Responses ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Allografts ◽  
Artery Disease

After cardiac transplantation, graft damage occurs secondary to ischemia-reperfusion injury and acute rejection. This damage ultimately leads to the development of graft coronary artery disease (GCAD), which limits long-term graft survival. Apoptosis is directly involved in graft injury, contributing to the development of GCAD. To assess the role of the antiapoptotic factor Bcl-2 in the process of GCAD, we transplanted hearts from FVB transgenic mice overexpressing human Bcl-2 under the control of α-myosin heavy chain promoter into allogenic C57BL/6 mice. Bcl-2 overexpression led to reduced cytochrome c–mediated caspase-9–dependent cardiomyocyte apoptosis and local inflammation (neutrophil infiltration and proinflammatory cytokine production) in cardiac allografts during ischemia-reperfusion injury and also led to reduced immune responses (inflammatory cell infiltration, production of TH1 cytokines and chemokines, and expression of adhesion molecules) during acute and chronic rejection without affecting host CD4+ and CD8+ cell responses in the spleen. Thus, local Bcl-2 expression directly contributes to the modulation of local immune responses in allograft rejection, resulting in attenuated GCAD. In conclusion, our findings suggest that the modulation of Bcl-2 expression by pharmacologic up-regulation or gene transfer may be of clinical benefit in the short- and long-term function of cardiac allografts.

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