PhD Scientific Days 2020

Molecular Sciences V. Lectures

New Therapeutic Opportunity in the Treatment of Ischemia-Reperfusion Induced Acute Renal Failure

Előadó neve

Dr. Pajtók, Csenge

Előadó munkahelye

Semmelweis Egyetem, I. sz. Gyermekgyógyászati Klinika

Előadó telefonszáma

+36306543170

Előadó e-mail címe

pajtok.csenge@gmail.com

Az előadás címe

New Therapeutic Opportunity in the Treatment of Ischemia-Reperfusion Induced Acute Renal Failure

Szerző(k) neve és munkahelye

Csenge Pajtók1, Domonkos Pap2, Beáta Szebeni2, Apor Veres-Székely1, István M. Takács1, Eszter Lévai1, Katalin Adrienna Kékesi3, Gábor Juhász4, Attila J. Szabó1,2, Ádám Vannay 1,2

1 1st Department of Paediatrics, Semmelweis University, Budapest
2 MTA-SE Pediatrics and Nephrology Research Group, Budapest
3 Laboratory of Proteomics, Institute of Biology, Eötvös Loránd University, Budapest
4 Department of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Budapest

Szekció

Molecular Sciences V. Lectures

Language of the presentation

English

Section, first choice

Molecular Sciences

Section, second choice

Clinical Medicine

Összefoglaló szövege

Introduction: Acute renal failure (ARF) has a high risk of morbidity and mortality without reliable therapeutic intervention. The most common cause of ARF is renal ischemia reperfusion (I/R) injury, which may associated with various clinical situations including major surgery, cardiac arrest or organ transplantation.
Aim: Our aim was to better understand the pathomechanism of renal I/R injury find new biomarkers or therapeutic targets.
Methods: Two-dimensional gel electrophoresis and proteomic evaluation was carried out on rat kidneys following I/R injury. The significantly changed proteins were analyzed by bioinformatics approaches. The role of Parkinson’s diseases 7 (PARK7) in oxidative stress (H2O2) induced cell death was investigeted by its overexpression or pharmacological modulation in the HEK-293 kidney epithelial cells. We also examined the effect of the modulation of PARK7 in I/R induced mice models of ARF in vivo.
Results: PARK7 was identified as central factor related to I/R induced oxidative stress in the kidney. PARK7 overexpression and its pharmacological modulation decreased H2O2 induced apoptosis of HEK-293 cells. Accordingly, pharmacological modulation of PARK7 improved renal function in mice following I/R induced ARF.
Conclusion: Our data suggest that PARK7 plays a role in the reduction of renal I/R injury associated oxidative damage probably through activation of antioxidant or anti-apoptotic mechanisms. Therefore, PARK7 may serve as therapeutic target in the treatment of I/R injury induced ARF.

Grant support: This paper was supported by 20382-3/2018 FEKUTSTRAT grants and Semmelweis Science and Innovation Fund.

Additional Information

Supervisor: Domonkos Pap
e-mail address: pap.doma@gmail.com

Bemutatás módja

Szóbeli

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

4740

Start

16:30

End

16:45

Authors (legacy)

Csenge Pajtók1, Domonkos Pap2, Beáta Szebeni2, Apor Veres-Székely1, István M. Takács1, Eszter Lévai1, Katalin Adrienna Kékesi3, Gábor Juhász4, Attila J. Szabó1,2, Ádám Vannay 1,2

1 1st Department of Paediatrics, Semmelweis University, Budapest
2 MTA-SE Pediatrics and Nephrology Research Group, Budapest
3 Laboratory of Proteomics, Institute of Biology, Eötvös Loránd University, Budapest
4 Department of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Budapest