PhD Scientific Days 2024

Poster Session F - Molecular Medicine 3.

PARK7 as a new therapeutic target in pulmonary fibrosis

Előadó neve

Dr. Pap, Domonkos

Előadó munkahelye

Pediatric Center, MTA Center of Excellence, Semmelweis University, Budapest, Hungary / HUN-REN–SU Pediatrics and Nephrology Research Group, Budapest, Hungary

Előadó telefonszáma

06304847648

Előadó e-mail címe

pap.doma@gmail.com

Az előadás címe

PARK7 as a new therapeutic target in pulmonary fibrosis

Szerző(k) neve és munkahelye

Dr. Domonkos Pap¹, Apor Veres-Székely^2,3, Beáta Szebeni^2,3, Csenge Szász², Péter Bokrossy², Réka Zrufkó², Attila J. Szabó^2,3, Ádám Vannay², HUN-REN–SU Pediatrics and Nephrology Research Group, Budapest, Hungary⁴

1: Pediatric Center, MTA Center of Excellence, Semmelweis University, Budapest
2: Pediatric Center, MTA Center of Excellence, Semmelweis University, Budapest, Hungary
3: HUN-REN–SU Pediatrics and Nephrology Research Group, Budapest, Hungary
4: Ádám Vannay

Bemutatás módja

Poszter

Szekció

Poster Session F - Molecular Medicine 3.

Language of the presentation

English

Preferred session

Molecular Medicine

Összefoglaló szövege

Introduction: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by excessive scarring, increasing breathlessness, and death within three to four years after diagnosis. Development of IPF is a result of an aberrant, repetitive alveolar epithelial injury, in which the oxidative stress plays a dominant role. Parkinson’s Diseases 7 (PARK7) molecule is a central mediator of the antioxidant defence mechanisms of various organs, however, its role in IPF and the underlying mechanisms is still unknown.

Aims: In the present study, we aimed to investigate the role and therapeutic potential of PARK7 in IPF.

Method: Pulmonary expression of PARK7 was investigated in the bleomycin induced mouse model of lung fibrosis. The effect of pharmacological PARK7 activation with Comp-23 on the synthesis of extracellular matrix (ECM) components, including collagen-1 (Col1a1) and fibronectin (FN) in the lungs was investigated in vivo. The effect of Comp-23 treatment on oxidative damage (H2O2, bleomycin) induced death of lung alveolar epithelial cells (A549) was investigated in vitro.

Results: We found increased PARK7 expression in the fibrotic lung of mice treated with bleomycin. PARK7 activation with Comp-23 treatment diminished the bleomycin induced Col1a1 and FN levels in the lungs. Comp-23 treatment decreased the H2O2 and bleomycin induced oxidative stress and cell death of A549 cells.

Conclusion: Our data suggest that PARK7 protects the alveolar epithelial cells against oxidative damage thereby reducing the pathologic alterations in the lung leading to the development of IPF. Therefore, PARK7 may serve as a potential therapeutic target in the treatment of IPF.

Funding: K-142728, TKP2021-EGA-24, ELKH-POC-2022-024, ÚNKP-23-3-I-SE-36, ÚNKP-23-3-I-SE-42, ÚNKP-23-4-II-SE-29, ÚNKP-23-5-SE-15; Hungarian Academy of Sciences, János Bolyai Research Scholarship.

University

Semmelweis University

Supervisor

Ádám Vannay

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

7422

Start

14:50

End

14:53