Translational Medicine I. (Poster discussion will take place on the terrace of the room during the Coffee Break)
Dr. Daradics, Noemi
Semmelweis University; Department of Surgery, Transplantation and Interventional Gastroenterology; Hepato-Pancreatico-Biliary (HPB) Surgical Research Center Hungary; Budapest, Hungary
206701424
daradics.noemi@gmail.com
Cyclophilin D inhibition as a potential mitochondrial therapy following associating liver partition and portal vein ligation for staged hepatectomy in a mouse knockout model
Noemi Daradics1, Gergo Horvath2, Laszlo Tretter2, Agnes Paal3, Andras Fulop1, Andras Budai3, Attila Szijarto1
1 – Semmelweis University; Department of Surgery, Transplantation and Interventional Gastroenterology; Hepato-Pancreatico-Biliary (HPB) Surgical Research Center Hungary; Budapest, Hungary
2 – Semmelweis University; Department of Medical Biochemistry, Budapest, Hungary
3 – Semmelweis University; 2nd Department of Pathology; Budapest, Hungary
Poszter
Translational Medicine I. (Poster discussion will take place on the terrace of the room during the Coffee Break)
Hungarian
Theoretical and Translational Medicine
Aim: Inhibition of cyclophilins has been already proposed to be efficient as a mitochondrial therapy in liver diseases. To investigate the effect of Cyclophilin D (CypD) inhibition on mitochondrial function, biogenesis and liver regeneration following Associating Liver Partition and Portal vein ligation for Staged hepatectomy (ALPPS) a CypD knockout (KO) mice model was created.
Methods: Male wild type (WT) (n=30) and CypD KO (n=30) mice underwent ALPPS procedure. Animals were terminated pre-operatively and 24, 48, 72 or 168 h after the operation. Mitochondrial functional studies and proteomic analysis of mitochondria were performed. Regeneration rate along with mitotic activity were assessed.
Results: The CypD KO group displayed improved mitochondrial function, as both ATP production (P < 0.001) and oxygen consumption (P < 0.05) were increased compared to the WT group. The level of mitochondrial biogenesis coordinator peroxisome proliferator-activated receptor γ co-activator 1-α (PGC1-α) was also elevated in the CypD KO group (P < 0.001), which resulted in the induction of the mitochondrial oxidative phosphorylation system. Liver growth was increased in the CypD KO group compared to the WT group (P < 0.001).
Conclusions: Our study demonstrates the effect of CypD inhibition on the mitochondrial vulnerability following ALPPS. Based on our results we propose that CypD inhibition should be further investigated as a possible mitochondrial therapy following ALPPS.
Semmelweis University, Károly Rácz Doctoral School of Clinical Medicine
Prof. Dr. Szijártó Attila
I do not give consent to the publication of my abstract on the website of the congress.
Szabad
elfogadva
poszter
nem rendelkezett róla
5973
11:15
11:20
Noemi Daradics1, Gergo Horvath2, Laszlo Tretter2, Agnes Paal3, Andras Fulop1, Andras Budai3, Attila Szijarto1
1 – Semmelweis University; Department of Surgery, Transplantation and Interventional Gastroenterology; Hepato-Pancreatico-Biliary (HPB) Surgical Research Center Hungary; Budapest, Hungary
2 – Semmelweis University; Department of Medical Biochemistry, Budapest, Hungary
3 – Semmelweis University; 2nd Department of Pathology; Budapest, Hungary