The proteomic profile of a mouse model of proliferative vitreoretinopathy

Proliferative vitreoretinopathy (PVR) develops as a complication of retinal detachment surgery and represents a devastating condition leading to serious vision loss. A good animal model that permits extensive functional studies and drug testing is crucial in finding better therapeutic modalities for...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Márkus Bernadett
Pató Zsuzsanna
Sarang Zsolt
Albert Réka
Tőzsér József
Petrovski Goran
Csősz Éva
Dokumentumtípus: Cikk
Megjelent: Elsevier 2017
Sorozat:FEBS OPEN BIO 7 No. 8
doi:10.1002/2211-5463.12252

mtmt:3255497
Online Access:http://publicatio.bibl.u-szeged.hu/12222
Leíró adatok
Tartalmi kivonat:Proliferative vitreoretinopathy (PVR) develops as a complication of retinal detachment surgery and represents a devastating condition leading to serious vision loss. A good animal model that permits extensive functional studies and drug testing is crucial in finding better therapeutic modalities for PVR. A previously established mouse model, using dispase injection, was analyzed from the proteomic point of view, examining global protein profile changes by 2D electrophoresis, image analysis and HPLC-tandem mass spectrometry-based protein identification. The easy applicability of the mouse model was used to study the role of transglutaminase 2 (TG2) in PVR formation by proteomic examination of dispase-induced TG2 knockout vitreous samples. Our data demonstrate that, despite the altered appearance of crystallin proteins, the lack of TG2 did not prevent the development of PVR.
Terjedelem/Fizikai jellemzők:1166-1177
ISSN:2211-5463