"IGF-1R Regulates the Extracellular Level of Active MMP-2, Pathological Neovascularization and Functionality in Retinas of OIR Mouse Model."

LORENC VE; SUBIRADA CALDARONE PAULA; PAZ MC; FERRER D; LUNA JD; CHIABRANDO GA; SANCHEZ MC

MOLECULAR NEUROBIOLOGY

HUMANA PRESS INC

Lugar: Oregon; Año: 2017

0893-7648

n ischemic proliferative diseases such as retinopathies, persistent hypoxia leads to the release of numerous neovascular factors that participate in the formation of abnormal vessels and eventually cause blindness. The up-regulation and activation of metalloproteinases (MMP-2 and MMP-9) represent a final common pathway in this process. Although many regulators of the neovascular process have been identified, the complete role of the insulin-like growth factor 1 (IGF-1) and its receptor (IGF-1R) appears to be significantly more complex. In this study, we used an oxygen-induced retinopathy (OIR) mouse model as well as an in vitro model of hypoxia to study the role of MMP-2 derived from Müller glial cells (MGCs) and its relation with the IGF-1/IGF-1R system. We demonstrated that MMP-2 protein expression increased in P17 OIR mice, which coincided with the active phase of the neovascular process. Also, glutamine synthetase (GS) positive cells were also positive for MMP-2, whereas IGF-1R wa