Supplementary Material for: MicroRNA-126 Reduces Blood-Retina Barrier Breakdown via the Regulation of VCAM-1 and BCL2L11 in Ischemic Retinopathy
Bai X.
Luo J.
Zhang X.
Han J.
Wang Z.
Miao J.
Bai Y.
10.6084/m9.figshare.4539844.v1
https://karger.figshare.com/articles/dataset/Supplementary_Material_for_MicroRNA-126_Reduces_Blood-Retina_Barrier_Breakdown_via_the_Regulation_of_VCAM-1_and_BCL2L11_in_Ischemic_Retinopathy/4539844
<p>To evaluate the role of microRNA-126 (miR-126) in maintaining the
integrity of the blood-retina barrier (BRB), we established a mouse
model of oxygen-induced retinopathy (OIR) and measured the retinal
levels of miR-126 using recombinant plasmid pCMV-MIR or pCMV-MIR-126
intravitreal injections. We also detected VCAM-1 and BCL2L11 levels.
Retinal vaso-obliteration, VCAM-1 localization on retinal endothelial
cells, the blood-retina vascular permeability or albumin leakage in
retinas, TUNEL histology, Evans blue assays, or Western blotting for
detecting albumin or tight junction levels in the retina was performed.
We also detected the effect of miR-126 on the survival of Müller cells
in a mouse model using vimentin fluorescence staining. Our results
suggested that miR-126 may not only regulate the overexpression of
VCAM-1 or BCL2L11 and lead to the reduction of retinal endothelial cell
apoptosis, retinal vascular leakage, or retinal permeability in the OIR
mouse model, but may also protect hypoxic retinal Müller cells via the
STAT3 signaling pathway. We believe that miR-126 could also be a
potential therapeutic agent to maintain the stability of the BRB in
ischemic retinopathy.</p>
2017-01-11 12:53:59
MicroRNA-126
Vascular cell adhesion molecule 1
BCL2L11
Blood-retina barrier
Tight junction
Ischemic retinopathy