Expression of leukemia inhibitory factor in the rat retina following acute ocular hypertension

Molecular Medicine Reports
Qianqian HuRenyi Wu

Abstract

The aim of the present study was to investigate the expression of leukemia inhibitory factor (LIF) and its downstream signaling pathways in the rat retina following acute ocular hypertension. The intraocular pressure of the rats was elevated to 110 mmHg for 1 h by infusing the anterior chamber with normal saline. The retinal tissues were obtained 12 h, 24 h, and 2, 3 and 7 days after termination of the ocular hypertension. Hematoxylin and eosin and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed to assess the morphological changes and the apoptosis of retinal cells, respectively. Quantification of the retinal ganglion cells (RGCs) was performed using fluorogold retrograde (FG) staining. The expression levels of LIF, LIF receptor (LIFR), signal transducers and activators of transcription 3 (STAT3), phosphorylated STAT3 (P‑STAT3), Akt, phosphorylated‑Akt (P‑Akt), extracellular signal‑regulated kinase (ERK) and phosphorylated ERK (P‑ERK) were determined at different time‑points following acute ocular hypertension using western blot analysis. Reverse transcription‑quantitative polymerase chain reaction was performned to detect the mRNA expression levels of LIF and LIFR. The results revea...Continue Reading

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Citations

Jan 25, 2018·Reproduction : the Official Journal of the Society for the Study of Fertility·Hua LiKai Wang
Sep 4, 2018·Frontiers in Molecular Neuroscience·Saori InafukuKip M Connor
Dec 26, 2018·Oxidative Medicine and Cellular Longevity·Weiwei DuWei He
Mar 2, 2021·Neural Regeneration Research·Xiao-Bin LiuYing Xu

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Methods Mentioned

BETA
protein assay
electrophoresis

Software Mentioned

Image J
SPSS

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis