in-vivo-detection-analysis-rb-protein-sumoylation-human

<em>In Vivo</em> Detection and Analysis of Rb Protein SUMOylation in Human Cells

The post-translational modifications of proteins are critical for the proper regulation of intracellular signal transduction. Among these modifications, ...

Eye and ENT Hospital of Fudan University

Fudan University

Microglia-associated inflammation is closely related to the pathogenesis of retinal degenerative disorders. We have previously shown in vivo that naloxone protected photoreceptors from light-induced apoptosis possibly through inhibiting microglial activation. In this study, we attempted to explore the effect of lipopolysaccharide (LPS)-activated microglia on photoreceptor death and the influence of naloxone treatment using an in vitro retinal microglia and 661 W photoreceptor co-culture system. Immunofluorescent staining and ELISA measurements demonstrated that LPS activated microglia by changing the morphology and increasing the production of proinflammatory factors interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha. Flow cytometry analysis of annexin V/propidium iodide staining showed that LPS-activated microglia promoted the apoptosis of co-cultured 661 W photoreceptor cells. Naloxone inhibited microglial activation and decreased the release of IL-1beta and TNF-alpha but could not prevent photoreceptors from undergoing apoptosis. Considering the dual role of microglia-associated inflammation in both neurotoxicity and neuroprotection, modulating the function, rather than simply inhibiting their activation, might be a new therapeutic method for preventing photoreceptor degeneration.

Inhibition of LPS-induced retinal microglia activation by naloxone does not prevent photoreceptor death.

To evaluate the tear-film meniscus with optical coherence tomography (OCT) in patients with idiopathic dacryoadenitis and to determine its relationships with the clinical tests.

Changes in Tear Film Characteristics in Patients With Idiopathic Dacryoadenitis.

Persistent fetal vasculature (PFV) is a congenital developmental anomaly of the eye that accounts for about 5% of childhood blindness. The molecular mechanism of PFV remains unclear. As a glycosyltransferase of α-dystroglycan, LARGE mutations have been found in congenital muscular dystrophy patients with brain abnormalities. Spontaneous Large mutant mice displayed similar symptoms of human muscle-eye-brain disorders. However, the detailed roles of Large in ocular vasculature development still need to be uncovered.

Article	Year
Inhibition of LPS-induced retinal microglia activation by naloxone does not prevent photoreceptor death. Inflammation\| PubMed ID: 22869199	2013
Changes in Tear Film Characteristics in Patients With Idiopathic Dacryoadenitis. Ophthalmic plastic and reconstructive surgery\| PubMed ID: 26863039	2017
Large is required for normal astrocyte migration and retinal vasculature development. Cell & bioscience\| PubMed ID: 28428837	2017

Hui Ren

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