Vitreous Mediators in Retinal Hypoxic Diseases

Abstract

The causes of retinal hypoxia are many and varied. Under hypoxic conditions, a variety of soluble factors are secreted into the vitreous cavity including growth factors, cytokines, and chemokines. Cytokines, which usually serve as signals between neighboring cells, are involved in essentially every important biological process, including cell proliferation, inflammation, immunity, migration, fibrosis, tissue repair, and angiogenesis. Cytokines and chemokines are multifunctional mediators that can direct the recruitment of leukocytes to sites of inflammation, promote the process, enhance immune responses, and promote stem cell survival, development, and homeostasis. The modern particle-based flow cytometric analysis is more direct, stable and sensitive than the colorimetric readout of the conventional ELISA but, similar to ELISA, is influenced by vitreous hemorrhage, disruption of the blood-retina barrier, and high serum levels of a specific protein. Finding patterns in the expression of inflammatory cytokines specific to a particular disease can substantially contribute to the understanding of its basic mechanism and to the development of a targeted therapy.

Angiogenesis and Inflammation Crosstalk in Diabetic Retinopathy

“…Herein, the observed leukostasis increase regulated by factors can contribute to the formation of an acellular retinal capillary in diabetes. In accordance recent studies related increased of several cytokines, chemokines, and other factors in diabetes with levels of these molecules particularly elevated in the ocular fluid of diabetic patients [Goldberg et al, ; dell'Omo et al, ].…”

Hypoxia–Reoxygenation Affects Whole-Genome Expression in the Newborn Eye

“…Various soluble factors enter under hypoxic conditions the vitreous cavity by secretion, including cytokines, chemokines, and growth factors. 39 The low number of transcriptional changes after 21% and 40% reoxygenation can be explained by the rather modest hypoxia applied in the present model. The use of 100% oxygen after hypoxia can exacerbate the damage in the CNS.…”

“…40 Herein, both chemokine (C-C motif) ligand 12 (Ccl12; inflammation), hexokinase 2 (Hk2; glycolysis), the NMDA2A glutamate receptor (Grin2a; excitotoxicity), the signal transducer and activator of transcription 3 (Stat3), and insulin-like growth factor I receptor (Igfr1; angiogenesis) were upregulated after 100% O 2 during reoxygenation, in line with other studies. 9,39 Pathway Analysis Pathway analyses performed by using GSEA independently of the BAMarray analyses found several interesting pathway systems. Apoptosis and voltage-gated calcium channel complex were both initiated by hypoxia when followed by room air.…”

Effects of Exogenous Neuroglobin (Ngb) on retinal inflammatory chemokines and microglia in a rat model of transient hypoxia

“…Retinal hypoxia underlies numerous ophthalmological conditions such as retinal vascular occlusions, diabetic retinopathy, retinopathy of prematurity and uveitis 10,[13][14][15][16] . During transient hypoxia, an endogenous www.nature.com/scientificreports www.nature.com/scientificreports/ neuroprotective mechanism exists in the retina that prevents apoptosis from minor or transient hypoxic insults.…”