Sequential morphological and functional features of retinal damage in mice exposed to different doses (40 vs. 20 mg/kg) of sodium iodate (NaIO3) were analyzed. Retinal morphology, apoptosis (TUNEL assay), and function (electroretinography; ERG) were examined at several time points after NaIO3 administration. The higher dose of NaIO3 caused progressive degeneration of the whole retinal area and total suppression of scotopic and photopic ERG. In contrast, the lower dose induced much less severe degeneration in peripheral part of retina along with a moderate decline of b- and a-wave amplitudes in ERG, corroborating the presence of regions within retina that retain their function. The peak of photoreceptor apoptosis was found on the 3rd day, but the lower dose induced more intense reaction within the central retina than in its peripheral region. In conclusion, these results indicate that peripheral area of the retina reveals better resistance to NaIO3 injury than its central part.

CL wear may predispose individuals to meibomian gland dysfunction, which is not usually investigated unless significant symptoms are present. Therefore, we recommend to routinely examine CL wearers for meibomian gland dysfunction manifestations and to introduce specific prophylaxis if required.

Transplantation of genetically modified MSCs that produce neurotrophic growth factors may represent a useful strategy for treatment of different forms of retinopathies in the future.

Age-related macular degeneration (AMD) is the most common cause of blindness among the elderly, especially in Western countries. Although the prevalence, risk factors, and clinical course of the disease are well described, its pathogenesis is not entirely elucidated. AMD is associated with a variety of biochemical abnormalities, including complement components deposition in the retinal pigment epithelium-Bruch's membrane-choriocapillaris complex. Although the complement system (CS) is increasingly recognized as mediating important roles in retinal biology, its particular role in AMD pathogenesis has not been precisely defined. Unrestricted activation of the CS following injury may directly damage retinal tissue and recruit immune cells to the vicinity of active complement cascades, therefore detrimentally causing bystander damage to surrounding cells and tissues. On the other hand, recent evidence supports the notion that an active complement pathway is a necessity for the normal maintenance of the neurosensory retina. In this scenario, complement activation appears to have beneficial effect as it promotes cell survival and tissue remodeling by facilitating the rapid removal of dying cells and resulting cellular debris, thus demonstrating anti-inflammatory and neuroprotective activities. In this review, we discuss both the beneficial and detrimental roles of CS in degenerative retina, focusing on the diverse aspects of CS functions that may promote or inhibit macular disease.

Purpose. The aim of this study was to investigate the relationships between MGL and ocular symptoms, several systemic conditions, and key markers of ocular surface health. Methods. We included into the study 91 healthy volunteers between the ages of 20 and 77 years. We analyzed meibomian gland morphology, function, and lid margin alterations. We correlated our findings with self-reported ocular symptoms, systemic medical history, lifestyle factors, and tear film abnormalities. Results. We observed that a high ocular surface disease index, a history of either chalazion or hordeolum, experience of puffy eyelids upon waking, and foreign body sensation all appeared to be predictors of an abnormal meiboscore after adjusting for age and sex (p = 0.0007; p = 0.001; p = 0.02; p = 0.001, resp.). Multivariate logistic regression model including age and sex showed that there were three independent predictors of abnormal meiboscore: older age (OR = 1.03, 95% CI = 1.01–1.04 per year, p = 0.006), postmenopausal hormone therapy (OR = 4.98, 95% CI = 1.52–16.30, p = 0.007), and the use of antiallergy drugs (OR = 5.85, 95% CI = 2.18–15.72, p = 0.0004). Conclusion. Our findings extend current knowledge on the pathophysiology of MGL.

We aimed to explore the expression of systemic inflammatory factors and selected intracellular miRNAs that regulate inflammatory signaling pathways potentially involved in age-related macular degeneration (AMD) pathogenesis. A total of 179 patients with wet AMD, 175 with dry AMD and 121 controls were enrolled in the study. Soluble inflammatory factors were analyzed in plasma samples using Luminex technology. Expression of selected miRNAs was analyzed in isolated nucleated peripheral blood cells (PBNCs) using real-time qPCR. Wet AMD was an independent factor associated with higher concentrations of IL-6 (β = +0.24, p = 0.0004), GM-CSF (β = +0.31, p < 0.001), IFN-γ (β = +0.58, p < 0.001), higher expression of miRNA-23a-3p (β = +0.60, p < 0.0001), miRNA-30b (β = +0.32, p < 0.0001), miRNA-191-5p (β = +0.28, p < 0.0001) and lower concentration of IL-1β (β = −0.25, p = 0.0003), IL-5 (β = −0.45, p < 0.001), IL-10 (β = −0.45, p < 0.001), IL-12 (β = −0.35, p < 0.001), lower expression of miRNA-16-5p (β = −0.31, p < 0.0001), miRNA-17-3p (β = −0.18, p = 0.01), miRNA-150-5p (β = −0.18, p = 0.01) and miRNA-155-5p (β = −0.47, p < 0.0001). Multivariate analysis revealed that dry AMD was an independent factor associated with higher concentration of GM-CSF (β = +0.34, p < 0.001), IL-6 (β = +0.13, p = 0.05), higher expression of miRNA-23a-3p (β = +0.60, p < 0.0001), miRNA-126-3p (β = +0.23, p = 0.0005), miRNA-126-5p (β = +0.16, p = 0.01), miRNA 146a (β = +0.14, p = 0.03), and mRNA191-5p (β = +0.15, p = 0.03) and lower concentrations of TNF-α (β = +0.24, p = 0.0004), IL-1β (β = −0.39, p < 0.001), IL-2 (β = −0.20, p = 0.003), IL-5 (β = −0.54, p < 0.001), IL-10 (β = −0.56, p < 0.001), IL-12 (β = −0.51, p < 0.001), lower expression of miRNA-16-5p (β = −0.23, p = 0.0004), miRNA-17-3p (β = −0.20, p = 0.003) and miRNA-17-5p (β = −0.19, p = 0.004). Negative correlations between visual acuity and WBC, lymphocyte count, TNF-α, IL-1 β, IL-2, IL-4, IL-6, IL-10 concentrations and miRNA-191-5p, as well as positive correlations between visual acuity and miRNA-126-3p, -126-5p, and -155-5p PBNCs expression were found in AMD patients. No such correlations were found in the control group. Our results may suggest the role of both intra- and extracellular mechanisms implicated in inflammatory response regulation in multifactorial AMD pathogenesis.

ABSTRACT. Age-related macular degeneration (AMD) shares several pathological and epidemiological similarities with systemic atherosclerosis (AS). First, an association between AS and AMD is apparent from the analyses of the histological and biochemical structure of atherosclerotic plaques in the vascular walls and retinal drusen, the hallmark of AMD. Second, there is considerable evidence implicating endothelial dysfunction in the pathogenesis of both disorders, and cellular oxidative stress appears to be a common denominator underlying this process. Moreover, there are observations that the complement system (CS) triggering inflammatory response contributes to the onset and advancement of both diseases. The CS plays a role in the generation of drusen and neovascularization in AMD as well as in vascular endothelium activation, cell damage and ultimately atherosclerotic plaque formation in the course of systemic arteriosclerosis. It is widely recognized that both AMD and AS are not only related to local stimulation of the CS, but also result in its systemic activation. In addition, a specific Y402H polymorphism of the complement inhibitor factor H has been found to be associated with the incidence of both AMD and AS. Here, we propose a linking hypothesis between CS activation, endothelial dysfunction and the pathogenesis of two common and age-related pathological processes, AS and AMD. We also discuss the potential therapeutic value of pharmacological modulation of CS activation in these disorders.

EPCs may play a considerable role in vascular development in preterm infants.