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MLA 2025 Annual Meeting Research Awards
Get PDFThe MLA Research Caucus is pleased to announce the winners for best research papers and posters presented at the MLA 2025 Pittsburgh annual meeting
Editors\u27 Note
No full textGuest Editors, Kimberly Yousey-Elsener and Lisa Mann introduce the first issue JSAIII\u27s special series on Career Preparation and Outcomes
Potential Role of Cigarette Smoke Exposure on Elastin Sensitization and Aortic Pathophysiology in a Mouse Model of Abdominal Aortic Aneurysm
Get PDFIn the US, 200,000 people annually are diagnosed with abdominal aortic aneurysm (AAA) and it accounts for over 15,000 deaths per year. The current paradigm for AAA progression includes cytotoxic T cell activation inducing inflammatory monocyte and macrophage recruitment. These cells secrete collagen and elastin degrading enzymes, leading to loss of structural integrity, aortic dilatation, and eventual rupture. Studies in AAA patients show an increase in cytotoxic T lymphocyte number and activity, a significant decrease in the number and immuno-suppressive activity of the T-regulatory (Treg) cells responsible for governing autoimmune responses, and decreased levels of circulating IL-10. Data from our group suggest that the immune system is sensitized to elastin in patients with early AAA. Cigarette smoking is one of the strongest risk factors for development of AAA in humans and smoke exposure has been shown to exacerbate aneurysm formation in mice. Our working hypothesis is that cigarette smoke causes lung damage via activation of tissue proteases which in turn generates antigenic elastin fragments that trigger an inflammatory reaction in the abdominal aorta resulting in an aneurysm.
The current study will evaluate the effect of cigarette smoke exposure in mice on the relative ratios of populations of pro-inflammatory and anti-inflammatory T-cell subtypes, serum levels of IL-10, miRNA related to IL-10, aortic pathology, and an assessment of potential self-sensitization to elastin. The results of this study will be used to develop a delayed type hypersensitivity assay for elastin that could be used to easily assess the presence of AAA in human patients
The Impact of Neuritin 1 on Retinal Ganglion Cell Survival in Human Donor Glaucomatous Eyes using the Translaminar Autonomous System
Get PDFPurpose: Glaucoma is a progressive optic neuropathy characterized by degeneration of retinal ganglion cells (RGCs), thinning of the retinal nerve layer, and atrophy of the optic nerve. Disease progression is characterized by increased intraocular pressure (IOP) and visual field loss. The only efficacious therapy for treating glaucoma is modification of IOP through pharmacological or surgical intervention. Although these interventions slow disease progression, they do not prevent RGC death entirely. Decreased axonal transport of essential neurotrophic factors contributes to RGC death. Neurotrophic factor supplementation has shown to improve RGC survival and sustain retinal function. We have previously demonstrated that secreted human Neuritin-1 (hNRN1) exhibits neuroprotection, regeneration, and preservation of RGC function in non-glaucomatous human eyes perfused in the ex-vivo Translaminar Autonomous System (TAS). We will investigate the effects of hNRN1 in glaucomatous human donor eyes within the TAS to evaluate if hNRN1 can protect RGC loss in diseased retinas.
Methods: Three pairs of glaucomatous human donor eyes were obtained from eye banks in accordance with the Declaration of Helsinki. Posterior cups were perfused using the TAS for 6-7 days under high and normal pressures with and without hNRN1. We then assessed RGC survival by measuring apoptosis, inflammation, and retinal markers using qRT-PCR and immunostaining. Retinal activity was measured using the OcuScience® Ex Vivo electroretinogram.
Results: Posterior eye cups were successfully maintained in the TAS under normal and highpressure conditions for 6-7 days. Human NRN1 treated eyes showed differential expression of various inflammatory and apoptotic markers. Decreased extra cellular matrix deposition (Collagen, Fibronectin, Laminin) and improved retinal activity was seen within the treated glaucomatous eyes.
Conclusions: The TAS model can mimic pressure induced pathogenesis in human glaucoma. Data from this study shows that hNRN1 may serve as a potential therapeutic target by promoting RGC survival in glaucoma patients
