Age-Related Macular Degeneration Models Induced by Polyethylene Glycol (PEG) | Chapter 11 | Medicine and Medical Research: New Perspectives Vol. 8

Age-related macular degeneration (AMD) is a leading cause of irreversible blindness worldwide.  olyethylene glycol (PEG) can activate the alternative pathway of the complement system and induce choroidal neovascularization (CNV) in mice, has been recently reported. Currently, no other investigator has demonstrated CNV after PEG injection in the mouse eye. AMD pathogenesis in mice through subretinal PEG treatment of RPE cells and retinal layers. Male C57BL/6 mice were injected (subretinal) with 2 μL of solution containing 0.5 mg and 1.0 mg of PEG or PBS in control groups. Eyes were harvested on days 1, 3, and 5 after injection and processed for analysis. Sections were immunohistochemically stained for complement component C3, membrane attack complex (MAC), and cytokeratin 18. Light and laser confocal microscopy was used for image capturing. PEG increased deposition of C3 and MAC on RPE cells and on all retinal layers after 1.0 mg injection. PEG induced loss of cellular contacts between RPE cells and migration of RPE cells in the subretinal space at day 1 after PEG injection. After 0.5 mg PEG injection, increased size of RPE cells was detected at days 3 and 5. Apoptotic bodies were observed in an outer nuclear layer at days 3 and 5 after 0.5 mg PEG treatment. RPE cells with dark cytoplasm and condensed chromatin were observed. Higher doses of PEG induce CNV, encourage RPE cell proliferation and death, and damage photoreceptors in mice. This simple and fast model may be useful to explore the pathogenesis of both dry and wet AMD.

 

Author (s) Details

Reece Mitchell
Department of Ophthalmology, Jones Eye Institute, Pat and Willard Walker Eye Research Center, 4301 West Markham, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, United States.

 

Connor Logan
Department of Ophthalmology, Jones Eye Institute, Pat and Willard Walker Eye Research Center, 4301 West Markham, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, United States.

 

Valeriy V. Lyzogubov
Department of Ophthalmology, Jones Eye Institute, Pat and Willard Walker Eye Research Center, 4301 West Markham, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, United States.

 

Nalini S. Bora
Department of Ophthalmology, Jones Eye Institute, Pat and Willard Walker Eye Research Center, 4301 West Markham, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, United States.

 

Puran S. Bora
Department of Ophthalmology, Jones Eye Institute, Pat and Willard Walker Eye Research Center, 4301 West Markham, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, United States.

 

Please see the book here:- https://doi.org/10.9734/bpi/mmrnp/v8/2312

Pivotal Roles of APN/AdipoRs Signaling in Maintaining Ocular Homeostasis and Protecting against Eye Ailments | Chapter 10 | Advancement and New Understanding in Medical Science Vol. 10

 This comprehensive review critically examines the latest findings and breakthroughs that underscore the pivotal roles of APN/AdipoRs signaling in maintaining ocular homeostasis and protecting against eye ailments. Explaining the complex interactions between ocular diseases and the flexible fat-associated adipokine adiponectin (APN) has garnered a lot of attention in recent years. Discovering the complex connection between aging eye problems and adipocytokine and its receptors (AdipoRs) has become an exciting area of medical research. Here, we meticulously explore the intriguing mechanisms by which APN protein influences retinal function and overall visual acuity. Drawing from an extensive array of cutting-edge studies, the article highlights APN’s multifaceted functions, ranging from anti-inflammatory properties and oxidative stress reduction to angiogenic regulation within retinal and macula tissues Targeting common aging eye diseases with treatment approaches could be made possible by the role that APN/AdipoRs play in mediating these effects. Furthermore, the interaction between APN signaling pathways and age-related macular degeneration (AMD) is unraveled in this review. The single-cell RNA-seq results validate the expression of both the receptor isoforms (AdipoR1/R2) in retinal cells. The transcriptomic analysis showed lower expression of AdipoR1/2 in dry AMD pathogenesis compared to healthy subjects. The inhibitory adiponectin peptide (APN1) demonstrated over 75% suppression of choroidal neovascularization (CNV), whereas the control peptide did not exert any inhibitory effect on CNV. The elucidation of these relationships fosters a deeper understanding of adipose tissue’s profound influence on ocular health, presenting new prospects for personalized treatments and preventative measures. Because APN1 inhibits CNV and leakage, it can be used to treat human AMD. In conclusion, this review provides a captivating journey into the enthralling world of APN, intertwining the realms of adipose biology and ophthalmology in aging. The remarkable connection between fat, in the form of adiponectin, and t654r4dexzsight opens exciting avenues for advancing eye health and improving patient outcomes.

Author(s) Details:

Mayank Choubey,
Department of Foundations of Medicine, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.

Munichandra B. Tirumalasetty,
Department of Foundations of Medicine, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.

Nalini S. Bora,
Department of Ophthalmology, Jones Eye Institute, Pat & Willard Walker Eye Research Center, 4301 West Markham, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

Puran S. Bora,
Department of Ophthalmology, Jones Eye Institute, Pat & Willard Walker Eye Research Center, 4301 West Markham, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

Please see the link here: https://stm.bookpi.org/ANUMS-V10/article/view/13958