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Summary: Humanin G treatment reduced protein levels of inflammatory markers that are elevated in age-related macular degeneration.
Source: Impact Journals
Inflammatory processes drive the progression of age-related macular degeneration (AMD) — a leading cause of vision loss in the United States.
In this new aging In a study, researchers at the University of California Irvine and the University of Southern California compared the protein levels of inflammatory markers in normal and AMD retinal pigment epithelium (RPE) transmitochondrial cybrid cells and examined the effects of treatment with exogenous humanin G.
Humanin G (HNG) is a mitochondrial-derived peptide that is cytoprotective in AMD and may protect against mitochondrial and cellular stress induced by damaged AMD mitochondria.
“The aim of this study was to test our hypothesis that inflammation-associated marker protein levels are elevated in AMD and that treatment with HNG leads to a reduction in their protein levels.”
Humanin G protein levels were measured in plasma from AMD patients and normal subjects using an ELISA assay. Humanin G was added to AMD and normal (control) cybrids derived from clinically characterized AMD patients and normal (control) subjects.
Cell lysates were extracted from untreated and HNG-treated AMD and normal cybrids, and the Luminex XMAP multiplex assay was used to measure levels of inflammatory proteins.
The researchers found that there were different levels of inflammatory proteins between normal and AMD plasma samples. Compared to control plasma samples, AMD plasma showed higher protein levels of inflammatory markers.
However, plasma levels of endogenous humanin protein were 36.58% lower in AMD patients than in age-matched healthy subjects. After treatment with Humanin G, the researchers observed a significant reduction in protein levels of inflammatory markers that were elevated in the transferred AMD-RPE cybrid cells.
“In conclusion, we present new findings that: a) show reduced humanin protein levels in AMD plasma compared to normal plasma; b) suggest the role of inflammatory markers in AMD pathogenesis; and c) highlight the beneficial effects of humanin G in reducing inflammation in AMD.”
To the teams’ knowledge, this is the first study to find significantly reduced humanin protein levels in AMD patients, confirming humanin’s critical role in maintaining tissue homeostasis and normal eye function.
“Our discovery is novel and may contribute to the development of therapeutic tools to reduce inflammation to alleviate the pathology of AMD disease,” the researchers conclude.
There is news from research about this age-related macular degeneration
Author: press office
Source: Impact Journals
Contact: Press Office – Impact Journals
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Original research: Open access.
“Effect of humanin G (HNG) on inflammation in age-related macular degeneration (AMD)” by Sonali Nashine et al. aging
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abstract
Effect of humanin G (HNG) on inflammation in age-related macular degeneration (AMD)
Inflammation plays a crucial role in the etiology and pathogenesis of AMD (age-related macular degeneration). Humanin G (HNG) is a mitochondrial-derived peptide (MDP) that is cytoprotective in AMD and may protect against mitochondrial and cellular stress induced by damaged AMD mitochondria.
The aim of this study was to test our hypothesis that inflammation-associated marker protein levels are elevated in AMD and treatment with HNG leads to a reduction in their protein levels. Humanin protein levels were measured in plasma from AMD patients and normal subjects using an ELISA assay. Humanin G was added to AMD and normal cybrids (control), which had identical nuclei from mitochondrial-deficient ARPE-19 cells but differed in mitochondrial DNA (mtDNA) content, derived from clinically characterized AMD patients and normal (control) subjects came from.
Cell lysates were extracted from untreated and HNG-treated AMD and normal cybrids, and the Luminex XMAP multiplex assay was used to measure levels of inflammatory proteins. AMD plasma showed reduced humanin protein levels but higher protein levels of inflammatory markers compared to control plasma samples.
In AMD-RPE hybrid cells, humanin G reduced CD62E/E selectin, CD62P/P selectin, ICAM-1, TNF-α, MIP-1α, IFN-γ, IL-1β, IL-13 and IL-17A protein levels, suggesting that humanin G can rescue AMD cybrids from mtDNA-mediated inflammation.
Finally, we present new findings that: A) show reduced humanin protein levels in AMD plasma versus normal plasma; B) propose the role of inflammatory markers in AMD pathogenesis and C) highlight the beneficial effects of humanin G in reducing inflammation in AMD.
