Gene expression in retinal ischemic post-conditioning

Kadzielawa, Konrad; Mathew, Biji; Stelman, Clara R.; Lei, Arden Zhengdeng; Torres, Leianne; Roth, Steven

doi:10.1007/s00417-018-3905-0

Cited by 10 publications

(10 citation statements)

References 64 publications

(84 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Retinae were harvested 10 days after ischemia, shortly after our electrophysiologic assessments of functional outcome at 7 days postischemia, so the proteome profiles reported here do not necessarily represent the acute phase of a dynamic postischemic response nor ones representative of long-term recovery, but somewhere intermediate between the two. To this point, few of the changes in the retinal protein profile we measured in response to ischemia, with and without parental RHC, were found at the RNA level in response to ischemia, with and without postconditioning, in rats 41 ; the same is true for respective pathway analyses in this and our study. However, beyond species differences, this is not necessarily unexpected given that we measured retinae at 10 days postischemia and Roth's group measured at 1 day postischemia, and that mRNA abundance does not necessarily translate to protein abundance.…”

Section: Discussionsupporting

confidence: 72%

Intermittent Hypoxia Promotes Functional Neuroprotection from Retinal Ischemia in Untreated First-Generation Offspring: Proteomic Mechanistic Insights

Harman

Guidry

Gidday

2020

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

Purpose Stress can lead to short- or long-term changes in phenotype. Accumulating evidence also supports the transmission of maladaptive phenotypes, induced by adverse stressors, through the germline to manifest in subsequent generations, providing a novel mechanistic basis for the heritability of disease. In the present study in mice, we tested the hypothesis that repeated presentations of a nonharmful conditioning stress, demonstrated previously to protect against retinal ischemia, will also provide ischemic protection in the retinae of their untreated, first-generation (F1) adult offspring. Methods Swiss–Webster ND4 outbred mice were mated following a 16-week period of brief, every-other-day conditioning exposures to mild systemic hypoxia (repetitive hypoxic conditioning, RHC). Retinae of their 5-month-old F1 progeny were subjected to unilateral ischemia. Scotopic electroretinography quantified postischemic outcomes. The injury-resilient retinal proteome was revealed by quantitative mass spectrometry, and bioinformatic analyses identified the biochemical pathways and networks in which these differentially expressed proteins operate. Results Significant resilience to injury in both sexes was documented in F1 mice derived from RHC-treated parents, relative to matched F1 adult progeny derived from normoxic control parents. Ischemia-induced increases and decreases in the expression of many visual transduction proteins that are integral to photoreceptor function were abrogated by parental RHC, providing a molecular basis for the observed functional protection. Conclusions Our proteomic analyses provided mechanistic insights into the molecular manifestation of the inherited, injury-resilient phenotype. To our knowledge, this is the first study in a mammalian model documenting the reprogramming of heritability to promote disease resilience in the next generation.

show abstract

Section: Discussionsupporting

confidence: 72%

Intermittent Hypoxia Promotes Functional Neuroprotection from Retinal Ischemia in Untreated First-Generation Offspring: Proteomic Mechanistic Insights

Harman

Guidry

Gidday

2020

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

show abstract

“…KEGG analysis also showed that the NF-kappa B signaling pathway, Jak-STAT signaling pathway, Toll-like receptor signaling pathway, PI3K-Akt signaling pathway, TNF signaling pathway, MAPK signaling pathway, Calcium signaling pathway, cAMP signaling pathway, and Apoptosis were significantly enriched. These findings were in agreement with previous studies [12,[35][36][37][38][39][40][41]. Different expression profile between RIRI and DHF+RIRI revealed reversed pathways responsible for DHF treatment.…”

Section: Discussionsupporting

confidence: 93%

7,8-Dihydroxyflavone alleviates apoptosis and inflammation induced by retinal ischemia-reperfusion injury via activating TrkB/Akt/NF-kB signaling pathway

Yu¹,

Wang²,

Xing³

et al. 2022

Int. J. Med. Sci.

View full text Add to dashboard Cite

“…(i) Intravitreal administration: An intravitreal injection of MSCs is feasible as a means to reach the dysfunctional retinal ganglion cells. Injection of MSCs into the vitreous in a rodent model rescued the retina from ischemic damage by suppression of apoptosis, preserved autophagy, and attenuation of inflammation and vascular permeability [ 59 – 61 ]. Intravitreally transplanted MSCs may also function by donating functional mitochondria to retinal ganglion cells [ 62 ].…”

Section: Main Textmentioning

confidence: 99%

Emerging concepts in the treatment of optic neuritis: mesenchymal stem cell-derived extracellular vesicles

et al. 2021

Self Cite

View full text Add to dashboard Cite

Background Optic neuritis (ON) is frequently encountered in multiple sclerosis, neuromyelitis optica spectrum disorder, anti-myelin oligodendrocyte glycoprotein associated disease, and other systemic autoimmune disorders. The hallmarks are an abnormal optic nerve and inflammatory demyelination; episodes of optic neuritis tend to be recurrent, and particularly for neuromyelitis optica spectrum disorder, may result in permanent vision loss. Main Body Mesenchymal stem cell (MSC) therapy is a promising approach that results in remyelination, neuroprotection of axons, and has demonstrated success in clinical studies in other neuro-degenerative diseases and in animal models of ON. However, cell transplantation has significant disadvantages and complications. Cell-free approaches utilizing extracellular vesicles (EVs) produced by MSCs exhibit anti-inflammatory and neuroprotective effects in multiple animal models of neuro-degenerative diseases and in rodent models of multiple sclerosis (MS). EVs have potential to be an effective cell-free therapy in optic neuritis because of their anti-inflammatory and remyelination stimulating properties, ability to cross the blood brain barrier, and ability to be safely administered without immunosuppression. Conclusion We review the potential application of MSC EVs as an emerging treatment strategy for optic neuritis by reviewing studies in multiple sclerosis and related disorders, and in neurodegeneration, and discuss the challenges and potential rewards of clinical translation of EVs including cell targeting, carrying of therapeutic microRNAs, and prolonging delivery for treatment of optic neuritis. Graphical Abstract

show abstract

Gene expression in retinal ischemic post-conditioning

Cited by 10 publications

References 64 publications

Intermittent Hypoxia Promotes Functional Neuroprotection from Retinal Ischemia in Untreated First-Generation Offspring: Proteomic Mechanistic Insights

Intermittent Hypoxia Promotes Functional Neuroprotection from Retinal Ischemia in Untreated First-Generation Offspring: Proteomic Mechanistic Insights

7,8-Dihydroxyflavone alleviates apoptosis and inflammation induced by retinal ischemia-reperfusion injury via activating TrkB/Akt/NF-kB signaling pathway

Emerging concepts in the treatment of optic neuritis: mesenchymal stem cell-derived extracellular vesicles

Contact Info

Product

Resources

About