Autophagy and post-ischemic conditioning in retinal ischemia

Mathew, Biji; Chennakesavalu, Mohansrinivas; Sharma, Monica; Torres, Leianne; Stelman, Clara R.; Tran, Sophie; Patel, Raj; Burg, Nathan; Salkovski, Maryna; Kadzielawa, Konrad; Seiler, Figen A.; Aldrich, Leslie N.; Roth, Steven

doi:10.1080/15548627.2020.1767371

Cited by 45 publications

(20 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because autophagy is an essential survival mechanism in photoreceptor cells, it plays a key role in sustaining photoreceptor function by facilitating photoreceptor outer segment degradation and visual pigment recycling ( Mathew et al, 2021a ; Villarejo-Zori et al, 2021 ). Although the mechanism by which autophagy protects photoreceptors and the relationship between DR and autophagy are ambiguous, more recent studies have corroborated the importance of autophagic flux.…”

Section: Involved Cellsmentioning

confidence: 99%

Diabetic retinopathy: Involved cells, biomarkers, and treatments

et al. 2022

View full text Add to dashboard Cite

Diabetic retinopathy (DR), a leading cause of vision loss and blindness worldwide, is caused by retinal neurovascular unit dysfunction, and its cellular pathology involves at least nine kinds of retinal cells, including photoreceptors, horizontal and bipolar cells, amacrine cells, retinal ganglion cells, glial cells (Müller cells, astrocytes, and microglia), endothelial cells, pericytes, and retinal pigment epithelial cells. Its mechanism is complicated and involves loss of cells, inflammatory factor production, neovascularization, and BRB impairment. However, the mechanism has not been completely elucidated. Drug treatment for DR has been gradually advancing recently. Research on potential drug targets relies upon clear information on pathogenesis and effective biomarkers. Therefore, we reviewed the recent literature on the cellular pathology and the diagnostic and prognostic biomarkers of DR in terms of blood, protein, and clinical and preclinical drug therapy (including synthesized molecules and natural molecules). This review may provide a theoretical basis for further DR research.

show abstract

Section: Involved Cellsmentioning

confidence: 99%

Diabetic retinopathy: Involved cells, biomarkers, and treatments

et al. 2022

View full text Add to dashboard Cite

show abstract

“…The R28 cells are immortalized, rat retinal origin, heterogenous, precursor cells with differentiation potential [ 26 ]. According to the published methods, R28 cells were differentiated to neuronal phenotype with the addition of a modified form of cAMP and laminin and grown using DMEM [ 44 , 45 , 46 ]. Studies by Seigel et al utilizing R28 cells demonstrate the expression of neuron-specific markers such as MAP2, Syntaxin, NSE, and Nestin, along with neurotransmission receptors [ 26 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis

Candadai

Liu

Verma

et al. 2021

Cells

View full text Add to dashboard Cite

Visual dysfunction resulting from optic neuritis (ON) is one of the most common clinical manifestations of multiple sclerosis (MS), characterized by loss of retinal ganglion cells, thinning of the nerve fiber layer, and inflammation to the optic nerve. Current treatments available for ON or MS are only partially effective, specifically target the inflammatory phase, and have limited effects on long-term disability. Fingolimod (FTY) is an FDA-approved immunomodulatory agent for MS therapy. The objective of the current study was to evaluate the neuroprotective properties of FTY in the cellular model of ON-associated neuronal damage. R28 retinal neuronal cell damage was induced through treatment with tumor necrosis factor-α (TNFα). In our cell viability analysis, FTY treatment showed significantly reduced TNFα-induced neuronal death. Treatment with FTY attenuated the TNFα-induced changes in cell survival and cell stress signaling molecules. Furthermore, immunofluorescence studies performed using various markers indicated that FTY treatment protects the R28 cells against the TNFα-induced neurodegenerative changes by suppressing reactive oxygen species generation and promoting the expression of neuronal markers. In conclusion, our study suggests neuroprotective effects of FTY in an in vitro model of optic neuritis.

show abstract

“…This suggests that the timing of intervention is important; autophagy activation at early stage of a developing condition may be beneficial. Tat-BECN1 inhibits apoptotic cell death in many in vitro or in vivo models: during renal ischemia/reperfusion, pretreatment with Tat-BECN1 inhibits apoptosis and prevents renal injury ( Livingston et al, 2019 ); under oxygen glucose deprivation, the in vitro model of ischemia, Tat-BECN1 decreases apoptosis of endothelial progenitor cells ( Jiang et al, 2020 ) and retinal neurons ( Mathew et al, 2021 ); Tat-BECN1 blocks cardiomyocytes apoptosis under pressure overload ( Shirakabe et al, 2016 ); it also alleviates cisplatin (a cancer drug known for nephrotoxicity)-induced cell death in renal proximal tubule cells ( Wang S. et al, 2021 ) or PKM2 silence-induced apoptosis in acute myeloid leukemia cell line with mutated nucleophosmin ( Wang L. et al, 2019 ). Tat-BECN1 not only reduces apoptosis but enhances proliferation in synovial intima cells leading to synovial hyperplasia in mouse knee joints ( Rockel et al, 2020 ); it augments cardiac hypertrophy in autosomal dominant polycystic kidney disease mouse model ( Atwood et al, 2020 ).…”

Section: Effects Of Tat-becn1 On Cell Deathmentioning

confidence: 99%

Development of an autophagy activator from Class III PI3K complexes, Tat-BECN1 peptide: Mechanisms and applications

Lu²,

Zhao³

2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Impairment or dysregulation of autophagy has been implicated in many human pathologies ranging from neurodegenerative diseases, infectious diseases, cardiovascular diseases, metabolic diseases, to malignancies. Efforts have been made to explore the therapeutic potential of pharmacological autophagy activators, as beneficial health effects from caloric restriction or physical exercise are linked to autophagy activation. However, the lack of specificity remains the major challenge to the development and clinical use of autophagy activators. One candidate of specific autophagy activators is Tat-BECN1 peptide, derived from Beclin 1 subunit of Class III PI3K complexes. Here, we summarize the molecular mechanisms by which Tat-BECN1 peptide activates autophagy, the strategies for optimization and development, and the applications of Tat-BECN1 peptide in cellular and organismal models of physiology and pathology.

show abstract

Autophagy and post-ischemic conditioning in retinal ischemia

Cited by 45 publications

References 61 publications

Diabetic retinopathy: Involved cells, biomarkers, and treatments

Diabetic retinopathy: Involved cells, biomarkers, and treatments

Neuroprotective Effects of Fingolimod in a Cellular Model of Optic Neuritis

Development of an autophagy activator from Class III PI3K complexes, Tat-BECN1 peptide: Mechanisms and applications

Contact Info

Product

Resources

About