ArticleMolecular vision2020
Accumulation of Asn450Tyr mutant myocilin in ER promotes apoptosis of human trabecular meshwork cells.
Article in Molecular vision, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Protein misfolding and mitochondrial dysfunction in glaucoma.Frontiers in cell and developmental biology · 2025Review
- The S341P mutant MYOC renders the trabecular meshwork sensitive to cyclic mechanical stretch.Heliyon · 2024Article
- Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review).Molecular medicine reports · 2024Review
- Serine to proline mutation at position 341 of MYOC impairs trabecular meshwork function by causing autophagy deregulation.Cell death discovery · 2024Article
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Integrated analysis of long non-coding RNAs and mRNAs associated with glaucomaFrontiers in endocrinology · 2023Article
- Structure‒function‒pathogenicity analysis of C-terminal myocilin missense variants based on experiments and 3D models.Frontiers in genetics · 2022Article
- Thrombospondin-1 Signaling Through the Calreticulin/LDL Receptor Related Protein 1 Axis: Functions and Possible Roles in Glaucoma.Frontiers in cell and developmental biology · 2022Review
- Myocilin Gene Mutation Induced Autophagy Activation Causes Dysfunction of Trabecular Meshwork Cells.Frontiers in cell and developmental biology · 2022Article
- The Potential Role of Small-Molecule PERK Inhibitor LDN-0060609 in Primary Open-Angle Glaucoma Treatment.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: In a previous study, we identified the Asn450Tyr mutant myocilin gene ( Methods: Primary HTM cells were infected with lentivirus with wild-type myocilin ( Results: We found that non-secretion of Myoc-N450Y induced ER stress by colocalization with the ER marker calreticulin (CALR), and upregulating the expression of ER stress markers in primary HTM cells. Moreover, overexpression of Myoc-N450Y inhibited the viability and induced apoptosis of primary HTM cells, and inhibition of PI3K/AKT signaling was induced by ER stress. Reduction in ER stress with 4-PBA decreased the level of ER stress markers, promoted secretion, and prevented accumulation of myocilin in the Myoc-N450Y group. Apoptosis was rescued, and inhibition of PI3K/AKT signaling was reversed, after PBA treatment in primary HTM cells with Myoc-N450Y overexpression. Conclusions: The study results suggest that Myoc-N450Y promotes apoptosis of primary HTM cells via the ER stress-induced apoptosis pathway, in which the PI3K/AKT signaling pathway plays a crucial role.
Indexed as
Identifiers
32818018PMC7406863W3047545192What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.