ArticleInvestigative ophthalmology & visual science2021
iPSC-Derived Trabecular Meshwork Cells Stimulate Endogenous TM Cell Division Through Gap Junction in a Mouse Model of Glaucoma.
Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Tracer Techniques in Ophthalmology: Ocular Applications and Systemic Connections.Diagnostics (Basel, Switzerland) · 2026Review
- Bioengineered 3D Human Trabecular Meshwork Models for Outflow Physiology and Glaucoma Research.Bioengineering (Basel, Switzerland) · 2026Review
- Experimental models to study oxidative stress in glaucoma: integratingFrontiers in pharmacology · 2026Review
- iPSC-derived ITGA6-positive cells restore aqueous humor outflow in glaucoma eyes.Nature communications · 2025Article
- Advances in Regenerative Medicine, Cell Therapy, and 3D Bioprinting for Glaucoma and Retinal Diseases.Advances in experimental medicine and biology · 2025Review
- A comprehensive analysis of induced pluripotent stem cell (iPSC) production and applications.Frontiers in cell and developmental biology · 2025Review
- Glial connexins in glaucoma.Frontiers in neuroscience · 2025Review
- iPSC-derived cells stimulate ABCG2Cell proliferation · 2024Article
- New Perspectives in Stem Cell Transplantation and Associated Therapies to Treat Retinal Diseases: From Gene Editing to 3D Bioprinting.Stem cell reviews and reports · 2024Review
- Serine to proline mutation at position 341 of MYOC impairs trabecular meshwork function by causing autophagy deregulation.Cell death discovery · 2024Article
- Posterior corneoscleral limbus: Architecture, stem cells, and clinical implications.Progress in retinal and eye research · 2023Review
- Exogenously delivered iPSCs disrupt the natural repair response of endogenous MPCs after bone injury.Scientific reports · 2023Article
- Application of a Magnetic Platform in α6 Integrin-Positive iPSC-TM Purification.Bioengineering (Basel, Switzerland) · 2023Article
- iPSCs-Based Therapy for Trabecular Meshwork.Handbook of experimental pharmacology · 2023Article
- Review
- Systemic Treatment with Pioglitazone Reverses Vision Loss in Preclinical Glaucoma Models.Biomolecules · 2022Article
- Magnetic Nano-Platform Enhanced iPSC-Derived Trabecular Meshwork Delivery and Tracking Efficiency.International journal of nanomedicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Purpose: Decreased trabecular meshwork (TM) cellularity has been implicated as a major reason for TM dysfunction and aqueous humor (AH) outflow abnormalities in primary open angle glaucoma. We previously found that transplantation of induced pluripotent stem cell (iPSC)-derived TM cells can restore TM function and stimulate endogenous TM cell division. The goal of the present study is to investigate whether signaling via gap junctions is involved in this process. Methods: Differentiated iPSCs were characterized morphologically, transcriptionally, and immunohistochemically. After purification, iPSC-TM were co-cultured with mouse TM (MTM) cells to mimic the transplantation procedure. Through the pharmacological antagonists and short hairpin RNA (shRNA) technique, the gap junction function in iPSC-based therapy was determined. Results: In the co-culture system, iPSC-TM increase MTM cell division as well as transfer of Ca2+ to MTM. This effect was blocked by treatment with the gap junction inhibitors carbenoxolone (CBX) or flufenamic acid (FFA). The shRNA mediated knock down of connexin 43 (Cx43) expression in iPSC-TM also results in decreased Ca2+ transfer and lower MTM proliferation rates. In vivo, Cx43 downregulation in transplanted iPSC-TM weakened their regenerative role in an Ad5.myocilinY437H mouse model of glaucoma. Mice receiving these cells exhibited lower TM cellularity and higher intraocular pressure (IOP) than those receiving unmodified iPSC-TM. Conclusions: Our findings reveal a crucial role of gap junction, especially Cx43, in iPSC-based TM regeneration, and provides insights to enhance the regenerative effect of iPSCs in glaucoma therapy.
Indexed as
Identifiers
What 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.