ArticleThe Journal of international medical research2018
Lens-specific deletion of the Msx2 gene increased apoptosis by enhancing the caspase-3/caspase-8 signaling pathway.
Article in The Journal of international medical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Unveiling ZNF124 as a novel determinant in neurodegeneration: orchestration of photoreceptor homeostasis through MSX2 transcriptional regulation.Cell death & disease · 2026Article
- Genetic and environmental factors contributing to anophthalmia and microphthalmia: Current understanding and future directions.World journal of clinical pediatrics · 2025Review
- A grape-supplemented diet prevented ultraviolet (UV) radiation-induced cataract by regulating Nrf2 and XIAP pathways.The Journal of nutritional biochemistry · 2024Article
- Disruption of common ocular developmental pathways in patient-derived optic vesicle models of microphthalmia.Stem cell reports · 2024Article
- Association analysis of apoptosis-related gene caspase3, Integrin a subunit 1 and glutathione sulfur transferase M1 gene polymorphisms and susceptibility to gastric cardia carcinoma.Journal of medical biochemistry · 2023Article
- Lens-specific conditional knockout of Msx2 in mice leads to ocular anterior segment dysgenesis via activation of a calcium signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective To investigate the influence of Msx2 conditional gene knockout during lens development in mice. Methods Lens-specific Msx2 knockout mice were generated using the Cre-loxP system. The eyes of Msx2 conditional knockout ( Msx2CKO) and wild-type ( Msx2WT) mice were examined during embryonic and early postnatal periods using histological, immunofluorescence, in situ hybridization, cell proliferation, apoptosis, and mRNA microarray analyses. Results Msx2CKO mice exhibited small lens formation and microphthalmia after birth, while Msx2CKO embryos exhibited a persistent lens stalk, small lens formation, and microphthalmia. Conditional deletion of Msx2 also led to an increased apoptosis rate, a significant reduction in FoxE3 expression, and an upregulation of Prox1 expression in the lens vesicle during the early embryonic period. Microarray comparison of Msx2CKO and Msx2WT lens transcriptomes identified a large number of differentially expressed genes. Real-time PCR showed that Casp8 and Casp3 expression was upregulated in Msx2CKO mice at post-natal day 1. Conclusion The activation of apoptosis through the caspase-8/caspase-3 signaling pathway, together with the downregulation of FoxE3 expression, appeared to account for the smaller lens formation in Msx2CKO mice.
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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.