ArticleIn vitro cellular & developmental biology. Animal2022
Chloroquine regulates the proliferation and apoptosis of palate development on mice embryo by activating P53 through blocking autophagy in vitro.
Article in In vitro cellular & developmental biology. Animal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Integrated Phosphoproteomics Identifies TGFβ-Dependent Phosphorylation Events Linking Kinase Signaling to Autophagy in Palatogenesis.Proteomes · 2026Article
- Salvianolic acid A alleviates HScientific reports · 2024Article
- Inhibition ofInternational journal of molecular sciences · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cleft lip and palate is one of the most frequent congenital developmental defects. Autophagy is a highly conserved process of cell self-degradation in eukaryotes, involving multiple biological processes in which chloroquine (CQ) is the most common inhibitor. However, whether CQ affects and how it affects palate development is unknown. Mouse embryonic palatal cells (MEPCs) were treated with CQ to observe cell viability, apoptosis, migration, osteogenic differentiation by cell proliferation assay, flow cytometric analysis, scratch assay, and alizarin red staining. PI staining was used to measure cell cycle distribution. Immunofluorescence (IF) assay and transmission electron microscopy were used to detect autophagosomes. The autophagy-related factors (LC3 and P62), apoptosis-related markers (P53, caspase-3 cleaved caspase-3, BAX, and BCL-2), and cell cycle-related proteins (P21, CDK2, CDK4, cyclin D1, and cyclin E) were all measured by western blot. CQ inhibited the proliferation of MEPCs by arresting the G0/G1 phase of the cell cycle in a concentration- and time-dependent manner with cell cycle-related proteins P21 upregulated and CDK2, CDK4, cyclin D1, and cyclin E downregulated. Then we detected CQ also induced cell apoptosis in a dose-dependent manner by decreasing the BCL-2/BAX ratio and increasing cleaved caspase-3. Next, it was investigated that migration and osteogenesis of MEPCs decreased with CQ treatment in a dose-dependent manner. Meanwhile, CQ blocked the autophagy pathway by upregulating LC3II and P62 expressions which activated the P53 pathway. CQ activates P53 which affects MEPC biological characteristics by changing the proliferation and apoptosis of MEPCs through inhibiting autophagy.
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