Chloroquine regulates the proliferation and apoptosis of palate development on mice embryo by activating P53 through blocking autophagy in vitro

Chen, Jing; Yao, Yaxia; Wang, Xiaotong; Wang, Yijia; Li, Tianli; Du, Juan

doi:10.1007/s11626-022-00704-8

Cited by 2 publications

(2 citation statements)

References 66 publications

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“…It has been found that exposure of cells to oxidative stress leads to senescence by activating p53 through the initiation of the DNA damage response pathway and activating the downstream factor p21. Activated p21 blocks the G1 cell cycle and inhibits the activity of cell cycle proteins, such as Cyclin E1 32 . In our results SalA inhibited p53, p21 and promoted Cyclin E1 expression levels, these results indicated that SalA rescued H 2 O 2 -induced cellular senescence.…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid A alleviates H2O2-induced endothelial oxidative injury via miR-204-5p

Qiao,

Cao,

Chen

et al. 2024

Sci Rep

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Oxidative stress induced endothelial dysfunction plays a particularly important role in promoting the development of cardiovascular diseases (CVDs). Salvianolic acid A (SalA) is a water-soluble component of traditional Chinese medicine Salvia miltiorrhiza Bunge with anti-oxidant potency. This study aims to explore the regulatory effect of SalA on oxidative injury using an in vitro model of H2O2-induced injury in human umbilical vein endothelial cells (HUVECs). In the study, we determined cell viability, the activities of Lactate dehydrogenase (LDH) and Superoxide dismutase (SOD), cell proliferation rate and intracellular reactive oxygen species (ROS). Flow cytometry was used to detect cell apoptosis. Western-blotting was used to evaluate the expression of cell senescence, apoptosis, autophagy and pyroptosis protein factors. The expression level of miRNA was determined by qRT-PCR. Compared with H2O2-induced HUVECs, SalA promoted cell viability and cell proliferation rate; decreased LDH and ROS levels; and increased SOD activity. SalA also significantly attenuated endothelial senescence, inhibited cell apoptosis, reversed the increase of LC3 II/I ratio and NLRP3 accumulation. Furthermore, miR-204-5p was regulated by SalA. Importantly, miR-204-5p inhibitor had similar effect to that of SalA on H2O2-induced HUVECs. Our results indicated that SalA could alleviate H2O2-induced oxidative injury by downregulating miR-204-5p in HUVECs.

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Section: Discussionmentioning

confidence: 99%

Salvianolic acid A alleviates H2O2-induced endothelial oxidative injury via miR-204-5p

Qiao,

Cao,

Chen

et al. 2024

Sci Rep

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“…A total of 1 mL of fixative solution was added and kept at 4 °C for 30 min. The staining solution was added and kept for 1 h. Finally, the images were captured with a light microscope after the fixative solution was removed [ 59 ].…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Cxcr4 Disrupts Mouse Embryonic Palatal Mesenchymal Cell Migration and Induces Cleft Palate Occurrence

Zheng

Zhao

Wang

et al. 2023

IJMS

Self Cite

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Many processes take place during embryogenesis, and the development of the palate mainly involves proliferation, migration, osteogenesis, and epithelial–mesenchymal transition. Abnormalities in any of these processes can be the cause of cleft palate (CP). There have been few reports on whether C-X-C motif chemokine receptor 4 (CXCR4), which is involved in embryonic development, participates in these processes. In our study, the knockdown of Cxcr4 inhibited the migration of mouse embryonic palatal mesenchymal (MEPM) cells similarly to the use of its inhibitor plerixafor, and the inhibition of cell migration in the Cxcr4 knockdown group was partially reversed by supplementation with C-X-C motif chemokine ligand 12 (CXCL12). In combination with low-dose retinoic acid (RA), plerixafor increased the incidence of cleft palates in mice by decreasing the expression of Cxcr4 and its downstream migration-regulating gene Rac family small GTPase 1 (RAC1) mediating actin cytoskeleton to affect lamellipodia formation and focal complex assembly and ras homolog family member A (RHOA) regulating the actin cytoskeleton to affect stress fiber formation and focal complex maturation into focal adhesions. Our results indicate that the disruption of cell migration and impaired normal palatal development by inhibition of Cxcr4 expression might be mediated through Rac1 with RhoA. The combination of retinoic acid and plerixafor might increase the incidence of cleft palate, which also provided a rationale to guide the use of the drug during conception.

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Chloroquine regulates the proliferation and apoptosis of palate development on mice embryo by activating P53 through blocking autophagy in vitro

Cited by 2 publications

References 66 publications

Salvianolic acid A alleviates H2O2-induced endothelial oxidative injury via miR-204-5p

Salvianolic acid A alleviates H2O2-induced endothelial oxidative injury via miR-204-5p

Inhibition of Cxcr4 Disrupts Mouse Embryonic Palatal Mesenchymal Cell Migration and Induces Cleft Palate Occurrence

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