ZNF862 induces cytostasis and apoptosis via the p21-RB1 and Bcl-xL-Caspase 3 signaling pathways in human gingival fibroblasts.

OBJECTIVE: This study investigates the effects of ZNF862 on the proliferation and apoptosis of human gingival fibroblasts and their related mechanisms. BACKGROUND: As a major transcription factor family, zinc finger proteins (ZFPs) regulate cell differentiation, growth, and apoptosis through their conserved zinc finger motifs, which allow high flexibility and specificity in gene regulation. In our previous study, ZNF862 mutation was associated with hereditary gingival fibromatosis. Nevertheless, little is known about the biological function of ZNF862. Therefore, this study was aimed to reveal intracellular localization of ZNF862, the influence of ZNF862 on the growth and apoptosis of human gingival fibroblasts (HGFs) and its potential related mechanisms. METHODS: Immunohistochemistry, immunofluorescence staining, and western blotting were performed to determine the intracellular localization of ZNF862 in HGFs. HGFs were divided into three groups: ZNF862 overexpression group, ZNF862 interference group, and the empty vector control group. Then, the effects of ZNF862 on cell proliferation, migration, cell cycle, and apoptosis were evaluated. qRT-PCR and western blotting were performed to further explore the mechanism related to the proliferation and apoptosis of HGFs. RESULTS: ZNF862 was found to be localized in the cytoplasm of HGFs. In vitro experiments revealed that ZNF862 overexpression inhibited HGFs proliferation and migration, induced cell cycle arrest at the G0/G1-phase and apoptosis. Whereas, ZNF862 knockdown promoted HGFs proliferation and migration, accelerated the transition from the G0/G1 phase into the S and G2/M phase and inhibited cell apoptosis. Mechanistically, the effects of ZNF862 on HGFs proliferation and apoptosis were noted to be dependent on inhibiting the cyclin-dependent kinase inhibitor 1A (p21)-retinoblastoma 1 (RB1) signaling pathway and enhancing the B-cell lymphoma-extra-large (Bcl-xL)-Caspase 3 signaling pathway. CONCLUSION: Our results for the first time reveal that ZNF862 is localized in the cytoplasm of HGFs. ZNF862 can inhibit the proliferation of HGFs by inhibiting the p21-RB1 signaling pathway, and it also promotes the apoptosis of HGFs by enhancing the Bcl-xL-Caspase 3 signaling pathway.

Multiple idiopathic cervical root resorption: A systematic review.

The current literature on multiple idiopathic cervical root resorption (MICRR), a rare and aggressive form of external root resorption, is limited to case reports and series. Therefore, we performed a systematic review of this condition. A comprehensive search of PubMed, Embase, Web of science, Cochrane Library, CNKI, and WANFANG was conducted using key terms relevant to MICRR, supplemented by a grey literature search. Risk of bias was assessed using Cochrane's and Joanna Briggs Institute's tools. A total of 36 studies with 47 cases were included. MICRR is more common among younger females and may be related to hormonal changes and denosumab use. Initially, the premolars are usually affected but all permanent teeth may eventually be involved. Cone-beam computed tomography is recommended for diagnosis and assessment of resorptive lesions. The management is focused on complete removal and restoration of the resorptive tissue to maintain the tooth's structural integrity. However, MICRR usually has a poor prognosis. Due to its invasive and aggressive behavior, MICRR requires greater attention.

Pharmaceutical excipient salts effect on micellization and drug solubilization of PEO-PPO-ph-PPO-PEO block copolymer.

Hydrophobic modification PEO-PPO copolymer BP123 was synthesized, with two aromatic rings in the centre linked to PEO-PPO blocks, and the identical PEO and PPO block numbers were possessed with commercial copolymer P123. The influence of three common pharmaceutical excipient salts sodium chloride (NaCl), sodium citrate (NaCA) and sodium benzoate (NaBZ) on self-assembly behaviors of BP123 and P123 was investigated via cloud point, surface tension, pyrene fluorescence and dynamic light scattering. Solubilization for hydrophobic drug simvastatin (SV) and in vitro drug release behavior were assessed accordingly. In the presence of NaCl or NaCA, cloud point and critical micellization concentration (CMC) decreased, micelles became more hydrophobic, micellar size and drug solubilization increased, drug release rate slowed, and the impact of NaCA was more significant than NaCl. Oppositely, cloud point and CMC increased with the addition of NaBZ. NaBZ could participate in the formation of micelles by hydrophobic aromatic ring, which greatly raised solubilization of SV. Moreover, a different performance occurred when NaBZ was added to BP123 or P123, due to the hydrophobic benzene rings in BP123, which prominently enhanced the interaction with hydrophobic drug, leading to obvious delay of drug release for BP123. This work is conducive to turning copolymer property in diverse pharmaceutical applications and in drug delivery systems as drug carriers.