1.Research advance in preparation and functional modification of porous polytetrafluoroethylene artificial blood vessels
Rong XU ; Haojie WANG ; Mengxiang GENG ; Kai MENG ; Hui WANG ; Keqin ZHANG ; Huijing ZHAO
Chinese Journal of Tissue Engineering Research 2024;28(5):759-765
BACKGROUND:Medium-and large-diameter polytetrafluoroethylene artificial blood vessels have been widely used in clinical practice.However,most of the products were imported from other countries.Small-diameter porous polytetrafluoroethylene vessels are easy to form thrombosis and intimal hyperplasia,resulting in an extremely low long-term patency rate,which is difficult to fulfill clinical requirements. OBJECTIVE:To review and summarize the research progress of polytetrafluoroethylene in the field of artificial blood vessels,which can provide a reference for the functional modification of small-diameter polytetrafluoroethylene artificial blood vessels and the improvement of their long-term patency rate. METHODS:The relevant articles published from October 2022 to March 2023 in CNKI,Web of Science,Wiley Online Library,SpringerLink,Science Direct and IOP Science databases were searched by the first author.The search terms in Chinese were"porous polytetrafluoroethylene,vascular graft,electrospinning,medical application,functional modification".The search terms in English were"ePTFE,porous polytetrafluoroethylene,vascular graft,electrospinning,medical application,functional modification".All the articles about the preparation and modification of polytetrafluoroethylene artificial blood vessels were retrieved. RESULTS AND CONCLUSION:The preparation and functional modification of porous polytetrafluoroethylene artificial blood vessels were still research hotspots and difficult problems.From the research progress in and outside China in recent years,the preparation of porous polytetrafluoroethylene artificial blood vessels mainly adopted the rapid thermal stretching method,but the preparation of polytetrafluoroethylene artificial blood vessels by electrospinning was a promising new method.By analyzing and summarizing different functional modification methods,it was found that the long-term patency rate of porous polytetrafluoroethylene artificial blood vessels had been improved.However,the functional modification of small-diameter polytetrafluoroethylene artificial blood vessels still needed further exploration and optimization.
2.Lysosomal membrane protein Sidt2 knockout induces apoptosis of human hepatocytes in vitro independent of the autophagy-lysosomal pathway.
Jiating XU ; Mengya GENG ; Haijun LIU ; Wenjun PEI ; Jing GU ; Mengxiang QI ; Yao ZHANG ; Kun LÜ ; Yingying SONG ; Miaomiao LIU ; Xin HU ; Cui YU ; Chunling HE ; Lizhuo WANG ; Jialin GAO
Journal of Southern Medical University 2023;43(4):637-643
OBJECTIVE:
To explore the regulatory mechanism of human hepatocyte apoptosis induced by lysosomal membrane protein Sidt2 knockout.
METHODS:
The Sidt2 knockout (Sidt2-/-) cell model was constructed in human hepatocyte HL7702 cells using Crispr-Cas9 technology.The protein levels of Sidt2 and key autophagy proteins LC3-II/I and P62 in the cell model were detected using Western blotting, and the formation of autophagosomes was observed with MDC staining.EdU incorporation assay and flow cytometry were performed to observe the effect of Sidt2 knockout on cell proliferation and apoptosis.The effect of chloroquine at the saturating concentration on autophagic flux, proliferation and apoptosis of Sidt2 knockout cells were observed.
RESULTS:
Sidt2-/- HL7702 cells were successfully constructed.Sidt2 knockout significantly inhibited the proliferation and increased apoptosis of the cells, causing also increased protein expressions of LC3-II/I and P62(P < 0.05) and increased number of autophagosomes.Autophagy of the cells reached a saturated state following treatment with 50 μmol/L chloroquine, and at this concentration, chloroquine significantly increased the expressions of LC3B and P62 in Sidt2-/- HL7702 cells.
CONCLUSION
Sidt2 gene knockout causes dysregulation of the autophagy pathway and induces apoptosis of HL7702 cells, and the latter effect is not mediated by inhibiting the autophagy-lysosomal pathway.
Humans
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Lysosome-Associated Membrane Glycoproteins/metabolism*
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Autophagy
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Apoptosis
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Hepatocytes
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Lysosomes/metabolism*
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Chloroquine/pharmacology*
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Nucleotide Transport Proteins/metabolism*