1.Application progress of collagen membranes in oral medicine.
Yiqin WANG ; Junliang WEN ; Xinhang YU ; Jun CHEN ; Wenjie LI
Journal of Central South University(Medical Sciences) 2025;50(6):1088-1098
Collagen membrane has attracted much attention from researchers due to its excellent properties such as wide source, degradable absorption, and low immunogenicity. However, they are limited by poor mechanical stability and rapid degradation. To enhance their physicochemical properties and biological functions, researchers have developed various strategies, including cross-linking, incorporation of growth factors or drugs, combination with other biomaterials, optimization of composition and structure, and substitution with marine-derived collagen. These advances aim to expand the clinical applications of collagen membranes in oral medicine. With the urgent demand for high-performance biomaterials in oral medicine, summarizing recent progress on collagen membranes provides valuable insights into their mechanisms, clinical efficacy, and limitations, offering reference for optimized design and broader clinical use. Furthermore, further trends may include integrating advanced manufacturing technologies to develop personalized collagen membranes, which could significantly improve therapeutic outcomes in oral diseases.
Collagen/therapeutic use*
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Humans
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Biocompatible Materials/chemistry*
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Membranes, Artificial
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Oral Medicine/methods*
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Tissue Engineering/methods*
2.PARP1 promotes the progression of hepatocellular carcinoma by regulating expression of POU2F2
Ziqiang WEN ; Junliang LAN ; Bo ZHOU ; Qiwei XU
China Oncology 2024;34(9):848-856
Background and purpose:Hepatocellular carcinoma(HCC)is a major disease seriously threatening human health.Poly(ADP-ribose)polymerase-1(PARP1)is an enzyme that catalyzes poly ADP-ribosylation.Given the role of PARP1 in DNA damage repair,it is generally considered as an oncogene.However,the expression of PARP1 and its mechanism in HCC are not yet clear.This study aimed to investigate the role of PARP1 in the occurrence and development of HCC and its potential mechanisms.Methods:First,we analyzed the expression pattern of PARP1 in The Cancer Genome Atlas(TCGA)and Clinical Proteomic Tumor Analysis Consortium(CPTAC)HCC database,and identified the expression trend of PARP1 in our HCC cohort using real-time fluorescence quantitative polymerase chain reaction(RTFQ-PCR)and Western blot.Then,the enzyme activity of PARP1 was inhibited by PJ34,an inhibitor of PARP1 and the expression of PARP1 in HCC cell lines was downregulated with small RNA interference technology.Based on these models,the following experiments were conducted:First,the effect of PARP1 on cell viability was assessed by cell counting kit-8(CCK-8)assay and flow cytometry;Second,the expression levels of stemness-related genes in HCC cells were identified using RTFQ-PCR;Third,the effect of inhibition of PARP1 on migration and invasion of HCC cells was detected by migration and invasion assay(transwell assay).Finally,bioinformatic analysis was performed to identify new target genes and the pathways regulated by PARP1 in HCC progression.Rescue experiments were performed to determine whether PARP1 target genes were involved in the malignant phenotypes of HCC cells.Results:The expression of PARP1 was significantly up-regulated in HCC tissues in both TCGA and CPTAC database.RTFQ-PCR and Western blot assays showed that PARP1 was obviously up-regulated in HCC tissues compared to paracancerous tissues.Survival analysis showed that PARP1 expression was significantly negatively correlated with the prognosis of patients.The results of CCK-8,flow cytometry,RTFQ-PCR and transwell assay indicated that inhibition of PARP1 attenuated proliferation and activity of HCC cells,as well as weakened their stemness,migration and invasion.Bioinformatics analysis suggested that PARP1-regulated genes were enriched in the nuclear factor-κB(NF-κB)and necroptosis pathways,with POU class homeobox 2(POU2F2)potentially being a target gene of PARP1.Correlation analysis,along with RTFQ-PCR and Western blot detection,confirmed that the expression of POU2F2 was regulated by PARP1,while not affected by PJ34,indicating the effect of nonenzymatic function of PARP1 on POU2F2.CCK-8,flow cytometry and RTFQ-PCR results showed that the reintroduction of POU2F2 enhanced proliferative capacity,increased activity,and promoted stemness of HCC cell lines with PARP1 knockdown.Conclusion:By positively regulating the expression of POU2F2,PARP1 promotes malignant phenotypes of HCC cells,providing new insights for clinical treatment and drug development for HCC.
3.Relation between cryptogenic ischemic stroke and patent foramen ovale in young and middle-aged adults
Yongsheng ZHU ; Xin MENG ; Wen JIANG ; Junliang HAN ; Jun LI ; Xiaodong ZHOU ; Jun ZHANG
Chinese Journal of Ultrasonography 2014;23(7):568-572
Objective To compare the prevalence of patent foramen ovale (PFO) in young and middle-aged patients with cryptogenic ischemic stroke (CS) and in normal population.Methods The casecontrol study included consecutive 318 young and middle-aged patients with CS and 336 normal control subjects with matched age and sex for group comparisons.Stroke risk factors including hypertension,diabetes mellitus,hyperlipidemia,ischemic heart disease,atrial fibrillation,carotid atherosclerosis plagues and smoking,etc.were studied.Transesophageal echocardiography (TEE) were performed to detect the presence of PFO.The prevalence of PFO and difference of risk factor levels between the groups was compared.Then the odds ratios (OR) of a PFO was estimated in CS patients versus control subjects.Results The prevalence of PFO was significant higher in patients with CS than in control subjects (145/318,45.6 % versus 46/336,13.7%,P <0.001).The odds ratio(OR) for PFO in CS for patients versus control subjects was 5.3 (confidence interval,3.6 to 7.8).The mean size of PFO was larger in stroke group than that in control group (P < 0.001).There were no significant differences in levels of other stroke risk factors between two groups.Conclusions PFO may play an important role in etiology of CS in young and middleaged adults.Larger and longer PFOs may be more concomitant with ischemic attacks.More efforts should be employed in patients with CS to detect PFO for further treatment.

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