[1]张毓姣,郭智辉,孟艳斌,等.circ-0030042通过miR-145/PTEN轴调控对增生性瘢痕成纤维细胞增殖及迁移的影响[J].中国美容医学,2024,(1):49-53.[doi:10.15909/j.cnki.cn61-1347/r.006094]
　ZHANG Yujiao,GUO Zhihui,MENG Yanbin,et al.Effect of circ-0030042 on Proliferation and Migration of Fibroblasts in Hypertrophic Scar by Regulation of miR-145/PTEN Axis[J].Medical Aesthetics and Beauty,2024,(1):49-53.[doi:10.15909/j.cnki.cn61-1347/r.006094]
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circ-0030042通过miR-145/PTEN轴调控对增生性瘢痕成纤维细胞增殖及迁移的影响()
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《中国美容医学》[ISSN:1008-6445/CN:61-1347/R]

卷:
期数:
2024年1期
页码:
49-53
栏目:
出版日期:
2024-01-10

文章信息/Info

Title:
Effect of circ-0030042 on Proliferation and Migration of Fibroblasts in Hypertrophic Scar by Regulation of miR-145/PTEN Axis
文章编号:
1008-6455（2024）01-0049-05
作者:
张毓姣1 ; 郭智辉2 ; 孟艳斌1 ; 高亚丽3 ; 段 鹏2 ; 郝振明1
[太原钢铁（集团）有限公司总医院 1.烧伤二科；2.烧伤一科；3.皮肤科 山西 太原 030000]
Author(s):
ZHANG Yujiao1 ; GUO Zhihui2 ; MENG Yanbin1 ; GAO Yali3 ; DUAN Peng2 ; HAO Zhenming1
[1.Department of Burn , 2.Department of Burn , 3.Department of Dermatology, General Hospital of Taiyuan Iron and Steel (Group) Co.,Ltd.,Taiyuan 030000,Shanxi,China]
关键词:
circ-0030042; miR-145/PTEN轴; 增生性瘢痕; 成纤维细胞; 细胞迁移/增殖
Keywords:
circ-0030042;  miR-145/PTEN shaft;  hypertrophic scarring;  fi broblast;  cell migration/proliferation
分类号:
R619+ .6
DOI:
10.15909/j.cnki.cn61-1347/r.006094
文献标志码:
A
摘要:
目的：探讨circ-0030042与人第10号染色体缺失的磷酸酶（Phosphatase and tensin homolog deleted on chromosome ten,PTEN）的相互作用关系，并分析其在增生性瘢痕（Hypertrophic scar,HS）患者中对成纤维细胞增殖与 迁移的影响及作用机制。方法：通过circRNA序列和定量聚合酶链反应（PCR技术）检测正常皮肤成纤维细胞（NSFBs）和 增生性瘢痕患者成纤维细胞（HSFBs）中circ-0030042的表达。用CCK8检测法检测转染48 h后的HSFBs细胞增殖情况。利用 stubRFP-sensGFP-LC3 基因转染、流式细胞仪及电子显微镜观察circ-0030042对miR-145/PTEN轴调控VEGF水平的表达。利用 生物信息学分析、RNA免疫沉淀、免疫荧光检测等方法，揭示circ-0030042介导HS患者成纤维细胞增殖与迁移的作用机制。 结果：circ-0030042在增生性瘢痕中显著上调，过表达时作为VEGF海绵抑制miR-145诱导的成纤维细胞，维持体内稳定性。 此外，circ-0030042通过海绵化VEGF水平并阻断其miR-145捕获转录因子（FOXO1）mRNA来影响自噬，而circ-0030042诱导 FOXO1 的抑制被VEGF水平过表达或circ-0030042结合减少所抵消。过表达circ-0030042对成纤维细胞的增殖抑制与VEGF表达 的抑制作用被过表达miR-145部分抵消。结论：干扰circ-0030042通过靶向下调miR-145/PTEN轴进而抑制HSFBs细胞的增殖与 迁移，进一步诱导恶性细胞凋亡。
Abstract:
Objective To investigate the interaction relationship between circ-0030042 and Phosphatase and tensin homolog deleted on chromosome ten ( PTEN ), and to analyze its effect and mechanism on fibroblast proliferation and migration in patients with proliferative scar (HS). Methods The expression of circ-0030042 in normal skin fibroblasts (NSFBs) and fi broblasts (HSFBs) of patients with proliferative scars was detected by circRNA sequence and quantitative polymerase chain reaction (PCR ).The proliferation of HSFBs cells after transfection 48 h was detected by CCK8 assay. The expression of circ 0030042 on the miR-145/PTEN axis to regulate VEGF levels was observed by stubRFP-sensGFP-LC3 gene transfection, flow cytometry and electron microscopy. Bioinformatics analysis, RNA immunoprecipitation, immunofluorescence and other methods were used to reveal the mechanism of CIRC-0030042 mediating fi broblast proliferation and migration in HS patients. Results Circ-0030042 is significantly up-regulated in hypertrophic scars. Overexpression of circ-0030042 acts as a VEGF sponge to inhibit miR-145-induced fibroblasts and maintain stability in vivo. In addition, circ-0030042 affects autophagy by spongeizing VEGF levels and blocking its miR-145-capturing transcription factor (FOXO1) mRNA, while circ 0030042-induced inhibition of FOXO1 is offset by overexpression of VEGF levels or decreased binding of circ-0030042. The proliferation inhibition of fibroblasts and VEGF expression by overexpression circ-0030042 were partially offset by overexpression miR-145. Conclusion Interference with circ-0030042 inhibits the proliferation and migration of HSFBs cells by targeting down-regulating the miR-145/PTEN axis, and further induces apoptosis in malignant cells.
更新日期/Last Update: 2024-01-24