Objective: Long intergenic noncoding RNA-p21 (lincRNA-p21) has been proved in the pathogenesis of aortic aneurysms, while its functionality in thoracic aortic aneurysms (TAA) and the mechanism of function remains unclear. Therefore our study aimed to investigate the role of lincRNA-p21 in TAA.Methods: Aortic media specimens and blood samples were collected from both patients with TAA and healthy controls. Expression of lincRNA-p21 in those tissues was detected by reverse-transcription quantitative polymerase chain reaction (qRT-PCR). Diagnostic values of lincRNA-p21 in aortic media and blood for TAA were evaluated by receiver operating characteristic curve analysis. LincRNA-p21 overexpression human vascular smooth muscle cells (VSMCs) were prepared and the effects of lincRNA-p21 overexpression on cell proliferation and apoptosis were explored by cell counting kit-8 assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, respectively. Expression of lincRNA-p21 and transforming growth factor β1 (TGF-β1) in VSMCs with different treatment was detected by qRT-PCR and Western blot analysis, respectively. Results: Expression of lincRNA-p21 in aortic media tissues and blood was significantly upregulated in TAA patients than in healthy controls. Expression of lincRNA-p21 in aortic media and blood can be used to effectively distinguish TAA patients form healthy controls. LincRNA-p21 overexpression inhibited proliferation and promoted apoptosis of VSMCs, while TGF-β1 inhibitor reduced those effects. LincRNA-p21 overexpression upregulated TGF-β1 expression, while TGF-β1 activator showed no significant effects on lincRNA-p21 expression in VSMC.Conclusion: LincRNA-p21 participates in TAA by regulating the proliferation and apoptosis of VSMCs through the activation of TGF-β1 signaling pathway. K E Y W O R D Shuman vascular smooth muscle cells, long intergenic noncoding RNA-p21, transforming growth factor β1, thoracic aortic aneurysms J Cell Biochem. 2019;120:4113-4120.wileyonlinelibrary.com/journal/jcb

The present study aimed to explore the therapeutic effect and underlying mechanism of epidermal growth factor (EGF) on the wound healing of diabetic foot ulcers (DFU). A total of 48 rabbits with DFU were randomly divided into 2 groups, comprising the treatment and control groups. Full-thickness skin (10×10 mm) was excised from the thigh of each rabbit. The wounds in the treatment group were treated with 100 mg/l EGF once a day for 1 month. The control group received no treatment. At 20 days following treatment, new granulation tissues that formed beyond the edge of the wound were collected for subsequent analysis. Tissues from rabbits in the treatment group produced a greater number of fibroblasts, which exhibited a fibroblastic morphology when compared with those in the control group. In the treatment group, a larger number of these fibroblasts were observed as clusters, and there were numerous blood vessels when compared with the control group. The fibroblasts in the control group exhibited an irregular morphology, contained fewer organelles and the surrounding collagenous fibers were sparse. These fibroblasts also demonstrated a disordered arrangement and it was revealed that the wound healed at a slower rate compared with the treatment group. Endogenous EGF mRNA detection revealed that there was a significant difference (P<0.05) in the relative gray value of EGF mRNA between the treatment (103.27±4.27) and control (63.88±4.36) groups. In conclusion, EGF may accelerate the healing of DFU, and exogenous EGF treatment may upregulate the expression of EGF mRNA in newly generated tissues.

To investigate the effects of soluble fms-like tyrosine kinase-1 on the vascular mimicry formation, proliferation, migration, and invasion of colorectal cancer SW480 cells. The recombinant plasmid pBLAST49-sFLT-1 or pBLAST49 control plasmid was transfected into SW480 cells to obtain hsFLT-1-SW480 or Ctrl-SW480 cells. The three-dimensional model culture, sulforhodamine B assay, scratch assay, and Transwell assay were performed to detect the vascular mimicry formation, proliferation, migration, and invasion of colorectal cancer SW480 cells, respectively. Western blotting was used to detect the expression of vascular endothelial-cadherin protein. Compared with Ctrl-SW480 cells, vascular mimicry formation ((0.85 ± 0.04) vs (7.40 ± 0.69), p < 0.05) and vascular endothelial-cadherin expression ((1.25 ± 0.08) vs (1.89 ± 0.03), p < 0.05) were significantly decreased, and the growth rate was also significantly decreased in hsFLT-1-SW480 cells ((32.54 ± 5.12) vs (88.13 ± 11.52), p < 0.05). Moreover, the migration ((0.46 ± 0.08) vs (0.94 ± 0.03), p < 0.05) and invasion capacity ((59.14 ± 3.64) vs (134.85 ± 10.16), p < 0.05) of SW480 cells were significantly inhibited upon soluble fms-like tyrosine kinase-1 transfection. soluble fms-like tyrosine kinase-1 inhibits cell proliferation, migration, and invasion of colorectal cancer SW480 cells through suppression of vascular mimicry formation, which provides a good basis for the development of new drugs for the treatment of colorectal cancer by targeting both angiogenesis and vascular mimicry formation.