Objective To evaluate the curative effect of endovascular treatment for Leriche syndrome.Methods The clinical data of 57 patients with Leriche syndrome,who were admitted to authors' hospital during the period from September 2010 to October 2014,were retrospectively analyzed.The curative effect of percutaneous transluminal angioplasty (PTA) was analyzed.Results Among the 57 patients (65 diseased limbs in total),simple PTA was employed in 2,catheter directed thrombolysis (CDT) with subsequent PTA and stenting in 5,and PTA plus stenting in 50.A total of 97 stents were implanted,the technical success rate was 100％.After the treatment,the ankle brachial index (ABI) increased from preoperative (0.42±0.22) to postoperative (0.83±0.15),the difference between the two data was statistically significant (P＜0.01).Thepatients were followed up for (9.8±2.8) months.The 6-month and 12-month primary patency rates were 95.4％ and 90.7％ respectively,the postoperative secondary patency rate was 96.4％.After the treatment,the symptoms of lower limb ischemia were improved in all patients.During perioperative period,iliac artery rupture due to balloon dilatation occurred in 2 patients,pseudoaneurysm at brachial aaery puncture point in one patient,hematoma at puncture point in 3 patients,cerebral infarction in 2 patients and myocardial infarction in one patient.One patient developed contrast-induced nephropathy and finally died of multiple organ dysfunction syndrome.The perioperative mortality was 1.75％.One patient developed in-stent obstruction in 3 months after two stage treatment,and artificial vascular bypass grafting had to be carried out.Conclusion For the treatment of Leriche syndrome,PTA is safe and reliable,it carries less complications and lower perioperative mortality with satisfactory short-term patency rate.(J Intervent Radiol,2017,26:221-224)

Objective To investigate the role of Wnt signaling pathway hypofunction mediated by dephosphorylation ofβ-catenin in the impaired wound healing of type 1 diabetic rats. Methods The back skin defect wounds were produced in rats with type 1 diabetes. These rats were divided into control, diabetes, lithium chloride treatment, and epidermal growth factor ( EGF) treatment groups. The situation of back wound healing, the ratio ofβ-catenin positive cells,β-catenin, phosphorylatedβ-catenin, and vascular endothelial growth factor ( VEGF) levels were detected. Results Compared to diabetes group, the wound granulation tissue was more mature, wound healing time was shorter, and healing rate, as well as the ratio ofβ-catenin positive cells, dephosphorylatedβ-catenin, and VEGF levels, were higher in normal group, lithium chloride treatment group, and EGF treatment group ( P<0. 05 or P<0. 01). Conclusion The hypofunction of Wnt signaling pathway is involved in the process of wound healing in type 1 diabetic rats, of which the dephosphorylation ofβ-catenin is the key point. EGF may play a beneficial role in the wound healing of type 1 diabetic rat models via Wnt pathway.

Objective To further investigate direct effects of dipeptidyl peptidase-4(DPP4) on calcification and to identify responsible signaling pathways in human vascular smooth muscle cells (HVSMC). Methods The effect of DPP-4 on calcification of HVSMC was observed by alizarin red, and Western blot was used to detect whether DPP4 induced calcification-related protein expressions through extracellular signal-regulated kinases 1/2 (ERK1/2) pathway. Results The Alizarin red staining results showed that calcified nodules in DPP4 group were significantly increased as compared with control group, similar to calcification group.The protein expressions of osteoprotegerin (OPG), osteopontin (OPN), Runt-related transcription factor 2 (RUNX2), and bone morphogenetic protein 2 (BMP2) were stimulated by DPP4 in a concentration- and time-dependent manner. The phosphorylation level of ERK1/2 was significantly increased after DPP4 incubation for 15 min (P<0.05). PD98059, an ERK1/2 inhibitor, significantly lowered DPP4-stimulated expressions of calcification-related proteins (P<0.05). Conclusion DPP4 may promote the calcification of HVSMC through ERK1/2 signaling pathways.

Objective To investigate the effect of ERK1/2 phosphorylation on the proliferation of human aorta vascular smooth muscle cells (HAVSMCs) stimulated by advanced glycation end products (AGEs) Methods CCK8 was used to test the effect of AGEs with different concentration on the proliferation of HAVSMCs, and the effect of PD98059, a specific inhibitor of ERK1/2, on HAVSMCs proliferation stimulated by AGEs was also detected. Flow Cytometer (FCM) was used to detect the cell cycle transformation induced by AGEs. Western Blot was used to detect the expression of relative proteins. Results 10 mg/L AGEs observably facilitated the proliferation and the DNA synthesis of HAVSMCs and PD98059 (40 umol/L) markedly inhibited the proliferation and cell cycle evolution of HAVSMCs induced by AGEs. Furthermore, ERK1/2 phosphorylation, and PCNA were regulated by AGEs and thus it showed time and dose dependent. Conclusion AGEs participates in the proliferation of HAVSMCs by activating ERK1/2 signal path.

Objective To investigate the effect of protein kinase B on calcifition of human aorta vascular smooth muscle cells(HASMCs) stimulated by advanced glycation end products (AGEs). Methods HASMCs were cultured in vitro and randomly divided into control group,DMSO group,AGEs group and AGEs+LY294002 group. The calcification of each group was examined by von Kusaa;the expression of protein was detected by west-ern blot and ALP levels in each group by Elisa. Results The expression of bone morphogenetic protein-2(BMP-2)and osteoprotegerin(OPG)in AGEs group was significantly higher than that in control group(P < 0.05). The expression of phosphorylated AKT in AGEs group was significantly higher than that in control group (P < 0.05), and it was time and concentration dependent. Compared with that in AGEs group ,the expression of BMP and OPG in AGEs + LY294002 group was significantly decreased (P < 0.01). Conclusion AKT signaling pathway may play an important role on calcifition of HASMCs caused by AGEs.

Objective To explore the molecular mechanism of dipeptidyl peptidase-4 ( DPP4) in the calcification of human vascular smooth muscle cells(HVSMCs). Methods The osteogenic differentiation of HVSMCs was induced by 200 ng/ ml DPP4 as calcification model. The differentially expressed long non-coding RNAs (lncRNAs) between DPP4 group and control group were analyzed by microarray, and the microarray results of LincRNA ENST00000540293 were validated by real-time PCR. After HVSMCs were incubated with LincRNA ENST00000540293 silencing positive reagent for 48 h, the expressions of calcification-related proteins osteoprotegerin (OPG) and bone morphogenetic protein 2(BMP-2) were detected by Western blotting and the formation of calcified nodules was observed by Alizarin red staining. Results The protein expressions of OPG and BMP-2 in HVSMCs were significantly increased after DPP4 intervention (P <0.05), with the increased formation of calcified nodules. RTqPCR showed that LincRNA ENST00000540293 expression was significantly decreased in DPP4 group as compared with the control group(P<0.05). The expressions of calcification-related proteins OPG and BMP-2 were significantly increased after LincRNA ENST00000540293 silence(P<0.05). Conclusion DPP4 may promote the calcification of HVSMC through inhibiting LincRNA ENST00000540293 expression.