ObjectiveTo explore the effects of PKD1 gene on mouse aortic smooth muscle (MOVAS) cells autophagy.MethodsThe shRNA and over-expression lentiviral vectors for the target gene of PKD1 were constructed. MOVAS cells were infected by a number of successful packaging shRNA (PKD1 knockdown) or ETS-1 (PKD1 over-expressing) lentiviral vectors, and qPCR was used to test interference and over-expressing effects. Then qPCR and Western blotting were used to detect the expression levels of autophagy markers including Atg5, Beclin1 and LC3 in control group, shPKD1 group and ETS-1 group.ResultsCompared with the control group, PKD1 mRNA level was decreased in the shPKD1 group (P<0.05); ETS-1 and PKD1 mRNA levels were increased in the ETS-1 group (P<0.05). In contrast with the control group, the mRNA levels of autophagy markers including Atg5 (P<0.05) and Beclin1 (P<0.01) were obviously decreased in the shPKD1 group, but they were obviously increased in the ETS-1 group (P<0.001). Protein levels of Atg5, Beclin1 and LC3 were significantly decreased in the shPKD1 group (P<0.05), but they were increased obviously in the ETS-1 group (P<0.05) in contrast with the control group.ConclusionPKD1 gene is involved in MOVAS cells autophagy, low expression of PKD1 gene can inhibit autophagy and high expression of PKD1 promotes autophagy in vascular smooth muscle cells.
Objective To evaluate the significance of lactate dehydrogenase (LDH) as a predictor of in-hospital mortality in patients with acute aortic dissection(AAD). Methods We conducted a retrospective analysis of the clinical data of 445 AAD patients who were admitted to the Second Xiangya Hospital of Central South University and the Changsha Central Hospital from January 2014 to December 2017 within a time interval of ≤14 days from the onset of symptoms to hospital admission, including 353 males and 92 females with the age of 45-61 years. LDH levels were measured on admission and the endpoint was the all-cause mortality during hospitalization. Results During hospitalization, 86 patients died and 359 patients survived. Increased level of LDH was found in non-survivors compared with that in the survived [269.50 (220.57, 362.58) U/L vs. 238.00 (191.25, 289.15) U/L, P<0.001]. A nonlinear relationship between LDH levels and in-hospital mortality was observed. Using multivariable logistic analysis, we found that LDH was an independent predictor of in-hospital mortality in the patients with AAD [OR=1.002, 95% CI (1.001 to 1.014), P=0.006]. Furthermore, using receiver operating characteristic (ROC) analysis, we observed that the best threshold of LDH level was 280.70 U/L, and the area under the curve was 0.624 (95% CI 0.556 to 0.689). Conclusion LDH level on admission is an independent predictor of in-hospital mortality in patients with AAD.