Publications by authors named "Xinran Bi"

3 Publications

  • Page 1 of 1

LncRNA MALAT1 promotes oxidized low-density lipoprotein-induced autophagy in HUVECs by inhibiting the PI3K/AKT pathway.

J Cell Biochem 2019 03 28;120(3):4092-4101. Epub 2018 Nov 28.

Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.

Emerging evidence suggests that long noncoding RNAs (lncRNAs) are involved in many biological processes, such as cell growth, differentiation, apoptosis, and autophagy. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), highly expressed in endothelial cells, is well conserved and implicated in endothelial cell migration and proliferation. However, whether MALAT1 participates in oxidized low-density lipoprotein (ox-LDL)-induced autophagy regulation in human umbilical vein endothelial cells (HUVECs) remains unknown. In this study, we observed that autophagy was upregulated and MALAT1 expression was markedly increased in HUVECs treated with ox-LDL. The ox-LDL-induced autophagy of HUVECs is significantly associated with the PI3K/AKT pathway. Furthermore, we found that MALAT1 overexpression inhibited PI3K, Akt and p70S6K phosphorylation and downregulated RHEB expression, simultaneously increasing ox-LDL-induced autophagy. MALAT1 silencing caused higher phosphorylated PI3K, Akt and p70S6K levels, upregulated RHEB expression and markedly suppressed autophagy. These results indicated that lncRNA MALAT1 promotes ox-LDL-induced autophagy in HUVECs partly through the PI3K/AKT signaling pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source Listing
March 2019

MicroRNA‑155 promotes ox‑LDL‑induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway.

Mol Med Rep 2018 Sep 29;18(3):2798-2806. Epub 2018 Jun 29.

Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.

Endothelial cell autophagy has a protective role in inhibiting inflammation and preventing the development of atherosclerosis, which may be regulated by microRNA (miR)‑155. The present study aimed to investigate the mechanisms of autophagy in the development of atherosclerosis. Human umbilical vein endothelial cells model in vitro and using oxidized low‑density lipoprotein (ox‑LDL) stimulated cells to simulate the atherosclerosis. MiR‑155 mimics, miR‑155 inhibitors, and a negative control were respectively transfected in human umbilical vein endothelial cells to analyzed alterations in the expression of miR‑155. It was demonstrated that overexpression of miR‑155 promoted autophagic activity in oxidized low‑density lipoprotein‑stimulated human umbilical vein endothelial cells, whereas inhibition of the expression of miR‑155 reduced autophagic activity. Overexpression of miR‑155 revealed that it regulated autophagy via the phosphatidylinositol‑3 kinase (PI3K)/RAC‑α serine/threonine‑protein kinase (Akt)/mechanistic target of rapamycin pathway (mTOR) signaling pathway. A luciferase reporter assay demonstrated that miR‑155 directly bound to the PI3K catalytic subunit a and Ras homolog enriched in brain 3'‑untranslated region and inhibited its luciferase activity. Therefore, the results of the present study suggested that miR‑155 promoted autophagy in vascular endothelial cells and that this may have occurred via targeting of the PI3K/Akt/mTOR pathway. Thus, miR‑155 may be considered as a potential therapeutic target for the treatment of atherosclerosis.
View Article and Find Full Text PDF

Download full-text PDF

Source Listing
September 2018

MiR-181b regulates autophagy in a model of Parkinson's disease by targeting the PTEN/Akt/mTOR signaling pathway.

Neurosci Lett 2018 05 30;675:83-88. Epub 2018 Mar 30.

Department of Neurology, The Affiliated Hospital of the Qingdao University, Qingdao, Shandong, 266100, China. Electronic address:

Objective: Parkinson's disease (PD) is the second most common neurodegenerative disease. Recent studies have shown that dysregulation of microRNA plays an important role in PD, and defects in autophagy are also critically associated with mechanisms underlying PD. We aim to investigate the effect of miR-181b on autophagy, particularly the involvement of miR-181b in the regulation of the phosphatase and tensin homolog (PTEN)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway and neuronal autophagy in a 1-methyl-4- phenylpyridinium iodide(MPP)-induced cellular model of Parkinson's disease.

Materials And Methods: We used MPP as a tool to construct the PD cell model, using miR-181b mimics or inhibitors to regulate the expression of miR-181b. PC12 cell viability was detected by MTT. The expression of miR-181b was determined by quantitative real-time PCR analysis. The expression of autophagy protein markers (LC3II) and PTEN/Akt/mTOR signaling proteins (PTEN, p-AKT,p-mTOR and p-p70S6K) were determined by Western blotting analysis.

Results: The expression of miR-181b and autophagy-related proteins was gradually decreased with increasing MPP content. Overexpression of miR-181b significantly decreased the LC3II/GAPDH ratio and increased cell viability compared to the MPP treated group, whereas inhibition of miR-181b attenuated these effects. In addition, we observed that PTEN expression was reduced by miR-181b mimics and induced by its inhibitors in MPP-treated PC12 cells. Additionally, the indicators of AKT/mTOR signaling, phosphorylated (active) AKT, mTOR and p70S6K were both increased by miR-181b mimics and decreased by its inhibitors.

Conclusions: Our results suggest that miR-181b regulates autophagy by targeting the PTEN/Akt/mTOR signaling pathway, thereby affecting cell viability in PD.
View Article and Find Full Text PDF

Download full-text PDF

Source Listing
May 2018