Role of autophagy induced by arecoline in angiogenesis of oral submucous fibrosis
| Autor: | Bingyu Zhu, Yingfang Wu, Xinchun Jian, Changyun Fang, Huiqiao Yu, Zhuo Dai, Jieying Peng |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Cell Survival Angiogenesis Arecoline Oral Submucous Fibrosis Umbilical vein 03 medical and health sciences 0302 clinical medicine Western blot Autophagy Human Umbilical Vein Endothelial Cells medicine Humans Viability assay General Dentistry Matrigel medicine.diagnostic_test Chemistry 030206 dentistry Cell Biology General Medicine medicine.disease 030104 developmental biology Otorhinolaryngology Oral submucous fibrosis embryonic structures cardiovascular system Cancer research medicine.drug |
| Zdroj: | Archives of Oral Biology. 102:7-15 |
| ISSN: | 0003-9969 |
| Popis: | Objectives To detect the expression of protein light chain 3 (LC3) and p62-SQSTM1 (p62) in the lamina propria of oral submucous fibrosis (OSF) and to determine the association of autophagy with OSF. To investigate the role of autophagy in angiogenesis of human umbilical vein endothelial cells (HUVECs) and to assess whether this effect was induced by arecoline. Methods LC3 and p62 expression was detected in OSF tissue through immunohistochemistry (IHC). Transmission electron microscopy (TEM) and Western blot were used to investigate the expression of autophagy in HUVECs. The role of autophagy in angiogenesis in HUVECs was investigated using the Matrigel assay. Results 1: LC3 expression was upregulated in OSF samples. In contrast, p62 was downregulated in early and intermediate stages but upregulated in advanced stages of OSF. 2: HUVECs treated with arecoline exhibited increased autophagosomes, LC3 expression and reduced p62 expression, when co-treated with chloroquine (CQ), which is a specific autophagy inhibitor, revealed the opposite trend. 3: Autophagy inhibited angiogenesis in HUVECs. Conclusions Our findings suggest that arecoline induces autophagy in HUVECs. The high level of autophagy could reduce cell viability and inhibit angiogenesis in HUVECs, potentially promoting the development of OSF. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect