Bingxiang Wang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Bingxiang Wang has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Chunlin Li
Department of Physiology, Center for Medical Research, the First Affiliated Hospital, Medical College of Qingdao University, Qingdao 266071, China
1 shared publication Dan Li
Institute of Clinical Medicine, Affiliated Hospital of Qingdao University, Qingdao
1 shared publicationJiaxiu Liu
Institute of Clinical Medicine, Affiliated Hospital of Qingdao University, Qingdao
1 shared publicationJingwei Chi
Institute of Clinical Medicine, Affiliated Hospital of Qingdao University, Qingdao
1 shared publicationLi Ma
Institute of Clinical Medicine, Affiliated Hospital of Qingdao University, Qingdao
1 shared publicationLikun Zhuang
Institute of Clinical Medicine, Affiliated Hospital of Qingdao University, Qingdao
1 shared publication
Latest Publications
- Open Access
- 1 January 2016
- Published by ACT Publishing Group in Journal of Cardiology and Therapy
- Vol. 3 (4) , 543-548
Functions of ANO1/TMEM16A, Ca2+-activated Cl- channels in Regulation of Blood Pressure and Vascular Remodeling
Since the molecule of Ca2+-activated Cl- channels (CaCC) had been identified as ANO1, major progresses have been made in recent studies on its roles in vascular functions. ANO1 has been confirmed to represent the CaCC channels in vascular smooth myocytes (VSMCs). Generally, ANO1 expresses more in resistance-size small arteries. When activated, it functions to control the VSMC membrane potentials by depolarization. As a result, the voltage-dependent Ca2+ channel is opened, leading to Ca2+ entry and VSMC contraction. Thus, the function of ANO1 is important for maintenance of normal blood pressure. Under influence of agonists, e.g., angiotensin II, ANO1 also participates in VSMC differentiation and remodeling which are mediated by KLF5, myocardin and SRF. The factors regulate the transcription of the ANO1 gene and other genes for VSMC differentiation and proliferation.
- 1 January 2016
- Published by ACT Publishing Group in Journal of Cardiology and Therapy
- Vol. 3 (4) , 543-548
Open AccessFunctions of ANO1/TMEM16A, Ca2+-activated Cl- channels in Regulation of Blood Pressure and Vascular Remodeling
Since the molecule of Ca2+-activated Cl- channels (CaCC) had been identified as ANO1, major progresses have been made in recent studies on its roles in vascular functions. ANO1 has been confirmed to represent the CaCC channels in vascular smooth myocytes (VSMCs). Generally, ANO1 expresses more in resistance-size small arteries. When activated, it functions to control the VSMC membrane potentials by depolarization. As a result, the voltage-dependent Ca2+ channel is opened, leading to Ca2+ entry and VSMC contraction. Thus, the function of ANO1 is important for maintenance of normal blood pressure. Under influence of agonists, e.g., angiotensin II, ANO1 also participates in VSMC differentiation and remodeling which are mediated by KLF5, myocardin and SRF. The factors regulate the transcription of the ANO1 gene and other genes for VSMC differentiation and proliferation.
- Open Access
- 12 August 2015
- Published by Public Library of Science (PLoS) in PLOS ONE
- Vol. 10 (8) , e0135345
7, 8-Dihydroxyflavone Protects an Endothelial Cell Line from H2O2 Damage
7, 8-dihydroxyflavone (7, 8-DHF), a selective agonist for TrkB receptors, has been well studied for its neurotrophic functions. However, its roles outside the neural tissues have scarcely been studied as yet. In this study, we investigated the protecting roles of 7, 8-DHF in EA.hy926 cells, a human umbilic vein endothelial cell line which was exposed to hydrogen peroxide (H2O2). We found that 7, 8-DHF significantly protected the cells from being damaged by H2O2 through suppression of apoptosis, attenuation of inflammatory factor releasing and inhibition of reactive oxygen species generation. The potent biological effects of 7, 8-DHF were probably executed via its binding to TrkB receptors because the receptor specific antagonist ANA-12 significantly blocked its protecting effects. The protecting roles of 7, 8-DHF in EA.hy926 cells suggest that it will be a promising compound to be developed into a health product that definitely benefits endothelial functions and prevents cardiovascular diseases.
- 12 August 2015
- Published by Public Library of Science (PLoS) in PLOS ONE
- Vol. 10 (8) , e0135345
Open Access7, 8-Dihydroxyflavone Protects an Endothelial Cell Line from H2O2 Damage
7, 8-dihydroxyflavone (7, 8-DHF), a selective agonist for TrkB receptors, has been well studied for its neurotrophic functions. However, its roles outside the neural tissues have scarcely been studied as yet. In this study, we investigated the protecting roles of 7, 8-DHF in EA.hy926 cells, a human umbilic vein endothelial cell line which was exposed to hydrogen peroxide (H2O2). We found that 7, 8-DHF significantly protected the cells from being damaged by H2O2 through suppression of apoptosis, attenuation of inflammatory factor releasing and inhibition of reactive oxygen species generation. The potent biological effects of 7, 8-DHF were probably executed via its binding to TrkB receptors because the receptor specific antagonist ANA-12 significantly blocked its protecting effects. The protecting roles of 7, 8-DHF in EA.hy926 cells suggest that it will be a promising compound to be developed into a health product that definitely benefits endothelial functions and prevents cardiovascular diseases.
- 1 May 2015
- Published by Elsevier in Journal of Molecular and Cellular Cardiology
- Vol. 82, 22-32
Overexpression of ANO1/TMEM16A, an arterial Ca2+-activated Cl− channel, contributes to spontaneous hypertension
- 1 May 2015
- Published by Elsevier in Journal of Molecular and Cellular Cardiology
- Vol. 82, 22-32
Overexpression of ANO1/TMEM16A, an arterial Ca2+-activated Cl− channel, contributes to spontaneous hypertension