Molecular recognition and interaction between human plasminogen Kringle 5 and voltage-dependent anion channel-1 by biological specificity technologies and molecular dynamic simulation

2021 ◽  
pp. 106710
Author(s):  
Zhang Jiaxin ◽  
Wang Kun ◽  
Xue Pengli ◽  
Chen Xiu ◽  
Liujiao Bian
Keyword(s):  
Molecular Recognition ◽  
Molecular Dynamic Simulation ◽  
Molecular Dynamic ◽  
Dynamic Simulation ◽  
Anion Channel ◽  
Voltage Dependent Anion Channel ◽  
Kringle 5 ◽  
Biological Specificity ◽  
Voltage Dependent ◽  
Human Plasminogen

scholarly journals The Voltage-dependent Anion Channel Is a Receptor for Plasminogen Kringle 5 on Human Endothelial Cells

2003 ◽  
Vol 278 (29) ◽  
pp. 27312-27318 ◽  
Author(s):  
Mario Gonzalez-Gronow ◽  
Theodosia Kalfa ◽  
Carrie E. Johnson ◽  
Govind Gawdi ◽  
Salvatore V. Pizzo
Keyword(s):  
Endothelial Cells ◽  
Anion Channel ◽  
Human Endothelial Cells ◽  
Voltage Dependent Anion Channel ◽  
Kringle 5 ◽  
Voltage Dependent

scholarly journals Voltage-Dependent Anion Channel-1, a Possible Ligand of Plasminogen Kringle 5

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0164834 ◽  
Author(s):  
Yin-ku Liang ◽  
Liu-jiao Bian
Keyword(s):  
Anion Channel ◽  
Voltage Dependent Anion Channel ◽  
Kringle 5 ◽  
Voltage Dependent

scholarly journals VDAC1 in the diseased myocardium and the effect of VDAC1-interacting compound on atrial fibrosis induced by hyperaldosteronism

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hadar Klapper-Goldstein ◽  
Ankit Verma ◽  
Sigal Elyagon ◽  
Roni Gillis ◽  
Michael Murninkas ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Apoptotic Cell ◽  
Anion Channel ◽  
Immunohistochemical Analysis ◽  
Voltage Dependent Anion Channel ◽  
Cardiac Tissues ◽  
Therapeutic Implications ◽  
Voltage Dependent ◽  
Models Of Lupus

AbstractThe voltage-dependent anion channel 1 (VDAC1) is a key player in mitochondrial function. VDAC1 serves as a gatekeeper mediating the fluxes of ions, nucleotides, and other metabolites across the outer mitochondrial membrane, as well as the release of apoptogenic proteins initiating apoptotic cell death. VBIT-4, a VDAC1 oligomerization inhibitor, was recently shown to prevent mitochondrial dysfunction and apoptosis, as validated in mouse models of lupus and type-2 diabetes. In the present study, we explored the expression of VDAC1 in the diseased myocardium of humans and rats. In addition, we evaluated the effect of VBIT-4 treatment on the atrial structural and electrical remodeling of rats exposed to excessive aldosterone levels. Immunohistochemical analysis of commercially available human cardiac tissues revealed marked overexpression of VDAC1 in post-myocardial infarction patients, as well as in patients with chronic ventricular dilatation\dysfunction. In agreement, rats exposed to myocardial infarction or to excessive aldosterone had a marked increase of VDAC1 in both ventricular and atrial tissues. Immunofluorescence staining indicated a punctuated appearance typical for mitochondrial-localized VDAC1. Finally, VBIT-4 treatment attenuated the atrial fibrotic load of rats exposed to excessive aldosterone without a notable effect on the susceptibility to atrial fibrillation episodes induced by burst pacing. Our results indicate that VDAC1 overexpression is associated with myocardial abnormalities in common pathological settings. Our data also indicate that inhibition of the VDAC1 can reduce excessive fibrosis in the atrial myocardium, a finding which may have important therapeutic implications. The exact mechanism\s of this beneficial effect need further studies.

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