Parviz MammadzadaKarolinska Institutet | KI · Department of Clinical Neuroscience
Parviz Mammadzada
M.D
About
11
Publications
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153
Citations
Citations since 2017
Introduction
Additional affiliations
February 2019 - present
March 2014 - present
Publications
Publications (11)
Understanding the mechanisms that underlie age-related macular degeneration (AMD) has led to the identification of key molecules. Hypoxia-inducible transcription factors (HIFs) have been associated with choroidal neovascularization and the progression of AMD into the neovascular clinical phenotype (nAMD). HIFs regulate the expression of multiple gr...
MicroRNAs (miRNAs) can provide insight into the pathophysiological states of ocular tissues such as proliferative diabetic retinopathy (PDR). In this study, differences in miRNA expression in vitreous from PDR patients with and without incidence of recurrent vitreous hemorrhage (RVH) after the initial pars-plana vitrectomy (PPV) were analyzed, with...
Objective—
Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede neo...
Ocular angiogenic diseases, such as proliferative diabetic retinopathy and neovascular age-related macular degeneration, are associated with severe loss of vision. These pathologies originate from different vascular beds, retinal and choroidal microvasculatures, respectively. The activation of endothelial cells (EC) plays pivotal roles in angiogene...
Purpose
To elaborate molecular differences between choroidal and retinal angiogenesis by generating and comparatively analyzing human primary choroidal and retinal endothelial cell (CEC and REC) lines.
Methods
Human CEC and REC were isolated by positive selection and cultured. Characterization was performed by immunostaining for endothelial cell (...
Cellular responses to hypoxia are mediated by the hypoxia-inducible factors (HIF). In normoxia, HIF-α proteins are regulated by a family of dioxygenases, through prolyl and asparagyl hydroxylation, culminating in proteasomal degradation and transcriptional inactivation. In hypoxia, the dioxygenases become inactive and allow formation of HIF transcr...
Purpose
Cellular responses to hypoxia are mediated by the hypoxia-inducible factors (HIF). In normoxia, HIF-α proteins are tightly regulated by a family of dioxygenases, both by proteasomal-mediated degradation and transcriptional inactivation. In hypoxic conditions, the dioxygenases become inactive and allow formation of HIF transcription factor,...
Purpose
To elaborate molecular differences between choroidal and retinal angiogenesis by generating and comparatively analyzing human primary choroidal and retinal endothelial cell (CEC and REC) lines.
Methods
Human CEC and REC were isolated by positive-selection and were cultured. Characterization was performed by immunostaining for endothelial c...
Purpose:
To elaborate molecular differences between choroidal and retinal angiogenesis by generating and comparatively analysing human primary choroidal and retinal endothelial cell (CEC and REC) lines.
Methods:
Human CEC and REC were isolated by positive selection and were cultured. Characterization was performed by immunostaining for endotheli...
Purpose In the eye, angiogenesis is associated with many pathological conditions. Retinal and choroidal endothelial cells (RE and CE cells) are the main cellular components of ocular angiogenesis. It is widely accepted that endothelial cells (EC) from different vascular beds show heterogeneity. Comparative study of RE and CE cells can lead to deepe...
Questions
Questions (5)
Hello everyone,
I have a recombinant protein which I believe can bind to VEGF. It is a weak interaction, therefore, hard to detect as you can imagine. The recombinant protein is synthezied by transfected cell culture, CO-IP-ed, and eluted by imidazole solution.
1. Is it possible to use ELISA method for detecting weak interactions? If yes, do I need to get rid of imidazole for doing that, or does imidazole not affect ELISA method?
2. Is there any better way to detect this kind of interactions?
Huge thanks in advance.
Hello dear colleagues!
I want to study the anti-angiogenic effects of my recombinant protein. I have been trying to establish proliferation/survival assay and migration/wound healing assay on HUVEC with no success. My aim is to compare the recombinant protein with avastin (bevacizumab). Which concentration of avastin is effective on HUVEC? What would be the FBS, ECGS and heparin % for these kind of assay? Is it mandatory to coat the wells with matrigel or collagen? Shall I starve the cells before the treatment. I'd appreciate any information.
Thanks.
I am trying to pull down the VEGF protein from cell culture media by using VEGF trapping protein. My WB looks pretty bad. I am using rabbit anti-mouse VEGF primary, and polyclonal swine anti rabbit secondary ECL. This is a photo of my last WB, I have repeated the experiment 3 times, but a similar WB results. Any idea why this appearance occurs?
Is there anyone that worked 6 his tag and could not detect it (with anti c terminus his antibody) ? I have a recombinant protein with 6 his tag at the c terminus but I am not able to get a signal from it on WB. I have heard that some people had the same problem with HIS tag.
I am not getting any signal from my WBs. I have been using the same protocol, which I was succesful at, but this specific protein which belongs to Vascular Endothelial Growth Factor Receptor ( VEGFR) (sFLT1s) is not the same but similiar in structure with them, is hard to detect.
Does anybody have any idea why this happens? Do I need to make some modifications in my protocol? Should I use a different temperature to boil the samples or doing something extra that can prevent degradation of my protein? I am not sure whether it is degraded or not. I have played with the primary and the secondary antibody concentration and still have no signal. I assume it is because of possible degradation.
