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Sickle Cell Disease: From Pathogenesis to Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 3301

Special Issue Editors


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Guest Editor
Children’s National Medical Center, George Washington University School of Medicine and Health Sciences, Washington, DC 20052, USA
Interests: sickle cell; coagulation; adhesion; inflammation; vasculopathy; nitric oxide

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Guest Editor
University of Ghana, College of Health Sciences, Department of Physiology, Legon, Ghana

Special Issue Information

Dear Colleagues,

A renaissance in the development of new therapies for sickle cell disease (SCD) is emerging. Many of these therapies have emanated from novel approaches to our understanding of sickle red blood cell biology and new insights into the genesis of sickle cell vaso-occlusive events. A growing number of clinical trials are developing new targets outside the sickle red blood cell with the hopes of mitigating the devasting cascade of physiologic events resulting in end-organ damage. Various new pathophysiologic mechanisms are being recognized, improving our understanding of sickle cell vasculopathy. They include increased inflammation, vascular adhesion, coagulopathy, and nitric oxide dysfunction. Novel and improved therapies remain to be discovered. For this Special Issue entitled “Sickle Cell Disease: From Pathogenesis to Therapies”, we invite papers on the following topics:

1) Role of the endothelium and adhesion in the vasculopathy of sickle cell disease: Implications for disease monitoring and novel therapeutics;

2) Impaired Nitric oxide function and implications for novel therapeutics;

3) Role of coagulopathy and platelet activation in the pathogenesis of SCD vasculopathy: Implications for disease monitoring and novel therapeutics

Assoc. Prof. Dr. Andrew D. Campbell
Dr. Charles Antwi-Boasiako
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Sickle Cell
  • Coagulation
  • Adhesion
  • Inflammation
  • Vasculopathy
  • Nitric Oxide

Published Papers (1 paper)

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Research

14 pages, 2295 KiB  
Article
Sickle Cell Trait Induces Oxidative Damage on Plasmodium falciparum Proteome at Erythrocyte Stages
by Alber Díaz-Castillo, Neyder Contreras-Puentes, Ciro Alvear-Sedán, Carlos Moneriz-Pretell, Erika Rodríguez-Cavallo and Darío Mendez-Cuadro
Int. J. Mol. Sci. 2019, 20(22), 5769; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20225769 - 16 Nov 2019
Cited by 6 | Viewed by 2874
Abstract
The presence of hemoglobin A-S (HbAS) in erythrocytes has been related to the high production of reactive oxygen species (ROS) and an increased in intracellular oxidative stress that affects the progress of Plasmodium erythrocytic cycle life and attenuates its serious clinical symptoms. Nevertheless, [...] Read more.
The presence of hemoglobin A-S (HbAS) in erythrocytes has been related to the high production of reactive oxygen species (ROS) and an increased in intracellular oxidative stress that affects the progress of Plasmodium erythrocytic cycle life and attenuates its serious clinical symptoms. Nevertheless, oxidative effects on P. falciparum proteome across the intraerythrocytic cycle in the presence of HbAS traits have not been described yet. Here, an immune dot-blot assay was used to quantify the carbonyl index (C.I) on P. falciparum 3D7 proteome at the different asexual erythrocytic stages. Protein carbonylation on parasites cultivated in erythrocytes from two donors with HbAS increased 5.34 ± 1.42 folds at the ring stage compared to control grown in hemoglobin A-A (HbAA) red blood cells. Whereas at trophozoites and schizonts stages were augmented 2.80 ± 0.52 and 3.05 ± 0.75 folds, respectively. Besides proteins involved in processes of the stress response, recognition and invasion were identified from schizonts carbonylated bands by combining SDS-PAGE with MALDI-TOF-TOF analysis. Our results reinforce the hypothesis that such oxidative modifications do not appear to happen randomly, and the sickle cell trait affects mainly a small fraction of parasite proteins particularly sensitive to ROS. Full article
(This article belongs to the Special Issue Sickle Cell Disease: From Pathogenesis to Therapies)
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