Advances in Red Blood Cells Research

Topic Information

Dear Colleagues,

Red blood cells (RBCs) are the most abundant cells in mammals, including humans. They serve a well-known and well-described vital function. Furthermore, they are increasingly recognized as biomarkers for various pathophysiological conditions ranging from RBC-related diseases, such as hereditary and acquired anemias, to states and diseases that are not primarily linked to RBCs, such as inflammation, cancer, diabetes, and cardiovascular disorders. Adaptation to environmental stressors such as hypoxia, hyper- and hypothermia, and practicing endurance and extreme sports also impacts the numbers and properties of red blood cells. Exploring the processes driving stem cells into erythroid differentiation and proliferation during erythropoiesis allows producing red blood cells of rare groups or those that may be used for transfusion for all patients. Today, “making one’s own red blood cells in a bioreaction” is a realistic future option; developing optimal methods for preserving red cells obtained from donors and storage in blood banks is of decisive importance for successful outcomes from blood transfusions. We are pleased to invite you to contribute original articles, short communications, reviews, and opinion articles (mini-reviews) covering the entire field of RBC research, including (but not limited to):

• Erythropoiesis;
• Membrane transport;
• Biophysical and biochemical RBC properties;
• Collective phenomena;
• The genesis, management, and treatment of diseases;
• The use of RBCs as drug carriers or biomarkers;
• Adaptations to stress.

Prof. Dr. Lars Kaestner
Prof. Dr. Anna Bogdanova
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomolecules biomolecules	4.8	9.4	2011	18.4 Days	CHF 2700
Cells cells	5.1	9.9	2012	17 Days	CHF 2700
International Journal of Molecular Sciences ijms	4.9	8.1	2000	16.8 Days	CHF 2900
Journal of Developmental Biology jdb	2.2	4.1	2013	20.3 Days	CHF 1800
Journal of Molecular Pathology jmp	-	-	2020	26.5 Days	CHF 1000

Preprints.org is a multidisciplinary platform offering a preprint service designed to facilitate the early sharing of your research. It supports and empowers your research journey from the very beginning.

MDPI Topics is collaborating with Preprints.org and has established a direct connection between MDPI journals and the platform. Authors are encouraged to take advantage of this opportunity by posting their preprints at Preprints.org prior to publication:

1. Share your research immediately: disseminate your ideas prior to publication and establish priority for your work.
2. Safeguard your intellectual contribution: Protect your ideas with a time-stamped preprint that serves as proof of your research timeline.
3. Boost visibility and impact: Increase the reach and influence of your research by making it accessible to a global audience.
4. Gain early feedback: Receive valuable input and insights from peers before submitting to a journal.
5. Ensure broad indexing: Web of Science (Preprint Citation Index), Google Scholar, Crossref, SHARE, PrePubMed, Scilit and Europe PMC.

Published Papers (4 papers)

Order results

Content type Publication Date

Result details

Normal Extended Compact

Journals

All Biomolecules Cells IJMS JDB JMP

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

Error

Oops... you haven't selected anything for export.

Ok

clear

attachment

Supplementary material:
Supplementary File 1 (ZIP, 1095 KiB)

20 pages, 35530 KiB  

Open AccessFeature PaperArticle

A Refined Single Cell Landscape of Haematopoiesis in the Mouse Foetal Liver

by Elena Ceccacci, Emanuela Villa, Fabio Santoro, Saverio Minucci, Christiana Ruhrberg and Alessandro Fantin

J. Dev. Biol. 2023, 11(2), 15; https://doi.org/10.3390/jdb11020015 - 23 Mar 2023

Cited by 4 | Viewed by 4750

Abstract

During prenatal life, the foetal liver is colonised by several waves of haematopoietic progenitors to act as the main haematopoietic organ. Single cell (sc) RNA-seq has been used to identify foetal liver cell types via their transcriptomic signature and to compare gene expression [...] Read more.

During prenatal life, the foetal liver is colonised by several waves of haematopoietic progenitors to act as the main haematopoietic organ. Single cell (sc) RNA-seq has been used to identify foetal liver cell types via their transcriptomic signature and to compare gene expression patterns as haematopoietic development proceeds. To obtain a refined single cell landscape of haematopoiesis in the foetal liver, we have generated a scRNA-seq dataset from a whole mouse E12.5 liver that includes a larger number of cells than prior datasets at this stage and was obtained without cell type preselection to include all liver cell populations. We combined mining of this dataset with that of previously published datasets at other developmental stages to follow transcriptional dynamics as well as the cell cycle state of developing haematopoietic lineages. Our findings corroborate several prior reports on the timing of liver colonisation by haematopoietic progenitors and the emergence of differentiated lineages and provide further molecular characterisation of each cell population. Extending these findings, we demonstrate the existence of a foetal intermediate haemoglobin profile in the mouse, similar to that previously identified in humans, and a previously unidentified population of primitive erythroid cells in the foetal liver. Full article

(This article belongs to the Topic Advances in Red Blood Cells Research)

►▼ Show Figures

Graphical abstract

attachment

Supplementary material:
Supplementary File 1 (ZIP, 2267 KiB)

17 pages, 6664 KiB  

Open AccessArticle

E-Cadherin Expression Distinguishes Mouse from Human Hematopoiesis in the Basophil and Erythroid Lineages

by Rosa A. Krimpenfort, Felix M. Behr, Marja Nieuwland, Iris de Rink, Ron Kerkhoven, Marieke von Lindern and Micha Nethe

Biomolecules 2022, 12(11), 1706; https://doi.org/10.3390/biom12111706 - 17 Nov 2022

Cited by 2 | Viewed by 2855

Abstract

E-cadherin is a key regulator of epithelial cell–cell adhesion, the loss of which accelerates tumor growth and invasion. E-cadherin is also expressed in hematopoietic cells as well as epithelia. The function of hematopoietic E-cadherin is, however, mostly elusive. In this study, we explored [...] Read more.

E-cadherin is a key regulator of epithelial cell–cell adhesion, the loss of which accelerates tumor growth and invasion. E-cadherin is also expressed in hematopoietic cells as well as epithelia. The function of hematopoietic E-cadherin is, however, mostly elusive. In this study, we explored the validity of mouse models to functionally investigate the role of hematopoietic E-cadherin in human hematopoiesis. We generated a hematopoietic-specific E-cadherin knockout mouse model. In mice, hematopoietic E-cadherin is predominantly expressed within the basophil lineage, the expression of which is dispensable for the generation of basophils. However, neither E-cadherin mRNA nor protein were detected in human basophils. In contrast, human hematopoietic E-cadherin marks the erythroid lineage. E-cadherin expression in hematopoiesis thereby revealed striking evolutionary differences between the basophil and erythroid cell lineage in humans and mice. This is remarkable as E-cadherin expression in epithelia is highly conserved among vertebrates including humans and mice. Our study therefore revealed that the mouse does not represent a suitable model to study the function of E-cadherin in human hematopoiesis and an alternative means to study the role of E-cadherin in human erythropoiesis needs to be developed. Full article

(This article belongs to the Topic Advances in Red Blood Cells Research)

►▼ Show Figures

Figure 1

16 pages, 3747 KiB  

Open AccessArticle

A Balance between Transmembrane-Mediated ER/Golgi Retention and Forward Trafficking Signals in Glycophorin-Anion Exchanger-1 Interaction

by Kate Hsu, Ting-Ying Lee, Jian-Yi Lin and Pin-Lung Chen

Cells 2022, 11(21), 3512; https://doi.org/10.3390/cells11213512 - 6 Nov 2022

Cited by 3 | Viewed by 2369

Abstract

Anion exchanger-1 (AE1) is the main erythroid Cl⁻/HCO₃⁻ transporter that supports CO₂ transport. Glycophorin A (GPA), a component of the AE1 complexes, facilitates AE1 expression and anion transport, but Glycophorin B (GPB) does not. Here, we dissected the [...] Read more.

Anion exchanger-1 (AE1) is the main erythroid Cl⁻/HCO₃⁻ transporter that supports CO₂ transport. Glycophorin A (GPA), a component of the AE1 complexes, facilitates AE1 expression and anion transport, but Glycophorin B (GPB) does not. Here, we dissected the structural components of GPA/GPB involved in glycophorin-AE1 trafficking by comparing them with three GPB variants—GPBhead (lacking the transmembrane domain [TMD]), GPBtail (mainly the TMD), and GP.Mur (glycophorin B-A-B hybrid). GPB-derived GP.Mur bears an O-glycopeptide that encompasses the R18 epitope, which is present in GPA but not GPB. By flow cytometry, AE1 expression in the control erythrocytes increased with the GPA-R18 expression; GYP.Mur^+/+ erythrocytes bearing both GP.Mur and GPA expressed more R18 epitopes and more AE1 proteins. In contrast, heterologously expressed GPBtail and GPB were predominantly localized in the Golgi apparatus of HEK-293 cells, whereas GBhead was diffuse throughout the cytosol, suggesting that glycophorin transmembrane encoded an ER/Golgi retention signal. AE1 coexpression could reduce the ER/Golgi retention of GPB, but not of GPBtail or GPBhead. Thus, there are forward-trafficking and transmembrane-driven ER/Golgi retention signals encoded in the glycophorin sequences. How the balance between these opposite trafficking signals could affect glycophorin sorting into AE1 complexes and influence erythroid anion transport remains to be explored. Full article

(This article belongs to the Topic Advances in Red Blood Cells Research)

►▼ Show Figures

Figure 1

19 pages, 969 KiB  

Open AccessReview

Krüppel-Like Factor 1: A Pivotal Gene Regulator in Erythropoiesis

by Cristian Antonio Caria, Valeria Faà and Maria Serafina Ristaldi

Cells 2022, 11(19), 3069; https://doi.org/10.3390/cells11193069 - 29 Sep 2022

Cited by 18 | Viewed by 3003

Abstract

Krüppel-like factor 1 (KLF1) plays a crucial role in erythropoiesis. In-depth studies conducted on mice and humans have highlighted its importance in erythroid lineage commitment, terminal erythropoiesis progression and the switching of globin genes from γ to β. The role of KLF1 in [...] Read more.

Krüppel-like factor 1 (KLF1) plays a crucial role in erythropoiesis. In-depth studies conducted on mice and humans have highlighted its importance in erythroid lineage commitment, terminal erythropoiesis progression and the switching of globin genes from γ to β. The role of KLF1 in haemoglobin switching is exerted by the direct activation of β-globin gene and by the silencing of γ-globin through activation of BCL11A, an important γ-globin gene repressor. The link between KLF1 and γ-globin silencing identifies this transcription factor as a possible therapeutic target for β-hemoglobinopathies. Moreover, several mutations have been identified in the human genes that are responsible for various benign phenotypes and erythroid disorders. The study of the phenotype associated with each mutation has greatly contributed to the current understanding of the complex role of KLF1 in erythropoiesis. This review will focus on some of the principal functions of KLF1 on erythroid cell commitment and differentiation, spanning from primitive to definitive erythropoiesis. The fundamental role of KLF1 in haemoglobin switching will be also highlighted. Finally, an overview of the principal human mutations and relative phenotypes and disorders will be described. Full article

(This article belongs to the Topic Advances in Red Blood Cells Research)

►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

 

Error

Oops... you haven't selected anything for export.

Ok

clear

Displaying articles 1-4