ArticleExperimental hematology2020
Reappraising the role of α5 integrin and the microenvironmental support in stress erythropoiesis.
Article in Experimental hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- ReducedInternational journal of molecular sciences · 2026Article
- Engineering Marrow-Mimetic Hydrogel Platforms Enhance Erythropoiesis: A Mechanobiology-Driven Approach for Transfusion Red Blood Cell Production.Gels (Basel, Switzerland) · 2025Article
- Targeting Stress Erythropoiesis Pathways in Cancer.Frontiers in physiology · 2022Review
- Gene Expression Analysis of Mevalonate Kinase Deficiency Affected Children Identifies Molecular Signatures Related to Hematopoiesis.International journal of environmental research and public health · 2021Article
- Adaptive Immunity and Pathogenesis of Diabetes: Insights Provided by the α4-Integrin Deficient NOD Mouse.Cells · 2020Article
- Stress erythropoiesis: definitions and models for its study.Experimental hematology · 2020Review
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We previously studied the role of β1 integrin and some of its different α partners relevant to erythropoiesis. Although clear and consistent answers regarding the role of α4β1 (VLA-4) were evident, the role of its companion integrin α5β1 (VLA-5) was clouded by inconsistent outcomes in all prior publications. Furthermore, the functional consequences of integrin deficiencies only in microenvironmental (ME) cells supporting erythroid cell expansion and maturation post stress have never been explored. In the study described here, we created several additional mouse models in the aim of addressing unanswered questions regarding functional consequences of single or combined integrin deficiencies in erythroid cells or only in ME supporting cells. Our novel and expansive data solidified the intrinsic requirement of both α4 and α5 integrins in erythroid cells for their proliferative expansion and maturation in response to stress; α5 integrin alone, deleted either early in all hematopoietic cells or only in erythroid cell, has only a redundant role in proliferative expansion and is dispensable for erythroid maturation. By contrast, α4 integrin, on its own, exerts a dominant effect on timely and optimal erythroid maturation. Deficiency of both α4 and α5 integrins in ME cells, including macrophages, does not negatively influence stress response by normal erythroid cells, in great contrast to the effect of ME cells deficient in all β1 integrins. Collectively the present data offer deeper insight into the coordination of different β1 integrin functional activities in erythroid cells or in ME cells for optimal erythroid stress response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.