ArticleThe Journal of biological chemistry2010
Vinculin is indispensable for repopulation by hematopoietic stem cells, independent of integrin function.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 24 citations in OpenAlex.
- Hematopoietic Stem and Progenitor Cells Establish Dynamic Podosome-Like Structures to Interact with Fibronectin.Advanced biology · 2026Article
- α1,3-fucosylation treatment improves cord blood CD34 negative hematopoietic stem cell navigation.iScience · 2024Article
- The extracellular matrix of hematopoietic stem cell niches.Advanced drug delivery reviews · 2022Review
- Article
- Review
- The Fate of Osteoblast-Like MG-63 Cells on Pre-Infected Bactericidal Nanostructured Titanium Surfaces.Materials (Basel, Switzerland) · 2019Article
- Preferential Colonization of Osteoblasts Over Co-cultured Bacteria on a Bifunctional Biomaterial Surface.Frontiers in microbiology · 2018Article
- Bone marrow niche-mimetics modulate HSPC function via integrin signaling.Scientific reports · 2017Article
- Paxillin is an intrinsic negative regulator of platelet activation in mice.Thrombosis journal · 2014Article
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vinculin is a highly conserved actin-binding protein that is localized in integrin-mediated focal adhesion complexes. Although critical roles have been proposed for integrins in hematopoietic stem cell (HSC) function, little is known about the involvement of intracellular focal adhesion proteins in HSC functions. This study showed that the ability of c-Kit(+)Sca1(+)Lin(-) HSCs to support reconstitution of hematopoiesis after competitive transplantation was severely impaired by lentiviral transduction with short hairpin RNA sequences for vinculin. The potential of these HSCs to differentiate into granulocytic and monocytic lineages, to migrate toward stromal cell-derived factor 1α, and to home to the bone marrow in vivo were not inhibited by the loss of vinculin. However, the capacities to form long term culture-initiating cells and cobblestone-like areas were abolished in vinculin-silenced c-Kit(+)Sca1(+)Lin(-) HSCs. In contrast, adhesion to the extracellular matrix was inhibited by silencing of talin-1, but not of vinculin. Whole body in vivo luminescence analyses to detect transduced HSCs confirmed the role of vinculin in long term HSC reconstitution. Our results suggest that vinculin is an indispensable factor determining HSC repopulation capacity, independent of integrin functions.
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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.