ArticleInternational journal of clinical and experimental pathology2013
TLR2-deficiency of cKit+ bone marrow cells is associated with augmented potency to stimulate angiogenic processes.
Article in International journal of clinical and experimental pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Toll-like receptor 2 deficiency exacerbates corneal angiogenesis in injury by impairing regulatory T cells.Theranostics · 2025Article
- Biological and pathophysiological roles of end-products of DHA oxidation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveToll-like receptor 2 (TLR2)-deficiency is associated with the preservation of vascular function and TLR2-deficient (TLR2(-/-)) mice exhibit increased neovascularization following induction of hindlimb ischemia. Hematopoietic stem cells play an important role in ischemia-induced angiogenesis and we now investigated whether the effects observed in TLR2(-/-) mice may be attributed to TLR2 deficiency on bone marrow-derived stem cells. APPROACH AND
resultscKit-positive (cKit(+)) bone marrow cells (BMC) were isolated from wild type (WT) and TLR2(-/-) mice employing MACS-bead technology. Co-incubation of TLR2(-/-)cKit(+) BMC with mature endothelial cells (ECs) resulted in increased tube formation of ECs on matrigel, augmented sprouting in a 3D-collagen matrix and increased migratory capacity compared to co-incubation with WT cKit(+) BMC. In an in vivo matrigel plug assay, TLR2(-/-)cKit(+) BMC exhibited enhanced formation of capillary-like networks. In a murine model of hindlimb ischemia, administration of TLR2(-/-) cKit(+) BMC to WT mice augmented capillary density and reperfusion of ischemic M. gastrocnemius muscle tissue to the level of TLR2(-/-) mice. Western Blot analysis revealed comparable expression of CXCR4 on TLR2(-/-)cKit(+) BMC but increased activation of the PI3K downstream signaling molecule protein kinase B (PKB/AKT) compared to WT cKit(+) cells.
conclusionsThe absence of TLR2 on cKit(+) BMC is associated with augmented potency to support angiogenic processes in vitro and in vivo. Functional inhibition of TLR2 may therefore provide a novel tool to enhance stem cell function for the treatment of vascular diseases.
Indexed as
Identifiers
24294367PMC3843261W309215909What OpenQuestion holds
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.