ArticlePloS one2014
TLR4 accessory molecule RP105 (CD180) regulates monocyte-driven arteriogenesis in a murine hind limb ischemia model.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Blood transcriptomic signatures associated with depression, or the risk for depression, in pregnant women from the Psychiatry Research And Motherhood - Depression (PRAM-D) study.Translational psychiatry · 2025Article
- Lipocalin 2 deficiency impacts angiogenesis after ischemia in vivo and in vitro.Vascular biology (Bristol, England) · 2025Article
- The Intriguing Role of TLR Accessory Molecules in Cardiovascular Health and Disease.Frontiers in cardiovascular medicine · 2022Review
- In Vivo Matrigel Plug Assay as a Potent Method to Investigate Specific Individual Contribution of Angiogenesis to Blood Flow Recovery in Mice.International journal of molecular sciences · 2021Article
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
- Variations in Surgical Procedures for Inducing Hind Limb Ischemia in Mice and the Impact of These Variations on Neovascularization Assessment.International journal of molecular sciences · 2019Review
- IRF3 and IRF7 mediate neovascularization via inflammatory cytokines.Journal of cellular and molecular medicine · 2019Article
- Consensus guidelines for the use and interpretation of angiogenesis assays.Angiogenesis · 2018Review
- RP105 alleviates myocardial ischemia reperfusion injury via inhibiting TLR4/TRIF signaling pathways.International journal of molecular medicine · 2018Article
- Activation of Toll-Like Receptor 9 Impairs Blood Flow Recovery After Hind-Limb Ischemia.Frontiers in cardiovascular medicine · 2018Article
- Article
- Inhibition of Mef2a Enhances Neovascularization via Post-transcriptional Regulation of 14q32 MicroRNAs miR-329 and miR-494.Molecular therapy. Nucleic acids · 2017Article
- Sphingolipid Metabolism Is Dysregulated at Transcriptomic and Metabolic Levels in the Spinal Cord of an Animal Model of Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2017Article
- Deficiency of the TLR4 analogue RP105 aggravates vein graft disease by inducing a pro-inflammatory response.Scientific reports · 2016Article
- The Toll of Vascular Insufficiency: Implications for the Management of Peripheral Arterial Disease.Journal of immunology research · 2016Review
- TLR4 Deters Perfusion Recovery and Upregulates Toll-like Receptor 2 (TLR2) in Ischemic Skeletal Muscle and Endothelial Cells.Molecular medicine (Cambridge, Mass.) · 2015Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsWe investigated the role of the TLR4-accessory molecule RP105 (CD180) in post-ischemic neovascularization, i.e. arteriogenesis and angiogenesis. TLR4-mediated activation of pro-inflammatory Ly6Chi monocytes is crucial for effective neovascularization. Immunohistochemical analyses revealed that RP105+ monocytes are present in the perivascular space of remodeling collateral arterioles. As RP105 inhibits TLR4 signaling, we hypothesized that RP105 deficiency would lead to an unrestrained TLR4-mediated inflammatory response and hence to enhanced blood flow recovery after ischemia. METHODS AND
resultsRP105-/- and wild type (WT) mice were subjected to hind limb ischemia and blood flow recovery was followed by Laser Doppler Perfusion Imaging. Surprisingly, we found that blood flow recovery was severely impaired in RP105-/- mice. Immunohistochemistry showed that arteriogenesis was reduced in these mice compared to the WT. However, both in vivo and ex vivo analyses showed that circulatory pro-arteriogenic Ly6Chi monocytes were more readily activated in RP105-/- mice. FACS analyses showed that Ly6Chi monocytes became activated and migrated to the affected muscle tissues in WT mice following induction of hind limb ischemia. Although Ly6Chi monocytes were readily activated in RP105-/- mice, migration into the ischemic tissues was hampered and instead, Ly6Chi monocytes accumulated in their storage compartments, bone marrow and spleen, in RP105-/- mice.
conclusionsRP105 deficiency results in an unrestrained inflammatory response and monocyte over-activation, most likely due to the lack of TLR4 regulation. Inappropriate, premature systemic activation of pro-inflammatory Ly6Chi monocytes results in reduced infiltration of Ly6Chi monocytes in ischemic tissues and in impaired blood flow recovery.
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