scholarly journals Murine macrophage chemokine receptor CCR2 plays a crucial role in macrophage recruitment and regulated inflammation in wound healing

2018 ◽  
Vol 48 (9) ◽  
pp. 1445-1455 ◽  
Author(s):  
Anna E. Boniakowski ◽  
Andrew S. Kimball ◽  
Amrita Joshi ◽  
Matt Schaller ◽  
Frank M. Davis ◽  
...  
Keyword(s):  
Wound Healing ◽  
Chemokine Receptor ◽  
Crucial Role ◽  
Murine Macrophage ◽  
Macrophage Recruitment ◽  
Chemokine Receptor Ccr2

The chemokine receptor CCR2 is involved in macrophage recruitment to the injured peripheral nervous system

2000 ◽  
Vol 110 (1-2) ◽  
pp. 177-185 ◽  
Author(s):  
Heike Siebert ◽  
Anika Sachse ◽  
William A Kuziel ◽  
Nobuyo Maeda ◽  
Wolfgang Brück
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Chemokine Receptor ◽  
Macrophage Recruitment ◽  
Chemokine Receptor Ccr2

Abstract 235: Interaction Between a Macrophage Chemokine Receptor, CCR2, and Its Ligand Plays a Crucial Role in Macrophage Recruitment Aand Regulated Inflammation in Normal Wound Healing

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Anna E Boniakowski ◽  
Andrew Kimball ◽  
Amrita Joshi ◽  
Ron Allen ◽  
Matt Schaller ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Wound Healing ◽  
Adoptive Transfer ◽  
Crucial Role ◽  
Wound Closure ◽  
Tissue Injury ◽  
Impaired Wound Healing ◽  
Macrophage Recruitment ◽  
Normal Wound Healing ◽  
Tnf Α

Background: Wound healing in chronic diseases, such as type 2 diabetes (T2D), is impaired due to dysregulated inflammation. Innate immune cells, particularly macrophages, play a significant role in regulated inflammation following tissue injury. After injury, CCR2+ monocytes are recruited to the peripheral wound. This recruitment is mediated in part by the CCR2 ligand, CCL2. Thus, we hypothesized that the CCL2/CCR2 interaction is vital for normal wound healing and appropriate inflammation, and that this signaling cascade is impaired in T2D. Methods: CCR2 -/- mice and littermate controls underwent 4mm hindlimb wounds, and wound closure was compared daily. Wound macrophages (CD3-CD19-NK1.1-CD11b+ cells) were analyzed on day 3 by flow cytometry for intracellular cytokine production. Adoptive transfer was performed using blood CD11b+ cells from WT C57BL/6 or CCR2 -/- mice isolated by magnetic sorting and transferred into CCR2 -/- mice via tail vein injection. Mice were then wounded and wound closure was compared between the two groups. C57BL/6 mice were maintained on normal or high fat diet for 12-14 weeks, wounds were created, and CD11b+ cells were isolated from wounds on day 2. ELISA for CCL2 was performed. Results: CCR2 -/- mice showed significantly impaired wound healing on days 2-7 compared with littermate controls. Macrophages isolated on day 3 from wounds of CCR2 -/- mice expressed significantly less inflammatory cytokines (IL-1β, TNF-α) by qPCR. Flow cytometry analysis revealed less Ly6C hi macrophages in the wounds, as well as macrophages that made significantly less IL-1β, NOS2, and TNF-α. When adoptive transfer was performed, wound healing was restored to normal in the mice that received WT compared to those that received CCR2 -/- CD11b+ cells (P< 0.01). Since CCR2 is important for normal wound inflammation, and we have previously shown that inflammation is impaired in the diet-induced obese (DIO) mice, we examined CCL2 in DIO wounds. CCL2 was significantly decreased in DIO wound macrophages on day 2. Conclusion: Appropriate CCR2/CCL2 interaction plays a crucial role in macrophage recruitment and regulated inflammation in normal wound healing. Impairment in CCR2/CCL2 signaling may be responsible, in part, for delayed early inflammation in T2D.

Discovery and Mapping of an Intracellular Antagonist Binding Site at the Chemokine Receptor CCR2

2014 ◽  
Vol 86 (4) ◽  
pp. 358-368 ◽  
Author(s):  
Annelien J.M. Zweemer ◽  
Julia Bunnik ◽  
Margo Veenhuizen ◽  
Fabiana Miraglia ◽  
Eelke B. Lenselink ◽  
...  
Keyword(s):  
Binding Site ◽  
Chemokine Receptor ◽  
Antagonist Binding ◽  
Chemokine Receptor Ccr2

scholarly journals The chemokine receptor CCR2 maintains plasmacytoid dendritic cell homeostasis

2017 ◽  
Vol 192 ◽  
pp. 72-78 ◽  
Author(s):  
Oriane Cédile ◽  
Line Østerby Jørgensen ◽  
Ida Frank ◽  
Agnieszka Wlodarczyk ◽  
Trevor Owens
Keyword(s):  
Dendritic Cell ◽  
Chemokine Receptor ◽  
Plasmacytoid Dendritic Cell ◽  
Cell Homeostasis ◽  
Chemokine Receptor Ccr2

scholarly journals Factor XIII-A: An Indispensable “Factor” in Haemostasis and Wound Healing

2021 ◽  
Vol 22 (6) ◽  
pp. 3055
Author(s):  
Fahad S. M. Alshehri ◽  
Claire S. Whyte ◽  
Nicola J. Mutch
Keyword(s):  
Bone Marrow ◽  
Wound Healing ◽  
Crucial Role ◽  
Factor Xiii ◽  
Severe Bleeding ◽  
Bleeding Diathesis ◽  
Unknown Mechanism ◽  
Protein Substrates ◽  
Physiological Processes ◽  
Isopeptide Bonds

Factor XIII (FXIII) is a transglutaminase enzyme that catalyses the formation of ε-(γ-glutamyl)lysyl isopeptide bonds into protein substrates. The plasma form, FXIIIA2B2, has an established function in haemostasis, with fibrin being its principal substrate. A deficiency in FXIII manifests as a severe bleeding diathesis emphasising its crucial role in this pathway. The FXIII-A gene (F13A1) is expressed in cells of bone marrow and mesenchymal lineage. The cellular form, a homodimer of the A subunits denoted FXIII-A, was perceived to remain intracellular, due to the lack of a classical signal peptide for its release. It is now apparent that FXIII-A can be externalised from cells, by an as yet unknown mechanism. Thus, three pools of FXIII-A exist within the circulation: plasma where it circulates in complex with the inhibitory FXIII-B subunits, and the cellular form encased within platelets and monocytes/macrophages. The abundance of this transglutaminase in different forms and locations in the vasculature reflect the complex and crucial roles of this enzyme in physiological processes. Herein, we examine the significance of these pools of FXIII-A in different settings and the evidence to date to support their function in haemostasis and wound healing.

scholarly journals Structural basis for the binding of the membrane-proximal C-terminal region of chemokine receptor CCR2 with the cytosolic regulator FROUNT

FEBS Journal ◽  
2014 ◽  
Vol 281 (24) ◽  
pp. 5552-5566 ◽  
Author(s):  
Kaori Esaki ◽  
Sosuke Yoshinaga ◽  
Tatsuichiro Tsuji ◽  
Etsuko Toda ◽  
Yuya Terashima ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Terminal Region ◽  
Structural Basis ◽  
Chemokine Receptor Ccr2

Chemokine CCL2 and chemokine receptor CCR2 in early active multiple sclerosis

2004 ◽  
Vol 11 (7) ◽  
pp. 445-449 ◽  
Author(s):  
T. L. Sorensen ◽  
R. M. Ransohoff ◽  
R. M. Strieter ◽  
F. Sellebjerg
Keyword(s):  
Multiple Sclerosis ◽  
Chemokine Receptor ◽  
Active Multiple Sclerosis ◽  
Chemokine Receptor Ccr2
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