The effect of CCL3 and CCR1 in bone remodeling induced by mechanical loading during orthodontic tooth movement in mice

Taddei, Silvana Rodrigues de Albuquerque; Queiroz-Junior, Celso Martins; Moura, Adriana Pedrosa; Andrade, Ildeu; Garlet, Gustavo; Proudfoot, Amanda E. I.; Teixeira, Mauro Martins; Silva, Tarcília A. da

doi:10.1016/j.bone.2012.09.036

Cited by 55 publications

(10 citation statements)

References 29 publications

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“…Previous studies have shown that AMPK is involved in the CCL3 signaling pathway [38]. We observed that the AMPK inhibitors, namely, Ara A and compound C, antagonize CCL3-mediated cancer migration and MMP-2 expression, suggesting that AMPK activation is an obligatory event in CCL3-induced migration activity in these cells.…”

Section: Discussionmentioning

confidence: 58%

AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma

Hsu

Chen

et al. 2013

Cell Commun Signal

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Chemokine (C-C motif) ligand 3 (CCL3), also known as macrophage inflammatory protein-1α, is a cytokine involved in inflammation and activation of polymorphonuclear leukocytes. CCL3 has been detected in infiltrating cells and tumor cells. Chondrosarcoma is a highly malignant tumor that causes distant metastasis. However, the effect of CCL3 on human chondrosarcoma metastasis is still unknown. Here, we found that CCL3 increased cellular migration and expression of matrix metalloproteinase (MMP)-2 in human chondrosarcoma cells. Pre-treatment of cells with the MMP-2 inhibitor or transfection with MMP-2 specific siRNA abolished CCL3-induced cell migration. CCL3 has been reported to exert its effects through activation of its specific receptor, CC chemokine receptor 5 (CCR5). The CCR5 and AMP-activated protein kinase (AMPK) inhibitor or siRNA also attenuated CCL3-upregulated cell motility and MMP-2 expression. CCL3-induced expression of MMP-2 and migration were also inhibited by specific inhibitors, and inactive mutants of AMPK, p38 mitogen activated protein kinase (p38 or p38-MAPK), and nuclear factor κB (NF-κB) cascades. On the other hand, CCL3 treatment demonstrably activated AMPK, p38, and NF-κB signaling pathways. Furthermore, the expression levels of CCL3, CCR5, and MMP-2 were correlated in human chondrosarcoma specimens. Taken together, our results indicate that CCL3 enhances the migratory ability of human chondrosarcoma cells by increasing MMP-2 expression via the CCR5, AMPK, p38, and NF-κB pathways.

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Section: Discussionmentioning

confidence: 58%

AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma

Hsu

Chen

et al. 2013

Cell Commun Signal

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“…Taddei et al . revealed that CCL3 deficiency decreased the mechanical loading-induced bone resorption in mice, suggesting an involvement of CCL3 in bone remodeling [ 39 ]. Our present data indicated that CCL3 is involved in bone repair through enhancement of macrophage recruitment to the damaged site after a femoral bone defect.…”

Section: Discussionmentioning

confidence: 99%

The Tissue Fibrinolytic System Contributes to the Induction of Macrophage Function and CCL3 during Bone Repair in Mice

et al. 2015

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Macrophages play crucial roles in repair process of various tissues. However, the details in the role of macrophages during bone repair still remains unknown. Herein, we examined the contribution of the tissue fibrinolytic system to the macrophage functions in bone repair after femoral bone defect by using male mice deficient in plasminogen (Plg –/–), urokinase-type plasminogen activator (uPA –/–) or tissue-type plasminogen activator (tPA –/–) genes and their wild-type littermates. Bone repair of the femur was delayed in uPA –/– mice until day 6, compared with wild-type (uPA +/+) mice. Number of Osterix-positive cells and vessel formation were decreased in uPA –/– mice at the bone injury site on day 4, compared with those in uPA +/+ mice. Number of macrophages and their phagocytosis at the bone injury site were reduced in uPA –/– and Plg –/–, but not in tPA –/– mice on day 4. Although uPA or plasminogen deficiency did not affect the levels of cytokines, including TNF-α, IL-1β, IL-6, IL-4 and IFN-γ mRNA in the damaged femur, the elevation in CCL3 mRNA levels was suppressed in uPA –/– and Plg –/–, but not in tPA –/– mice. Neutralization of CCL3 antagonized macrophage recruitment to the site of bone injury and delayed bone repair in uPA +/+, but not in uPA –/– mice. Our results provide novel evidence that the tissue fibrinolytic system contributes to the induction of macrophage recruitment and CCL3 at the bone injury site, thereby, leading to the enhancement of the repair process.

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“…We selected three random sagittal images of each animal for measurement, and then took the average of the results as the final measurement. Osteoclast and osteoblast counts were performed for positive cells attached to the alveolar bone surrounding the distal root in the TM model or within the area of subchondral bone of the tibia in the ACLT OA model 20 , 21 . In Safranin O stained sections, the histologic scoring system for severity of cartilage destruction in osteoarthritis was applied according to the 0 ~ 6 score of Chambers et al 22 .…”

Section: Methodsmentioning

confidence: 99%

Class A Scavenger Receptor Exacerbates Osteoclastogenesis by an Interleukin-6-Mediated Mechanism through ERK and JNK Signaling Pathways

Guo¹,

Ni²,

Ben³

et al. 2016

Int. J. Biol. Sci.

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Osteoclasts originate from bone marrow monocyte/macrophage lineage cells, which are important for bone health. Class A scavenger receptor (SR-A) is a multifunctional molecule that functions during differentiation of monocyte into macrophages and osteoclasts. To further characterize the role of SR-A in osteoclasts, we used the murine tooth movement model (TM) and the murine anterior cruciate ligament transection model of osteoarthritis (ACLT OA). In these two models the bones involved are of different origin and have different properties. Bone resorption was decreased in SR-A-/- mice compared to SR-A+/+ mice. Further evaluation showed that the number of multinucleated osteoclasts in SR-A-/- mice, compared to SR-A+/+ mice, was significantly decreased both in vivo and in vitro. The levels of interleukin-6 (IL-6) produced by osteoclasts were reduced in SR-A-/- mice compared to SR-A+/+ mice. In the in vitro marrow-derived osteoclast formation assay and in both mouse models, osteoclastogenesis was restored to normal in SR-A-/- mice by administration of recombinant murine IL-6. Moreover, neutralization of IL-6 reduced the number of osteoclasts formed in SR-A+/+ mice of TM model. Both extracellular signal-regulated kinase (ERK) and c-Jun N-terminal protein kinase (JNK), but not p38, signaling pathways were downregulated in receptor activator of nuclear factor-κB ligand (RANKL)-stimulated SR-A-/- osteoclasts. Importantly, when treated with either ERK or JNK inhibitor, the numbers of osteoclasts generated from RANKL-induced bone marrow derived-macrophages of SR-A+/+ mice, and their IL-6 production, were significantly decreased. This suggests that SR-A activates the ERK and JNK signaling pathways, and promotes production of IL-6 by osteoclasts to further stimulate osteoclast formation.

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The effect of CCL3 and CCR1 in bone remodeling induced by mechanical loading during orthodontic tooth movement in mice

Cited by 55 publications

References 29 publications

AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma

AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma

The Tissue Fibrinolytic System Contributes to the Induction of Macrophage Function and CCL3 during Bone Repair in Mice

Class A Scavenger Receptor Exacerbates Osteoclastogenesis by an Interleukin-6-Mediated Mechanism through ERK and JNK Signaling Pathways

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