Lectin‑type oxidized LDL receptor 1 modulates matrix metalloproteinase 2 production in peri‑implantitis

Abstract

Peri-implantitis is a disease in which inflammatory lesions that affect the surrounding soft and hard tissues develop. Matrix metalloproteinase 2 (MMP2) is hypothesized to be involved in this destructive process. However, the regulatory mechanism of action of MMP2 in the peripheral tissues of the implant are not fully understood. To determine the expression of MMP2 in peri-implantitis, peri-implant crevicular fluid (PICF) was collected from patients with peri-implantitis. The healthy volunteers' peripheral blood human macrophages infected with Porphyromonas gingivalis (P. gingivalis) were used as a cell model to explore the regulatory mechanism of MMP2 regarding dental implants. Western blotting, reverse transcriptionquantitative PCR and immunofluorescence staining were used to measure the expression of MMP2 in the present study. MMP2 expression was increased in the PICF of the patients with peri-implantitis and in human macrophages infected with P. gingivalis. Lectin-type oxidized LDL receptor 1 (LOX-1) mediated the expression of MMP2 in human macrophages upon infection of P. gingivalis, whereas dendritic cell-associated c-type lectin-1 did not appear to be involved in this regulatory process. However, JNK and ERK1/2 were involved in P. gingivalis induced MMP2 expression. The results of this study showed that MMP2 was involved in peri-implantitis. MMP2 was upregulated by LOX-1 in a JNK and ERKk1/2 signaling dependent manner in the cell model. The LOX-1/MMP2 signaling pathway may thus be a potential target for management of peri-implantitis.

Role of Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in inflammation and pathogen-associated interactions

“…Also, matrix metalloproteinase-2 (MMP-2) was found to be upregulated by LOX-1 in human macrophages infected by P. gingivalis . In this process, JNK and ERK1/2 also seemed to be involved in the LOX-1-dependent signaling process [ 113 ]. Additionally, it was found that LOX-1 is upregulated during infection in a process mediated by TLR2 and/or activation via MAPK in BMCs, which leads to osteoclastogenesis [ 123 ].…”

“…List of the agents interacting with LOX-1 in infections and in which cell and animal models the interaction was reported Interacting agent corneal epithelial cells, mouse corneas Upregulation, mediated by NF-κB Protein, mRNA[110,113] IL-1β Human corneal epithelial cells, mouse corneas Upregulation Protein, mRNA[113] VCAM-1 HMEC-1, HUVECs, RAW macrophages, mouse corneas Upregulation Protein, mRNA[111,112,118] E-Selectin HMEC-1, HUVECs, RAW macrophages, mouse corneas Upregulation, mediated by NF-κB Protein, mRNA[109-…”