Toll-like receptor 2 activation primes and upregulates osteoclastogenesis via lox-1

Autor: Y. Yoshinaga, Ryuji Sakagami, Fujio Okamoto, Koji Okabe, Hiroshi Kajiya, Kazuko Goto-T, Kimiko Ohgi
Rok vydání: 2018
Předmět:
Male
0301 basic medicine
MAPK/ERK pathway
Osteoclastogenesis
Endocrinology
Diabetes and Metabolism
Clinical Biochemistry
Bone Marrow Cells
Mice
03 medical and health sciences
0302 clinical medicine
Endocrinology
Osteogenesis
Toll-like receptor
Osteoclast
medicine
Animals
Periodontitis
Receptor
lcsh:RC620-627
biology
Chemistry
Macrophages
Research
Biochemistry (medical)
Cell Differentiation
Scavenger Receptors
Class E
Toll-Like Receptor 2
Lipoproteins
LDL
Lectin-like oxidized low-density-lipoprotein receptor 1
lcsh:Nutritional diseases. Deficiency diseases
TLR2
030104 developmental biology
medicine.anatomical_structure
Dyslipidemia
RANKL
030220 oncology & carcinogenesis
TLR4
Cancer research
biology.protein
Myeloid Differentiation Factor 88
lipids (amino acids
peptides
and proteins)
Signal Transduction
Zdroj: Lipids in Health and Disease, Vol 17, Iss 1, Pp 1-9 (2018)
Lipids in Health and Disease
ISSN: 1476-511X
DOI: 10.1186/s12944-018-0787-4
Popis: Background Lectin-like oxidized low-density-lipoprotein receptor 1 (Lox-1) is the receptor for oxidized low-density lipoprotein (oxLDL), a mediator in dyslipidemia. Toll-like receptor (TLR)-2 and − 4 are receptors of lipopolysaccharide (LPS) from Porphyromonas gingivalis, a major pathogen of chronic periodontitis. Although some reports have demonstrated that periodontitis has an adverse effect on dyslipidemia, little is clear that the mechanism is explained the effects of dyslipidemia on osteoclastogenesis. We have hypothesized that osteoclast oxLDL has directly effect on osteoclasts (OCs), and therefore alveolar bone loss on periodontitis may be increased by dyslipidemia. The present study aimed to elucidate the effect of Lox-1 on osteoclastogenesis associated with TLRs in vitro. Methods Mouse bone marrow cells (BMCs) were stimulated with macrophage colony-stimulating factor into bone marrow macrophages (BMMs). The cells were also stimulated with synthetic ligands for TLR2 (Pam3CSK4) or TLR4 (Lipid A), with or without receptor activator of nuclear factor kappa-B ligand (RANKL), and assessed for osteoclastogenesis by tartrate-resistant acid phosphatase (TRAP) staining, immunostaining, western blotting, flow activated cell sorting (FACS) analysis, real-time polymerase chain reaction (PCR), and reverse transcription PCR. Results Lox-1 expression was significantly upregulated by Pam3CSK4 and Lipid A in BMCs (p
Databáze: OpenAIRE
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