Gene expression patterns in bone following lipopolysaccharide stimulation

Yang, Jing; Su, Nan; Du, Xiaolan; Chen, Lin

doi:10.2478/s11658-014-0216-2

Cited by 8 publications

(8 citation statements)

References 46 publications

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“…These changes in osteoblasts might be a possible cause for bone loss and demineralization of bone in critically ill patients 88 . Our animal study also showed decreased bone mass and mRNA expression of OC in mice with systemic inflammation and sepsis caused by lipopolysaccharide (LPS) treatment 97 . Other animal experiments showed that the increased apoptosis or acute deficiency of osteoblasts might be another reason causing impaired of bone formation 23 , 98 .…”

Section: Extraskeletal Functions Of Bone Mediated By Bdfssupporting

confidence: 52%

Bone function, dysfunction and its role in diseases including critical illness

Su¹,

Yang²,

Xie³

et al. 2019

Int. J. Biol. Sci.

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The skeleton is one of the largest organs in the human body. In addition to its conventional functions such as support, movement and protection, the skeleton also contributes to whole body homeostasis and maintenance of multiple important non-bone organs/systems (extraskeletal functions). Both conventional and extraskeletal functions of the skeleton are defined as bone function. Bone-derived factors (BDFs) are key players regulating bone function. In some pathophysiological situations, including diseases affecting bone and/or other organs/systems, the disorders of bone itself and the subsequently impaired functions of extraskeletal organs/systems caused by abnormal bone (impaired extraskeletal functions of bone) are defined as bone dysfunction. In critical illness, which is a health status characterized by the dysfunction or severe damage of one or multiple important organs or systems, the skeleton shows rapid bone loss resulting from bone hyper-resorption and impaired osteoblast function. In addition, the dysfunctions of the skeleton itself are also closely related to the severity and prognosis of critical illness. Therefore, we propose that there is bone dysfunction in critical illness. Some methods to inhibit osteoclast activity or promote osteoblast function by the treatment of bisphosphonates or PTH1-34 benefit the outcome of critical illness, which indicates that enhancing bone function may be a potential novel strategy to improve prognosis of diseases including critical illness.

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Section: Extraskeletal Functions Of Bone Mediated By Bdfssupporting

confidence: 52%

Bone function, dysfunction and its role in diseases including critical illness

Su¹,

Yang²,

Xie³

et al. 2019

Int. J. Biol. Sci.

Self Cite

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“…However, the results of RT‐PCR showed that the BMP2 were up‐regulated in the infected ROBs. Previous studies indicated that inflammatory factors up‐regulated the mRNA expression of BMP2, however, down‐regulated the mRNA expression of Runx2 and reduced ALP activity in vivo or in vitro (Osta et al ., ; Bakker et al ., ; Yang et al ., ). In fact, the relationship between mRNA and protein expression levels informs about the combined outcomes of translation and protein degradation which are, in addition to transcription and mRNA stability, essential contributors to gene expression regulation (Abreu et al ., ).…”

Section: Discussionmentioning

confidence: 97%

Flavonoids of HerbaEpimediiEnhances Bone Repair in a Rabbit Model of Chronic Osteomyelitis During Post-infection Treatment and Stimulates Osteoblast Proliferation inVitro

Shou

Zhang²,

Shen

et al. 2016

Phytother. Res.

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Flavonoids are the active component of the Herba Epimedii (H. Epimedii), which is commonly used in Asia. This study is to investigate the effect of H. Epimedii on bone repair after anti-infection treatment in vivo. The bioactive-composition group of H. Epimedii (BCGE) contained four flavonoids with the total content of 43.34%. Rabbits with chronic osteomyelitis in response to injection with Staphylococcus aureus were treated with BCGE of 242.70 mg/kg/day intragastrically after vancomycin-calcium sulphate treatment. Micro-computerd tomography (CT), morphology, blood biochemistry and osteocalcin levels were assessed for effect evaluation. In addition, the rat calvarial osteoblasts infected with S. aureus were treated with vancomycin and BCGE. Cell viability, alkaline phosphatase activity, bone morphogenetic protein 2, Runt-related transcription factor 2, osteoprotegerin, receptor activator of nuclear factor-κB ligand mRNA levels and protein expression were assessed. Our results indicated that BCGE promoted bone repair via increasing the bone mass, the volume of bone, promoting osteocalcin secretion after vancomycin-calcium sulfate treatment. BCGE enhanced the cell proliferation, by regulating bone morphogenetic protein 2, runt-related transcription factor 2, and osteoprotegerin/receptor activator of nuclear factor κ-B ligand mRNA and protein expression to maintain the balance between bone formation and bone resorption. Therefore, BCGE is a potential adjuvant herbal remedy for the post-infection treatment of chronic osteomyelitis. Copyright © 2016 John Wiley & Sons, Ltd.

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“… 4 – 6 In the periapical area, LPS induces osteoclastogenic signaling, which culminates in bone resorption. 7 , 8 …”

Section: Introductionmentioning

confidence: 99%

Periapical bone response to bacterial lipopolysaccharide is shifted upon cyclooxygenase blockage

Ribeiro-Santos¹,

Silva

Petean

et al. 2019

J. Appl. Oral Sci.

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Objectives: Infection, inflammation and bone resorption are closely related events in apical periodontitis development. Therefore, we sought to investigate the role of cyclooxygenase (COX) in osteoclastogenesis and bone metabolism signaling in periapical bone tissue after bacterial lipopolysaccharide (LPS) inoculation into root canals. Methodology: Seventy two C57BL/6 mice had the root canals of the first molars inoculated with a solution containing LPS from E. coli (1.0 mg/mL) and received selective (celecoxib) or non-selective (indomethacin) COX-2 inhibitor. After 7, 14, 21 and 28 days the animals were euthanized and the tissues removed for total RNA extraction. Evaluation of gene expression was performed by qRT-PCR. Statistical analysis was performed using analysis of variance (ANOVA) followed by post-tests (α=0.05). Results: LPS induced expression of mRNA for COX-2 (Ptgs2) and PGE 2 receptors ( Ptger1, Ptger3 and Ptger4 ), indicating that cyclooxygenase is involved in periapical response to LPS. A signaling that favours bone resorption was observed because Tnfsf11 (RANKL), Vegfa, Ctsk , Mmp9, Cd36 , Icam, Vcam1 , Nfkb1 and Sox9 were upregulated in response to LPS. Indomethacin and celecoxib differentially modulated expression of osteoclastogenic and other bone metabolism genes: celecoxib downregulated Igf1r, Ctsk , Mmp9, Cd36 , Icam1, Nfkb1 , Smad3, Sox9 , Csf3, Vcam1 and Itga3 whereas indomethacin inhibited Tgfbr1, Igf1r , Ctsk, Mmp9 , Sox9, Cd36 and Icam1 . Conclusions: We demonstrated that gene expression for COX-2 and PGE 2 receptors was upregulated after LPS inoculation into the root canals. Additionally, early administration of indomethacin and celecoxib (NSAIDs) inhibited osteoclastogenic signaling. The relevance of the cyclooxygenase pathway in apical periodontitis was shown by a wide modulation in the expression of genes involved in both bone catabolism and anabolism.

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Gene expression patterns in bone following lipopolysaccharide stimulation

Cited by 8 publications

References 46 publications

Bone function, dysfunction and its role in diseases including critical illness

Bone function, dysfunction and its role in diseases including critical illness

Flavonoids of HerbaEpimediiEnhances Bone Repair in a Rabbit Model of Chronic Osteomyelitis During Post-infection Treatment and Stimulates Osteoblast Proliferation inVitro

Periapical bone response to bacterial lipopolysaccharide is shifted upon cyclooxygenase blockage

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