16 research outputs found
The actions of resolvin E1 on osteoblast function
No full textThesis (Ph.D.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at [email protected]. Thank you.Resolvins are endogenous anti-inflammatory I pro-resolving lipid mediators derived from omega-3 fatty acids. Resolvin E1 (RvE1) reverses periodontitis and promotes regeneration of alveolar bone in vivo. The goal of this project was to determine the mechanism of RvE1 impact on bone formation. RvE1 significantly enhanced bone formation relative to a vehicle control in a mouse craniotomy model of bone healing. Since RvE1 is reported to act through receptors expressed by cells of the innate immune system, the initial hypothesis tested was that RvE1 actions are mediated through bone macrophages. The hypothesis was rejected, as no impact of RvE1 on macrophage mediated bone formation was demonstrable. The alternative hypothesis was that RvE1 acts directly on osteoblasts. Using mouse neonatal osteoblasts, calcification of osteoblast cultures was demonstrated. Osteoblasts express the RvE1 receptor, ChemR23, at the mRNA and protein level. Examination of intracellular signaling by RvE1 demonstrated increased phosphorylation of rpS6 through the AKT-mTOR pathway. The specificity of RvE1 signaling through ChemR23 was demonstrated with ChemR23 specific blocking antibody that abrogated the phosphorylation of rpS6. Rapamycin, an inhibitor of mTOR, also blocked rpS6 phosphorylation.
To examine the mechanism of RvE1 treated osteoblast enhanced bone formation, secretion of bone specific proteins by osteoblasts after pro-inflammatory stimulation (IL-6) was examined with a focus on the osteoprotegerin (OPG) and receptor activator of NF-κB ligand (RANKL) axis, which regulates osteoclast differentiation. Secretion of RANKL and OPG by mouse neonatal osteoblasts stimulated with IL-6 and treated with RvE1 was measured by ELISA. IL-6 stimulation did not impact RANKL levels but decreased OPG production, thereby changing the RANKL/OPG to favor osteoclast activation and bone resorption. RvE1 blocked OPG changes, however, maintaining a RANKL/OPG more favorable to bone formation.
In conclusion, RvE1 has anabolic actions in a mouse model of bone healing mediated through RANKL/OPG. RvE1 signals the receptor ChemR23 on the osteoblast surface through the mTOR pathway and phosphorylation of rpS6. Functionally, RvE1 shifts the balance between OPG and RANKL to favor bone formation. Mediators of innate immunity thus also directly regulate bone cells
The action of anti-inflammatory agents in healthy temporomandibular joint synovial tissues is sex-dependent
No full textActivation of the Acquired Immune Response Reduces Coupled Bone Formation in Response to a Periodontal Pathogen
No full textVitamin D: A growing perspective
No full textVitamin D deficiency has been widely reported in all age groups in recent years. Rickets has never been eradicated in developed countries, and it most commonly affects children from recent immigrant groups. There is much evidence that current vitamin D guidelines for the neonatal period, 5-10 μ g (200-400 IU)-day, prevent rickets at the typical calcium intakes in developed countries. The annual incidence of vitamin D-deficiency rickets in developed countries ranges between 2.9 and 7.5 cases per 100,000 children. The prevalence of vitamin D deficiency in mothers and their neonates is remarkable, and the results of one study suggest that third-trimester 25-hydroxyvitamin D (25(OH)D) is associated with fetal bone mineral accrual that may affect prepubertal bone mass accumulation. Beyond infancy, the evidence indicates that 5 μ g (200 IU)-day of vitamin D has little effect on vitamin D status as measured by the serum 25(OH)D concentration. Two randomized clinical trials show that higher vitamin D intake improves one-year gain in bone density in adolescent girls. The functions of vitamin D extend beyond bone to include immune system regulation and anti-proliferative effects on cells. Early life vitamin D inadequacy is implicated in the risk of bone disease, autoimmune disease, and certain cancers later in life; however, long-term interventional studies do not exist to validate the widespread implementation of greater vitamin D consumption. Here we review the available data concerning vitamin D status and health effects of vitamin D in pregnancy through to and including adolescence. 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Alveolar Bone Resorption Following Coronal Versus Apical Approach in a Mucoperiosteal Flap Surgery Procedure in the Rat Mandible
No full text
Mineral maturity and crystallinity index are distinct characteristics of bone mineral
No full textThe purpose of this study was to test the hypothesis that mineral maturity and crystallinity index are two different characteristics of bone mineral. To this end, Fourier transform infrared microspectroscopy (FTIRM) was used. To test our hypothesis, synthetic apatites and human bone samples were used for the validation of the two parameters using FTIRM. Iliac crest samples from seven human controls and two with skeletal fluorosis were analyzed at the bone structural unit (BSU) level by FTIRM on sections 2–4 lm thick. Mineral maturity and crystallinity index were highly correlated in synthetic apatites but poorly correlated in normal human bone. In skeletal fluorosis, crystallinity index was increased and maturity decreased, supporting the fact of separate measurement of these two parameters. Moreover, results obtained in fluorosis suggested that mineral characteristics can be modified independently of bone remodeling. In conclusion, mineral maturity and crystallinity index are two different parameters measured separately by FTIRM and offering new perspectives to assess bone mineral traits in osteoporosis
Spectroscopic Characterization of Bone Composition : Alterations during Bone Formation, Maturation and Aging
No full textWnt3a transcriptionally up-regulates lysyl oxidase mRNA levels in C3H10T1/2 pluripotent progenitor cells.
No full text<p>Serum-depleted cells were treated with Wnt3a- or control-conditioned medium for 24 hours. Total RNA and protein were extracted and subjected to real time PCR and Western blotting analyses. <b>A)</b> The bar graph presents lysyl oxidase mRNA levels in response to Wnt3a in C3H10T1/2 cells (n = 6), mouse primary bone marrow stromal cells (BMSCs, n = 3), rat primary calvarial osteoblasts (n = 9), and a mouse pre-osteoblast cells (MC3T3-E1, n = 3). Data presented for C3H10T1/2 cells, BMSCs and primary calvarial osteoblasts were pooled from two independent experiments; data from MC3T3-E1 cells were from one experiment performed in triplicate. Data shown are means ± SD (*, p<0.05, N.S, not significant; Student's t-test). <b>B)</b> The bar graph shows the fold change of lysyl oxidase transcriptional activity in response to Wnt3a in C3H10T1/2 cells (n = 3). Data are from one representative experiment performed in triplicate of three independent experiments, all showing significantly increased lysyl oxidase transcription after Wnt3a treatment. Data shown are means ± SD (*, p<0.05; Student's t-test). <b>C)</b> The bar graph presents lysyl oxidase protein levels in response to Wnt3a in C3H10T1/2 cells (n = 3). Data shown are means ± SD (*, p<0.05; Student's t-test). <b>D)</b> Lysyl oxidase protein levels in response to Wnt3a in rat primary calvarial cells (n = 6). Data shown are means ± SD N.S, not significant; Student's t-test).</p
