Evaluation of a polyelectrolyte complex ­(PEC) composed of chitin derivatives ­and chitosan, which promotes the rat ­calvarial osteoblast differentiation

2001 ◽  
Vol 13 (1) ◽  
pp. 46-53 ◽  
Author(s):  
Takaichi Hamano ◽  
Daido Chiba ◽  
Katsuhiro Nakatsuka ◽  
Misao Nagahata ◽  
Akira Teramoto ◽  
...  
Keyword(s):  
Osteoblast Differentiation ◽  
Polyelectrolyte Complex ◽  
Calvarial Osteoblast ◽  
Chitin Derivatives

scholarly journals Effects of Farnesyl Pyrophosphate Accumulation on Calvarial Osteoblast Differentiation

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 3113-3122 ◽  
Author(s):  
Megan M. Weivoda ◽  
Raymond J. Hohl
Keyword(s):  
Bone Formation ◽  
Osteoblast Differentiation ◽  
Biosynthetic Pathway ◽  
Squalene Synthase ◽  
Farnesyl Pyrophosphate ◽  
Matrix Mineralization ◽  
Lower Serum Cholesterol ◽  
Calvarial Osteoblast ◽  
Isoprenoid Biosynthetic Pathway

Statins, drugs commonly used to lower serum cholesterol, have been shown to stimulate osteoblast differentiation and bone formation. Statins inhibit 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A reductase (HMGCR), the first step of the isoprenoid biosynthetic pathway, leading to the depletion of the isoprenoids farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). The effects of statins on bone have previously been attributed to the depletion of GGPP, because the addition of exogenous GGPP prevented statin-stimulated osteoblast differentiation in vitro. However, in a recent report, we demonstrated that the specific depletion of GGPP did not stimulate but, in fact, inhibited osteoblast differentiation. This led us to hypothesize that isoprenoids upstream of GGPP play a role in the regulation of osteoblast differentiation. We demonstrate here that the expression of HMGCR and FPP synthase decreased during primary calvarial osteoblast differentiation, correlating with decreased FPP and GGPP levels during differentiation. Zaragozic acid (ZGA) inhibits the isoprenoid biosynthetic pathway enzyme squalene synthase, leading to an accumulation of the squalene synthase substrate FPP. ZGA treatment of calvarial osteoblasts led to a significant increase in intracellular FPP and resulted in inhibition of osteoblast differentiation as measured by osteoblastic gene expression, alkaline phosphatase activity, and matrix mineralization. Simultaneous HMGCR inhibition prevented the accumulation of FPP and restored osteoblast differentiation. In contrast, specifically inhibiting GGPPS to lower the ZGA-induced increase in GGPP did not restore osteoblast differentiation. The specificity of HMGCR inhibition to restore osteoblast differentiation of ZGA-treated cultures through the reduction in isoprenoid accumulation was confirmed with the addition of exogenous mevalonate. Similar to ZGA treatment, exogenous FPP inhibited the mineralization of primary calvarial osteoblasts. Interestingly, the effects of FPP accumulation on osteoblasts were found to be independent of protein farnesylation. Our findings are the first to demonstrate that the accumulation of FPP impairs osteoblast differentiation and suggests that the depletion of this isoprenoid may be necessary for normal and statin-induced bone formation.

scholarly journals Porphyromonas gingivalis Lipids Inhibit Osteoblastic Differentiation and Function

2010 ◽  
Vol 78 (9) ◽  
pp. 3726-3735 ◽  
Author(s):  
Yu-Hsiung Wang ◽  
Jin Jiang ◽  
Qiang Zhu ◽  
Amer Z. AlAnezi ◽  
Robert B. Clark ◽  
...  
Keyword(s):  
Gene Expression ◽  
Porphyromonas Gingivalis ◽  
Osteoblast Differentiation ◽  
Marker Genes ◽  
Nodule Formation ◽  
Dependent Manner ◽  
Bone Homeostasis ◽  
Total Lipids ◽  
And Function ◽  
Calvarial Osteoblast

ABSTRACT Porphyromonas gingivalis produces unusual sphingolipids that are known to promote inflammatory reactions in gingival fibroblasts and Toll-like receptor 2 (TLR2)-dependent secretion of interleukin-6 from dendritic cells. The aim of the present study was to examine whether P. gingivalis lipids inhibit osteoblastic function. Total lipids from P. gingivalis and two fractions, phosphoglycerol dihydroceramides and phosphoethanolamine dihydroceramides, were prepared free of lipid A. Primary calvarial osteoblast cultures derived from 5- to 7-day-old CD-1 mice were used to examine the effects of P. gingivalis lipids on mineralized nodule formation, cell viability, apoptosis, cell proliferation, and gene expression. P. gingivalis lipids inhibited osteoblast differentiation and fluorescence expression of pOBCol2.3GFP in a concentration-dependent manner. However, P. gingivalis lipids did not significantly alter osteoblast proliferation, viability, or apoptosis. When administered during specific intervals of osteoblast growth, P. gingivalis total lipids demonstrated inhibitory effects on osteoblast differentiation only after the proliferation stage of culture. Reverse transcription-PCR confirmed the downregulation of osteoblast marker genes, including Runx2, ALP, OC, BSP, OPG, and DMP-1, with concurrent upregulation of RANKL, tumor necrosis factor alpha, and MMP-3 genes. P. gingivalis total lipids and lipid fractions inhibited calvarial osteoblast gene expression and function in vivo, as determined by the loss of expression of another osteoblast differentiation reporter, pOBCol3.6GFPcyan, and reduced uptake of Alizarin complexone stain. Finally, lipid inhibition of mineral nodule formation in vitro was dependent on TLR2 expression. Our results indicate that inhibition of osteoblast function and gene expression by P. gingivalis lipids represents a novel mechanism for altering alveolar bone homeostasis at periodontal disease sites.

Design and synthesis of 3-arylbenzopyran based non-steroidal vitamin-D3mimics as osteogenic agents

MedChemComm ◽  
2016 ◽  
Vol 7 (12) ◽  
pp. 2381-2394 ◽  
Author(s):  
Mohd. Imran Ahmad ◽  
Dushyant Singh Raghuvanshi ◽  
Sarita Singh ◽  
Aijaz A. John ◽  
Ravi Prakash ◽  
...  
Keyword(s):  
Osteoblast Differentiation ◽  
Osteoblast Cells ◽  
Design And Synthesis ◽  
Calvarial Osteoblast

27benhanced osteoblast differentiation at 1 pM in mouse calvarial osteoblast cells without inherent toxicity.

scholarly journals Activation of p38 Mitogen-Activated Protein Kinase Is Required for Osteoblast Differentiation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2068-2074 ◽  
Author(s):  
Yuanyu Hu ◽  
Emily Chan ◽  
Sherry X. Wang ◽  
Baojie Li
Keyword(s):  
Bone Marrow ◽  
P38 Mapk ◽  
Osteoblast Differentiation ◽  
Specific Inhibitor ◽  
Dominant Negative ◽  
Mitogen Activated Protein Kinase ◽  
Bone Morphogenetic Protein 2 ◽  
Differentiation Markers ◽  
Mineral Deposition ◽  
Calvarial Osteoblast

p38 MAPK is a conserved subfamily of MAPKs involved in inflammatory response, stress response, cell growth and survival, as well as differentiation of a variety of cell types. In this report we demonstrated that p38 MAPK played an important role in osteoblast differentiation using primary calvarial osteoblast, bone marrow osteoprecursor culture, and a murine cell line, MC3T3-E1. We found that p38 MAPK was activated as calvarial osteoblast differentiates along with extracellular signal-regulated kinases (ERKs). When p38 MAPK is inhibited with a specific inhibitor, the expression of differentiation markers, such as alkaline phosphatase and mineral deposition, were significantly reduced. MC3T3-E1 cells expressing dominant negative p38 MAPK also displayed signs of delay in ALP and mineral deposition. Differentiation of the bone marrow osteoprecursors was also impeded by the p38 MAPK inhibitor, justified by the same markers. Yet the inhibitory effects observed in calvarial osteoblasts and bone marrow osteoprogenitor cells could be partially prevailed by bone morphogenetic protein-2. Inhibition of ERKs with a specific drug did not significantly affect osteoblast differentiation even though ERK1/2 were also activated during osteoblast differentiation. These results taken together indicate that p38 MAPK, but not ERKs, is necessary for osteoblast differentiation.

Implant Surface Roughness Affects Osteoblast Gene Expression

2003 ◽  
Vol 82 (5) ◽  
pp. 372-376 ◽  
Author(s):  
G.B. Schneider ◽  
H. Perinpanayagam ◽  
M. Clegg ◽  
R. Zaharias ◽  
D. Seabold ◽  
...  
Keyword(s):  
Gene Expression ◽  
Real Time ◽  
Real Time Pcr ◽  
Osteoblast Differentiation ◽  
Tissue Culture Plastic ◽  
Implant Surface ◽  
Alizarin Red ◽  
Surface Microtopography ◽  
Expression Of Genes ◽  
Calvarial Osteoblast

The transcription factor Cbfa1 regulates osteoblast differentiation and expression of genes necessary for the development of a mineralized phenotype. The purpose of this study was to determine if Cbfa1 and BSPII gene expression are influenced by implant surface microtopography. Osteoblasts were cultured on 600-grit (grooved) or sandblasted (roughened) cpTi implant discs. Mineralization was evaluated by Alizarin-Red-S staining. Real Time PCR was used for quantitative analysis of Cbfa1 and BSPII gene expression. Enhanced mineralization was seen in osteoblasts grown on roughened implant surfaces relative to tissue culture plastic. Real Time PCR showed significant (P < 0.05) increases in Cbfa1 gene expression in cells grown on roughened, as compared with grooved, implant surfaces. BSPII gene expression was also increased on rough surfaces in the UMR cells, but was reduced in the rat calvarial osteoblast cultures. These results suggest that osteoblast gene expression and mineralization are affected by roughened implant surface microtopographies during osseointegration of dental implants.

scholarly journals EctopicMsx2Overexpression Inhibits andMsx2Antisense Stimulates Calvarial Osteoblast Differentiation

1999 ◽  
Vol 209 (2) ◽  
pp. 298-307 ◽  
Author(s):  
Milan Dodig ◽  
Tade Tadic ◽  
Mark S Kronenberg ◽  
Sanja Dacic ◽  
Yi-Hsin Liu ◽  
...  
Keyword(s):  
Osteoblast Differentiation ◽  
Calvarial Osteoblast

Author response for "Thrombomodulin functional domains support osteoblast differentiation and bone healing in diabetes in mice"

2020 ◽  
Author(s):  
Chung‐Hwan Chen ◽  
Chao‐Han Lai ◽  
Yi‐Kai Hong ◽  
Jui‐Ming Lu ◽  
Sung‐Yen Lin ◽  
...  
Keyword(s):  
Bone Healing ◽  
Osteoblast Differentiation ◽  
Author Response ◽  
Functional Domains ◽  
Diabetes In Mice
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