Effects of experimental conditions on the release of 45calcium from prelabeled fetal mouse long bones

Beek, Ermond van; Ruit, Marjanne Oostendorp-van de; Wee-Pals, L. van der; Bloys, H.; Bent, C. van de; Papapoulos, Socrates E.; Löwik, Clemens W.G.M.

doi:10.1016/8756-3282(95)00135-z

Cited by 11 publications

(3 citation statements)

References 14 publications

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“…Normal bone metabolism is a result of the equilibrium between bone formation by osteoblasts and bone resorption by osteoclasts. The mechanism of bone loss induced by glucocorticoids is two-fold, with decreased bone formation and increased bone resorption 28. Similar findings have been observed by Bhattacharya et al .,12 in Indian COPD patients.…”

Section: Discussionsupporting

confidence: 84%

Bone mineral density among elderly patients with chronic obstructive pulmonary disease patients in India

Hattiholi

Gaude

2013

Niger Med J

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Background:Osteoporosis is one of the major extra-pulmonary manifestations of chronic obstructive pulmonary disease (COPD), which limits the physical activity. The present study was undertaken to study the bone mineral density (BMD) and osteoporosis in the elderly COPD patients.Materials and Methods:This was a cross-sectional study carried out among elderly COPD patients. After a detailed clinical history spirometry was done to stage the severity of COPD. DEXA scan of the lumbar spine was performed using bone densitometer to determine osteoporosis. Statistical analysis was based on Chi-square test. Risk factors were identified by univariate and multivariate logistic regression analysis.Results:A total of 70 elderly COPD patients were included. Fourty-six patients (65.7%) had osteoporosis and 13 (18.6%) had osteopenia. Majority of the osteoporosis patients had stage III or stage IV COPD disease (77.2%). As the severity grade of COPD increased, the risk of osteoporosis also increased. Also, with the increasing severity of COPD, BMD decreased. Patients with lower body mass index (BMI) had higher prevalence of osteoporosis (45.7%). Using multivariate regression analysis, stage IV COPD, number of acute exacerbations >3 and steroid cumulative dose >1000 mg were independent risk factors for osteoporosis in elderly COPD patients.Conclusions:The prevalence of osteoporosis was 65.7%, and 18.6% had osteopenia. Stage III and IV patients had significantly lower BMI in elderly COPD patients. High clinical suspicion and early diagnosis and treatment are required in the evaluation of osteoporosis in elderly COPD patients.

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Section: Discussionsupporting

confidence: 84%

Bone mineral density among elderly patients with chronic obstructive pulmonary disease patients in India

Hattiholi

Gaude

2013

Niger Med J

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“…Mouse fetal metatarsals were isolated from FVB mouse embryos (time-paired; Harlan Laboratories, Indianapolis, IN, USA) at day 17.5 of gestation [26,27]. After isolation, metatarsals were individually cultured in 24-well plates in 200 µl/well in Minimal Essential Medium (MEM) α supplemented with 10% FBS, 100 U of penicillin-streptomycin (Gibco/Life Technologies) and 1% GlutaMAX supplement (Invitrogen, Carlsbad, CA, USA) for 48 h. After this equilibration period, metatarsals were treated with several concentrations of the small molecules, either alone or in combination with 10 ng/ml TNFα or IL-1β (R&D Systems, Minneapolis, MN, USA) or a combination of both for 1, 4 or 7 days.…”

Section: Methodsmentioning

confidence: 99%

Small molecule inhibitors of WNT/β-catenin signaling block IL-1β- and TNFα-induced cartilage degradation

et al. 2013

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IntroductionIn this study, we tested the ability of small molecule inhibitors of WNT/β-catenin signaling to block interleukin 1β (IL-1β)- and tumor necrosis factor α (TNFα)-induced cartilage degradation. Proinflammatory cytokines such as IL-1β and TNFα are potent inducers of cartilage degradation by upregulating matrix metalloproteinase (MMP) expression and activity. Because WNT/β-catenin signaling was found to be involved in IL-1β- and TNFα-induced upregulation of MMP activity, we hypothesized that inhibition of WNT/β-catenin signaling might block IL-1β- and TNFα-induced cartilage degradation. We tested the effect of small molecules that block the interaction between β-catenin and TCF/Lef transcription factors on IL-1β- and TNFα-induced cartilage degradation in mouse fetal metatarsals.MethodsWe used mouse fetal metatarsals treated with IL-1β and TNFα as an ex vivo model for cytokine-induced cartilage degradation. Metatarsals were treated with IL-1β and TNFα in combination with the small molecules PKF115-584, PKF118-310 and CGP049090 at different concentrations and then harvested them for histological and gene expression analysis.ResultsWe found that IL-1β- and TNFα-induced cartilage degradation in mouse fetal metatarsals was blocked by inhibiting WNT/β-catenin signaling using small molecule PKF115-584 and partially using CGP049090 dose-dependently. In addition, we found that PKF115-584 blocked IL-1β- and TNFα-induced MMP mRNA expression, but did not reverse the inhibitory effect of IL-1β on the expression of cartilage anabolic genes.ConclusionIn this study, we show that inhibition of WNT/β-catenin signaling by small molecules can effectively prevent IL-1β- and TNFα-induced cartilage degradation by blocking MMP expression and activity. Furthermore, we elucidate the involvement of WNT/β-catenin signaling in IL-1β- and TNFα-induced cartilage degradation.

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“…Animal experiments were approved by the ethical committee of the University Medical Centre Utrecht. Mouse fetal metatarsals were isolated from FVB mouse embryos (time‐paired, Harlan) at day 17.5 of gestation (van Beek et al , ; Haaijman et al , ). After isolation, the metatarsals were individually cultured in 24‐well plates in 200 µl/well minimal essential medium (MEM) α , supplemented with 10% FBS, 100 U/ml penicillin, 100 mg/ml streptomycin and 1% Glutamax (Invitrogen) for 48 h. After this equilibration period, the metatarsals were cultured in hypoxia or in the presence of 5.0 μ m O ‐phenanthroline, either alone or in combination with 10 ng/ml TNF α and IL‐1 β (R&D Systems), for 4 days for gene expression analysis or for 7 days for histological analysis.…”

Section: Methodsmentioning

confidence: 99%

O-Phenanthroline as modulator of the hypoxic and catabolic response in cartilage tissue-engineering models

Georgi

Landman

Blitterswijk

et al. 2014

J Tissue Eng Regen Med

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Hypoxia has been shown to be important for maintaining cartilage homeostasis as well as for inducing chondrogenic differentiation. Ensuring low oxygen levels during in vitro culture is difficult, therefore we assessed the chondro-inductive capabilities of the hypoxia-mimicking agent O-phenanthroline, which is also known as a non-specific matrix metalloproteinase (MMP) inhibitor. We found that O-phenanthroline reduced the expression of MMP3 and MMP13 mRNA levels during chondrogenic differentiation of human chondrocytes (hChs), as well as after TNFα/IL-1β exposure in an explant model. Interestingly, O-phenanthroline significantly inhibited matrix degradation in a TNFα/IL-1β-dependent model of cartilage degeneration when compared to control and natural hypoxia (2.5% O ). O-Phenanthroline had limited ability to improve the chondrogenic differentiation or matrix deposition in the chondrogenic pellet model. Additionally, O-phenanthroline alleviated MMP-induced cartilage degradation without affecting chondrogenesis in the explant culture. The data presented in this study indicate that the inhibitory effect of O-phenanthroline on MMP expression is dominant over the hypoxia-mimicking effect. Copyright © 2014 John Wiley & Sons, Ltd.

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Effects of experimental conditions on the release of 45calcium from prelabeled fetal mouse long bones

Cited by 11 publications

References 14 publications

Bone mineral density among elderly patients with chronic obstructive pulmonary disease patients in India

Bone mineral density among elderly patients with chronic obstructive pulmonary disease patients in India

Small molecule inhibitors of WNT/β-catenin signaling block IL-1β- and TNFα-induced cartilage degradation

O-Phenanthroline as modulator of the hypoxic and catabolic response in cartilage tissue-engineering models

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