Disruption of NF-κB1 prevents bone loss caused by mechanical unloading

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Paradoxical Response to Mechanical Unloading in Bone Loss, Microarchitecture, and Bone Turnover Markers

BACKGROUND Sclerostin, encoded by the SOST gene, has been implicated in the response to mechanical loading in bone. Some studies demonstrated that unloading leads to up-regulated SOST expression, which may induce bone loss. PURPOSE Most reported studies regarding the changes caused by mechanical unloading were only based on a single site. Considering that the longitudinal bone growth leads to...

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Swimming Activity Prevents the Unloading Induced Loss of Bone Mass, Architecture, and Strength in Rats

We investigated whether swimming activity associated with a three-week period of hypoactivity could prevent the deleterious effects of disuse on the tibias of tail-suspended rats. Forty Wistar rats were divided into five groups: (HS) permanently hindlimb suspension rats; (HS + Swim) rats submitted to unloading interrupted by swimming exercise; (HS + WB) hindlimb suspension rats with interruptio...

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The NF-κB1 transcription factor prevents the intrathymic development of CD8 T cells with memory properties.

The role of specific members of the NF-κB family of transcription factors in CD8 T-cell selection and development is largely unknown. Here, we show that mice lacking NF-κB1 develop a unique population of conventional CD8 single-positive (SP) thymocytes with memory T cell-like properties that populate peripheral immune organs. Development of this memory-like population is not due to PLZF(+) thym...

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Lack of NF-κB1 (p105/p50) attenuates unloading-induced downregulation of PPARα and PPARα-regulated gene expression in rodent heart

Objective: Unloading of the rodent heart activates the fetal gene program, decreases peroxisome proliferator-activated receptor α (PPARα) and PPARα-regulated gene expression (MCAD), and induces cardiomyocyte atrophy. NF-κB regulates the fetal gene program and PPARαregulated gene expression during cardiac hypertrophy and induces atrophy in skeletal muscle. Our objective was to test the hypothesi...

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Periostin expression contributes to cortical bone loss during unloading.

Periostin (a product of Postn gene) is a matricellular protein which is increased in periosteal osteoblasts and osteocytes upon mechanical stimulation. We previously reported that periostin-deficient mice (Postn(-/-)) have low bone mass and a diminished response to physical activity due to a lack of sclerostin (a product of Sost gene) inhibition by mechanical loading. Here we hypothesized that ...

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ژورنال

عنوان ژورنال: Journal of Bone and Mineral Research

سال: 2013

ISSN: 0884-0431

DOI: 10.1002/jbmr.1866