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Title:
Boneāfat linkage via interleukin-11 in response to mechanical loading | Journal of Bone and Mineral Metabolism
Description:
Positive regulators of bone formation, such as mechanical loading and PTH, stimulate and negative regulators, such as aging and glucocorticoid excess, suppress IL-11 gene transcription in osteoblastic cells. Signal transduction from mechanical loading and PTH stimulation involves two pathways: one is Ca2+āERKāCREB pathway which facilitates binding of āFosB/JunD to the AP-1 site to enhance IL-11 gene transcription, and the other is Smad1/5 phosphorylation that promotes IL-11 gene transcription via SBE binding and complex formation with āFosB/JunD. The increased IL-11 suppresses Sost expression via IL-11RαāSTAT1/3āHDAC4/5 pathway and enhances Wnt signaling in the bone to stimulate bone formation. Thus, IL-11 mediates stimulatory and inhibitory signals of bone formation by affecting Wnt signaling. Physiologically important stimulation of bone formation is exercise-induced mechanical loading, but exercise simultaneously requires energy source for muscle contraction. Exercise-induced stimulation of IL-11 expression in the bone increases the secretion of IL-11 from the bone. The increased circulating IL-11 acts like a hormone to enhance adipolysis as an energy source with a reduction in adipogenic differentiation via a suppression of Dkk1/2 expression in the adipose tissue. Such boneāfat linkage can be a mechanism whereby exercise increases bone mass and, at the same time, maintains energy supply from the adipose tissue.
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Keywords {š}
pubmed, article, bone, google, scholar, cas, matsumoto, formation, interleukin, central, signaling, mechanical, hiasa, masahiro, endo, access, gene, expression, fukumoto, rev, inoue, nat, privacy, cookies, content, journal, research, loading, transcription, pathway, wnt, exercise, differentiation, kido, factor, commun, miner, res, cytokine, information, publish, search, metabolism, stimulate, glucocorticoid, adipogenesis, open, mice, ito, receptor,
Topics {āļø}
wnt3a/β-catenin signalling pathway il-11rαāstat1/3āhdac4/5 pathway month download article/chapter extracellular-signal regulated kinase spaceflight-induced bone loss exercise-induced mechanical loading ca2+āerkācreb pathway fgf23-related hypophosphatemic diseases nishiyama dental academy exercise-induced stimulation full article pdf mineral metabolism aims boneāfat linkage stimulate osteoblast differentiation privacy choices/manage cookies related subjects stimulate bone formation stimulating osteoblast differentiation attenuating osteoblast differentiation enhances wnt signaling affecting wnt signaling impaired bone formation increases bone formation deltafosb transcription factor il11ra1 knockout mice renal stone formation systemic adipogenesis cortical bone mass interleukin-11 receptor signaling enhance adipolysis maintains energy supply check access instant access article journal bmp receptor signaling signaling cross-talk european economic area physiologically important stimulation x-linked hypophosphatemia unliganded fgf receptor lung fibro-inflammation 90-day bed rest restore normal gain fosb/āfosb gene article hiasa article log conditions privacy policy sims na il-11 mediates stimulatory decreased ap-1 activity
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headline:Boneāfat linkage via interleukin-11 in response to mechanical loading
description:Positive regulators of bone formation, such as mechanical loading and PTH, stimulate and negative regulators, such as aging and glucocorticoid excess, suppress IL-11 gene transcription in osteoblastic cells. Signal transduction from mechanical loading and PTH stimulation involves two pathways: one is Ca2+āERKāCREB pathway which facilitates binding of āFosB/JunD to the AP-1 site to enhance IL-11 gene transcription, and the other is Smad1/5 phosphorylation that promotes IL-11 gene transcription via SBE binding and complex formation with āFosB/JunD. The increased IL-11 suppresses Sost expression via IL-11RαāSTAT1/3āHDAC4/5 pathway and enhances Wnt signaling in the bone to stimulate bone formation. Thus, IL-11 mediates stimulatory and inhibitory signals of bone formation by affecting Wnt signaling. Physiologically important stimulation of bone formation is exercise-induced mechanical loading, but exercise simultaneously requires energy source for muscle contraction. Exercise-induced stimulation of IL-11 expression in the bone increases the secretion of IL-11 from the bone. The increased circulating IL-11 acts like a hormone to enhance adipolysis as an energy source with a reduction in adipogenic differentiation via a suppression of Dkk1/2 expression in the adipose tissue. Such boneāfat linkage can be a mechanism whereby exercise increases bone mass and, at the same time, maintains energy supply from the adipose tissue.
datePublished:2024-02-07T00:00:00Z
dateModified:2024-02-07T00:00:00Z
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Wnt signal
Sclerostin
Exercise
Bone formation
Adipolysis
Metabolic Diseases
Orthopedics
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description:Positive regulators of bone formation, such as mechanical loading and PTH, stimulate and negative regulators, such as aging and glucocorticoid excess, suppress IL-11 gene transcription in osteoblastic cells. Signal transduction from mechanical loading and PTH stimulation involves two pathways: one is Ca2+āERKāCREB pathway which facilitates binding of āFosB/JunD to the AP-1 site to enhance IL-11 gene transcription, and the other is Smad1/5 phosphorylation that promotes IL-11 gene transcription via SBE binding and complex formation with āFosB/JunD. The increased IL-11 suppresses Sost expression via IL-11RαāSTAT1/3āHDAC4/5 pathway and enhances Wnt signaling in the bone to stimulate bone formation. Thus, IL-11 mediates stimulatory and inhibitory signals of bone formation by affecting Wnt signaling. Physiologically important stimulation of bone formation is exercise-induced mechanical loading, but exercise simultaneously requires energy source for muscle contraction. Exercise-induced stimulation of IL-11 expression in the bone increases the secretion of IL-11 from the bone. The increased circulating IL-11 acts like a hormone to enhance adipolysis as an energy source with a reduction in adipogenic differentiation via a suppression of Dkk1/2 expression in the adipose tissue. Such boneāfat linkage can be a mechanism whereby exercise increases bone mass and, at the same time, maintains energy supply from the adipose tissue.
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Metabolic Diseases
Orthopedics
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