Inhibition of Insulin-like Growth Factor-1 (IGF-1) Expression by Prolonged Transforming Growth Factor-β1 (TGF-β1) Administration Suppresses Osteoblast Differentiation

Ochiai, Hirokazu; Okada, Shoko; Saito, Akiko; Hoshi, Kazuto; Yamashita, Haruto; Takato, Tsuyoshi; Azuma, Toshifumi

doi:10.1074/jbc.m111.279091

Cited by 83 publications

(80 citation statements)

References 40 publications

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“…Previously, we reported that repeated TGF-β1 treatment to HPDL cells downregulates ALP expression 4) . We observed subsequent decreased IGF-1 expression and inhibition of PI3K/Akt signaling 3) . In this study, we found that repeated Wnt3A treatment caused both decreased IGF-1 expression and decreased Akt phosphorylation, also previously observed following repeated TGF-β1 administration 3) .…”

Section: Discussionmentioning

confidence: 72%

“…IGF-1 knockout mice reportedly exhibit short-limb dwarfism, delays in mineralization, and increased chondrocyte apoptosis 27) . Our recent report revealed that the inhibition of autocrine IGF-1 expression may inhibit osteogenic differentiation 3) . We found that repeated Wnt3A administration suppressed both IGF-1 expression and Akt phosphorylation, indicating the inhibition of the IGF-1/PI3K…”

Section: Discussionmentioning

confidence: 99%

“…Previously, we reported that repeated TGF-β1 treatment reduced IGF-1 secretion, which subsequently downregulated PI3K signaling 3) . We examined whether the inhibitory effects caused by repeated Wnt3A treatment were reversed by IGF-1 administration.…”

Section: Effect Of Repeated Wnt3a Administration On the Smad And Pi3kmentioning

confidence: 99%

“…We previously reported an experimental model that allows the investigation of inhibitory effects of transforming growth factor-1 (TGF-1) on osteoblast differentiation and found that repeated or high-dose administration of TGF-1 inhibited osteoblast differentiation of HPDL cells by decreasing insulin-like growth factor-1 (IGF-1) expression and subsequently downregulating phosphatidylinositide 3-kinase (PI3K)/Akt signaling 3,4) . However, many aspects of the mechanisms by which HPDL cells differentiate into osteoblasts remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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The Comparison between Single vs Repeated Administration of Wnt3A of HPDL Cells

Yoshizawa

Ochiai-Shino

Tsukinowa

et al. 2015

J. Hard Tissue Biology.

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Developmental studies indicate the Wnt/ -catenin pathway biphasically regulates tissue differentiation. Bone morphogenetic protein (BMP) and Wnt signaling reported function in osteoblast differentiation, but few studies have investigated these complex mechanisms. We hypothesized that Wnt/ -catenin signaling acts, either promoting or inhibiting osteogenesis of human periodontal ligament (HPDL) cells depending on times of treatment of Wnt3A. HPDL cells were treated with single or repeated administration (12-or 24-h intervals) of 10 ng/ml of Wnt3A and cultured for 3 days. Single Wnt3A administration increased alkaline phosphatase (ALP) activity. Conversely, repeated Wnt3A administration significantly decreased the expression of osteoblast marker genes. Single Wnt3A administration resulted in Smad1/5 and Akt phosphorylation; however, repeated Wnt3A administration inhibited it. BMP2/7 or IGF-1 treatment was sufficient to reverse the inhibitory effects of repeated Wnt3A treatment. Single administration of a glycogen synthase kinase 3 inhibitors, CHIR99021, increased ALP expression, but repeated CHIR99021 administration significantly decreased ALP expression and ALP activity compared with single administration. These findings suggest that repeated activation of Wnt signaling inhibits osteoblast differentiation by suppressing the BMP2/7-Smad1/5 and phosphatidylinositide 3-kinase (PI3K) /Akt pathways in HPDL cells. This indicated that crosstalk between the Wnt, Smad1/5, and PI3K/Akt pathways is important for osteoblastic differentiation of HPDL cells.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Section: Effect Of Repeated Wnt3a Administration On the Smad And Pi3kmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Comparison between Single vs Repeated Administration of Wnt3A of HPDL Cells

Yoshizawa

Ochiai-Shino

Tsukinowa

et al. 2015

J. Hard Tissue Biology.

Self Cite

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“…Alternatively, downregulation of XRN1 may lead to increased expression of specific miRNAs and/or protein-coding RNAs which then promote the cancerous phenotype. Possible candidates are IGF-1, which is known to induce proliferation of osteoblasts [38][39][40] and/or pro-inflammatory RNAs such as FOS and MYC which are widely known to be involved in cancer progression.…”

Section: Human Diseases Associated With Xrn1mentioning

confidence: 99%

The roles of the exoribonucleases DIS3L2 and XRN1 in human disease

Pashler

Towler

Jones

et al. 2016

Biochemical Society Transactions

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RNA degradation is a vital post-transcriptional process which ensures that transcripts are maintained at the correct level within the cell. DIS3L2 and XRN1 are conserved exoribonucleases which are critical for the degradation of cytoplasmic RNAs. Although the molecular mechanisms of RNA degradation by DIS3L2 and XRN1 have been well studied, less is known about their specific roles in development of multicellular organisms or human disease. This review focusses on the roles of DIS3L2 and XRN1 in the pathogenesis of human disease, particularly in relation to phenotypes seen in model organisms. The known diseases associated with loss of activity of DIS3L2 and XRN1 are discussed, together with possible mechanisms and cellular pathways leading to these disease conditions.

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Spatiotemporal Control Strategies for Bone Formation through Tissue Engineering and Regenerative Medicine Approaches

White

Olabisi

2018

Adv Healthcare Materials

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Global increases in life expectancy drive increasing demands for bone regeneration. The gold standard for surgical bone repair is autografting, which enjoys excellent clinical outcomes; however, it possesses significant drawbacks including donor site morbidity and limited availability. Although collagen sponges delivered with bone morphogenetic protein, type 2 (BMP2) are a common alternative or supplement, they do not efficiently retain BMP2, necessitating extremely high doses to elicit bone formation. Hence, reports of BMP2 complications are rising, including cancer promotion and ectopic bone formation, the latter inducing complications such as breathing difficulties and neurologic impairments. Thus, efforts to exert spatial control over bone formation are increasing. Several tissue engineering approaches have demonstrated the potential for targeted and controlled bone formation. These approaches include biomaterial scaffolds derived from synthetic sources, e.g., calcium phosphates or polymers; natural sources, e.g., bone or seashell; and immobilized biofactors, e.g., BMP2. Although BMP2 is the only protein clinically approved for use in a surgical device, there are several proteins, small molecules, and growth factors that show promise in tissue engineering applications. This review profiles the tissue engineering advances in achieving control over the location and onset of bone formation (spatiotemporal control) toward avoiding the complications associated with BMP2.

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Inhibition of Insulin-like Growth Factor-1 (IGF-1) Expression by Prolonged Transforming Growth Factor-β1 (TGF-β1) Administration Suppresses Osteoblast Differentiation

Cited by 83 publications

References 40 publications

The Comparison between Single vs Repeated Administration of Wnt3A of HPDL Cells

The Comparison between Single vs Repeated Administration of Wnt3A of HPDL Cells

The roles of the exoribonucleases DIS3L2 and XRN1 in human disease

Spatiotemporal Control Strategies for Bone Formation through Tissue Engineering and Regenerative Medicine Approaches

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