Mechanisms by which the inhibition of specific intracellular signaling pathways increase osteoblast proliferation on apatite surfaces

Yang, Seungwon; Tian, Yan; Lee, Yun‐Jung; Yu, Frank H.; Kim, Hyun‐Man

doi:10.1016/j.biomaterials.2011.01.015

Cited by 27 publications

(15 citation statements)

References 47 publications

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“…Although ROCK inhibition up-regulated Akt phosphorylation through PTEN inhibition [10], [11], cell dissipation induced through ROCK inhibition was not reversed after the down-regulation of Akt activity using the PI3-K inhibitor, LY-294002 [Fig. 6C].…”

Section: Resultsmentioning

confidence: 99%

“…ROCK activity is highly activated to suppress cell cycle progression and cell migration when adhesion signaling is weak [9]–[12]. Furthermore, ROCK inhibition promotes cell proliferation through the down-regulation of phosphatase and tension homolog (PTEN) and the up-regulation of Akt phosphorylation [10], [11] or accelerates cell migration through the activation of Rac1 [12]. In the present study, we propose that the previous findings might explain the dormancy of tumor cells, manifested in cells that are not properly attached to the extracellular matrix (ECM) [13].…”

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confidence: 99%

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ROCK Inhibition Activates MCF-7 Cells

Yang

Kim

2014

PLoS ONE

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Dormant carcinoma cancer cells showing epithelial characteristics can be activated to dissipate into the surrounding tissue or organs through epithelial-mesenchymal transition (EMT). However, the molecular details underlying the activation of dormant cancer cells have been less explored. In this study, we examined the molecular pathway to activate dormant breast cancer cells. Rho-associated kinase (ROCK) inhibition disrupted cell junction, promoted cell proliferation and migration / invasion in both two-dimensional and three-dimensional substrates. The disintegration of cell junction upon ROCK inhibition, coupled with the loss of E-cadherin and b-catenin from the cell membrane, was associated with the activation of Rac1 upon ROCK inhibition. Migration / invasion also increased upon ROCK inhibition. However, the activation of MCF-7 cells upon ROCK inhibition was not associated with the up-regulation of typical EMT markers, such as snail and slug. Based on these results, we suggest the potential risk for dormant cancer cells to dissipate through non-typical EMT when ROCK activity is down-regulated.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

ROCK Inhibition Activates MCF-7 Cells

Yang

Kim

2014

PLoS ONE

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“…In addition, recent findings indicate that the RhoA signaling pathway has important roles in bone remodeling. For example, in osteoblast survival [26], the integrity of the actin cytoskeleton as well as migration [27] and differentiation [28][29][30] are regulated by RhoA signaling. We examined the effects of HA on RhoA activation in cells.…”

Section: Discussionmentioning

confidence: 99%

Hyaluronan inhibits BMP‐induced osteoblast differentiation

et al. 2015

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a b s t r a c tHyaluronan (HA), one of the major structural extracellular components in cartilage, regulates cellular responses via receptors such as CD44. However, the direct effects of HA on osteoblastic differentiation has not been studied in detail. Here, we investigated the effects of HA (molecular weight: 900-1200kDa) on osteoblastic differentiation that was induced by bone morphogenetic protein (BMP) in C2C12 cells (mouse myoblastic cells) and ST2 cells (mouse bone marrow cells). BMPinduced osteoblastic differentiation and Smad1/Smad5/Smad8 phosphorylation were downregulated by HA. Use of the CD44-blocking antibody restored HA-induced inhibition of osteoblastic differentiation and Smad1/Smad5/Smad8 phosphorylation. Our results indicate that HA inhibits BMPinduced osteoblastic differentiation through the CD44 receptor.

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“…9) although it did seem to inhibit proliferation on Sr5 which had the highest Sr content. It has been reported that osteoblasts proliferated very slowly on calcium phosphate apatite surfaces because of poor adhesion signaling in osteoblast-like cells on these surfaces 28,29) . This explained why lower cell numbers were observed on Sr0 to Sr5 than on plastic control in this study.…”

Section: Effect Of Sr On Cell Activitiesmentioning

confidence: 99%

Preparation of Sr-containing carbonate apatite as a bone substitute and its properties

Sakai

Valanezahad

Ozaki

et al. 2012

Dental Materials Journal

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Sr-containing carbonate apatite (SrCAp) specimens of varied Sr contents, ranging from 0 to 13.3 mol%, were prepared through a phosphate treatment of set gypsum-and-carbonate mixture at 100°C for 7 days. Effects of Sr content in SrCAp on microstructure, osteoblast-like cell (MC3T3-E1) attachment and proliferation, and alkaline phosphatase (ALP) activity were evaluated. Sr 2+ ion substituted Ca 2+ ion in the apatite lattice. Carbonate content was about 9-13.6 wt%, increasing in content level as Sr content increased. Sr addition benefited cell attachment but had no significant influence on cell proliferation, although the latter was inhibited at the highest Sr content. ALP activity reached a peak in specimen containing 3.4 mol% of Sr. The present study revealed that SrCAp is a promising candidate for use as a bone substitute material with good resorbabilty and osteoconductivity.

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Mechanisms by which the inhibition of specific intracellular signaling pathways increase osteoblast proliferation on apatite surfaces

Cited by 27 publications

References 47 publications

ROCK Inhibition Activates MCF-7 Cells

ROCK Inhibition Activates MCF-7 Cells

Hyaluronan inhibits BMP‐induced osteoblast differentiation

Preparation of Sr-containing carbonate apatite as a bone substitute and its properties

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