Photoactivation of TAZ via Akt/GSK3β signaling pathway promotes osteogenic differentiation

Feng, Jie; Sun, Qinyan; Liu, Lei; Xing, Da

doi:10.1016/j.biocel.2015.07.002

Cited by 18 publications

(14 citation statements)

References 71 publications

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“…In osteoporosis model rats, protein expression of phosphorylated PI3K and phosphorylated Akt in bone tissue was decreased dramatically (Xi et al, 2015). Akt activation promotes osteogenic differentiation (Feng et al, 2015). We therefore examined whether the PI3K/Akt signaling pathway is involved in the protective effects of SDSS.…”

Section: Discussionmentioning

confidence: 99%

The New Synthetic H2S-Releasing SDSS Protects MC3T3-E1 Osteoblasts against H2O2-Induced Apoptosis by Suppressing Oxidative Stress, Inhibiting MAPKs, and Activating the PI3K/Akt Pathway

Yan

et al. 2017

Front. Pharmacol.

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Reactive oxygen species (ROS) are important in osteoporosis development. Oxidative stress induces apoptosis of osteoblasts and arrest of their differentiation. Both Danshensu (DSS) and hydrogen sulfide (H2S) produce significant antioxidant effect in various systems. In this study, we synthesized SDSS, a novel H2S-releasing compound derived from DSS, and studied its antioxidant effect in an H2O2-induced MC3T3-E1 osteoblastic cell injury model. We first characterized the H2S releasing property of SDSS in both in vivo and in vitro models. HPLC chromatogram showed that intravenous injection of SDSS in adult rats released ADT-OH, a well proved H2S sustained-release moiety, within several minutes in the rat plasma. Using an H2S selective fluorescent probe, we further confirmed that SDSS released H2S in MC3T3-E1 osteoblastic cells. Biological studies revealed that SDSS had no significant toxic effect but produced protective effects against H2O2-induced MC3T3-E1 cell apoptosis. SDSS also reversed the arrest of cell differentiation caused by H2O2 treatment. This was caused by the stimulatory effect of SDSS on bone sialoprotein, runt-related transcription factor 2, collagen expression, alkaline phosphatase activity, and bone nodule formation. Further studies revealed that SDSS reversed the reduced superoxide dismutase activity and glutathione content, and the increased ROS production in H2O2 treated cells. In addition, SDSS significantly attenuated H2O2-induced activation of p38-, ERK1/2-, and JNK-MAPKs. SDSS also stimulated phosphatidylinositol 3-kinase/Akt signaling pathway. Blockade of this pathway attenuated the cytoprotective effect of SDSS. In conclusion, SDSS protects MC3T3-E1 cells against H2O2-induced apoptosis by suppressing oxidative stress, inhibiting MAPKs, and activating the phosphatidylinositol 3-kinase/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

The New Synthetic H2S-Releasing SDSS Protects MC3T3-E1 Osteoblasts against H2O2-Induced Apoptosis by Suppressing Oxidative Stress, Inhibiting MAPKs, and Activating the PI3K/Akt Pathway

Yan

et al. 2017

Front. Pharmacol.

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“…All three aspects were reported respectively to influence the differentiation of MSCs under some conditions [20,25,26]. In the present study, the main purpose was to investigate whether icariin-activated PI3K/Akt crosstalked with TAZ-Runx2 pathway from a transcriptional level and further regulated MSC osteogenesis, not translocation or phosphorylation of TAZ.…”

Section: Discussionmentioning

confidence: 99%

“…It was found that FGF2 treatment firstly activated ERK and then, activation of ERK would upregulate TAZ expression and facilitate its interaction with downstream Runx2 [21]. Moresignificantly, a recent report found that low-power laser irradiation (LPLI) activated the Akt/GSK3β pathway which further activated TAZ-related pathway to stimulate osteogenesis [25]. These reports suggest that TAZ may be a key effector of many drugs to promote osteogenesis and furthermore, crosstalking with the TAZ pathway may be the underlying mechanism by which some indirect signal molecules regulat osteogenesis, such as ERK and Akt/GSK3β.…”

Section: Conflict Of Interestmentioning

confidence: 99%

New pathway of icariin-induced MSC osteogenesis: transcriptional activation of TAZ/Runx2 by PI3K/Akt

et al. 2017

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“…In contrast, the mechanism, by which the initial activation of Akt leads to TAZ activation, is not clear. Although there are several reports that Akt activates TAZ, the underlying molecular mechanism is yet unknown [47,48]. One paper reported that Akt inhibits GSK3β and increases TAZ expression level [47].…”

Section: Plos Onementioning

confidence: 99%

Characterization of a novel compound that promotes myogenesis via Akt and transcriptional co-activator with PDZ-binding motif (TAZ) in mouse C2C12 cells

et al. 2020

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Photoactivation of TAZ via Akt/GSK3β signaling pathway promotes osteogenic differentiation

Cited by 18 publications

References 71 publications

The New Synthetic H2S-Releasing SDSS Protects MC3T3-E1 Osteoblasts against H2O2-Induced Apoptosis by Suppressing Oxidative Stress, Inhibiting MAPKs, and Activating the PI3K/Akt Pathway

The New Synthetic H2S-Releasing SDSS Protects MC3T3-E1 Osteoblasts against H2O2-Induced Apoptosis by Suppressing Oxidative Stress, Inhibiting MAPKs, and Activating the PI3K/Akt Pathway

New pathway of icariin-induced MSC osteogenesis: transcriptional activation of TAZ/Runx2 by PI3K/Akt

Characterization of a novel compound that promotes myogenesis via Akt and transcriptional co-activator with PDZ-binding motif (TAZ) in mouse C2C12 cells

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