Gardenamide A attenuated cell apoptosis induced by serum deprivation insult via the ERK1/2 and PI3K/AKT signaling pathways

Wang, R.; Yang, Jie; Li, Peng; Zhao, Jianhao; Ma, Nan; Huang, Jilin; Lazarovici, Philip; Chen, H.; Zheng, Wenhua

doi:10.1016/j.neuroscience.2014.11.056

Cited by 32 publications

(15 citation statements)

References 28 publications

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“…Protein kinase C is a driver of multiple signal transducing kinases, including ERK1/2 and p38 MAPK, which promote the proliferation and differentiation of chondrocytes . The major MAPK subtypes, including ERK1/2, JNK and p38MAPK, are known to participate in chondrogenic differentiation . ERK1/2 promotes cartilage formation by promoting early differentiation, p38 MAPK stimulates cartilage formation by acting on early and late cultures, and JNK acts as a negative regulator of cartilage formation.…”

Section: Discussionmentioning

confidence: 99%

“…38 Protein kinase C is a driver of multiple signal transducing kinases, including ERK1/2 and p38 MAPK, which promote the proliferation and differentiation of chondrocytes. 13 The major MAPK subtypes, including ERK1/2, JNK and p38MAPK, 39 are known to participate in chondrogenic differentiation. 40 SB203580 (p38 inhibitor) and PD98059 (ERK1/2 inhibitor) reduce the mRNA expression of p21 that is induced by NPW-23.…”

Section: Discussionmentioning

confidence: 99%

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Neuropeptide W regulates proliferation and differentiation of ATDC5: Possible involvement of GPR7 activation, PKA and PKC‐dependent signalling cascades

Wang

Zheng

Jiang

et al. 2019

J Cellular Molecular Medi

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Various neuropeptides related to the energy equilibrium affect bone growth in humans and animals. Neuropeptides W (NPW) are identical in the internal ligands of the two G‐protein receptors (GPRs) included in subtypes 7 and 8. Neuropeptides W inhibits proliferation in the cultivated rat calvarial osteoblast‐like (ROB) cells. This study examines the expression of NPW and GPR7 in murine chondrocyte and their function. An immunohistochemical analysis showed that NPW and GPR7 were expressed in the proliferative chondrocytes of the growth plates in the hind limbs of mice. The NPW mRNA quickly elevated in the early differentiation (7‐14 days) of ATDC5 cells, while NPW and GPR7 mRNA were reduced during the late stage (14‐21 days) of differentiation. Neuropeptide W‐23 (NPW‐23) promoted the proliferation of ATDC5 cells, which was attenuated by inhibiting the GPR7, protein kinase A (PKA), protein kinase C (PKC) and ERK1/2 pathways. Neuropeptide W‐23 enhanced the early cell differentiation, as evaluated by collagen type II and the aggrecan gene expression, which was unaffected by inhibiting the ERK1/2 pathway, but significantly decreased by inhibiting the PKA, PKC and p38 MAPK pathways. In contrast, NPW‐23 was not involved in the terminal differentiation of the chondrocytes, as evaluated by the mineralization of the chondrocytes and the activity of the alkaline phosphatase. Neuropeptides W stimulated the PKA, PKC, p38 MAPK and ERK1/2 activities in a dose‐ and time‐dependent manner in the ATDC5 cells. These results show that NPW promotes the proliferation and early differentiation of murine chondrocyte via GPR7 activation, as well as PKA and PKC‐dependent signalling cascades, which may be involved in endochondral bone formation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neuropeptide W regulates proliferation and differentiation of ATDC5: Possible involvement of GPR7 activation, PKA and PKC‐dependent signalling cascades

Wang

Zheng

Jiang

et al. 2019

J Cellular Molecular Medi

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“…Actually, PI3K/Akt signaling was found to be reversely associated with mitochondria oxidative stress and activation of PI3K/AKT signaling reduced ROS production (Dai et al, 2013; Zhu et al, 2015). Furthermore, phosphorylated Akt (p-Akt) not only acts to inhibit pro-apoptotic factors and stimulate anti-apoptotic factors, but also inactivates mitochondria-based oxidative stress (Wang et al, 2015; Xu et al, 2015). Hence, our findings support the hypothesis that sevoflurane ameliorated mROS formation post-ischemia by up-regulation of Trx2, Prx3, and HSP60 expression and interrupted the subsequent cascade reaction, which eventually resulted in improving mitochondrial biogenesis and integrity, possibly via the activation of the PI3K/Akt survival pathway.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane Post-conditioning Enhanced Hippocampal Neuron Resistance to Global Cerebral Ischemia Induced by Cardiac Arrest in Rats through PI3K/Akt Survival Pathway

Wang

Zhi

Huang

et al. 2016

Front. Cell. Neurosci.

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The purpose of this current study was to evaluate whether improvement of mitochondrial dysfunction was involved in the therapeutic effect of sevoflurane post-conditioning in global cerebral ischemia after cardiac arrest (CA) via the PI3K/Akt pathway. In the first experiment, animals were randomly divided into three groups: a sham group, a CA group, a CA+sevoflurane post-conditioning group (CA+SE). Sevoflurane post-conditioning was achieved by administration of 2.5% sevoflurane for 30 min after resuscitation. Sevoflurane post-conditioning has a significant neuroprotective effect by increasing survival rates and reducing neuronal apoptosis. Additionally, the gene and protein expression of PGC-1α, NRF-1, and TFAM, the master regulators of mitochondrial biogenesis, were up-regulated in the CA+SE group, when compared to the CA group. Similarly, in contrast to the CA group, mitochondria-specific antioxidant enzymes, including heat-shock protein 60 (HSP60), peroxiredoxin 3 (Prx3), and thioredoxin 2 (Trx2) were also increased in the CA+SE group. Finally, administration of sevoflurane ameliorated mitochondrial reactive oxygen species (ROS) formation and maintained mitochondrial integrity. In the second experiment, we investigated the relationship between the PI3K/Akt pathway and mitochondrial biogenesis and mitochondria-specific antioxidant enzymes in sevoflurane-induced neuroprotection. The selective PI3K inhibitor wortmannin not only eliminated the beneficial biochemical processes of sevoflurane by reducing the level of mitochondrial biogenesis-related proteins and aggravating mitochondrial integrity, but also reversed the elevation of mitochondria-specific antioxidant enzymes induced by sevoflurane. Therefore, our data suggested that sevoflurane post-conditioning provides neuroprotection via improving mitochondrial biogenesis and integrity, as well as increasing mitochondria-specific antioxidant enzymes by a mechanism involving the PI3K/Akt pathway.

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“…ERK pathway is the main pathway involved in the survival and adaptive protection of a variety of cell types activated by many growth factors and hormones [19]. The expression of phosphorylated ERK1/2 decreased gradually in a time-dependent manner, whereas the level of phosphorylated ERK1/2 showed little change in SKOV-3 cells treated with LY294002 (inhibitor of Akt, 10 μmol/l) compared with EPA alone (Fig.…”

Section: Effect Of Eicosapentaenoic Acid On Mitogen Activated Proteinmentioning

confidence: 95%

Eicosapentaenoic acid induced SKOV-3 cell apoptosis through ERK1/2–mTOR–NF-κB pathways

et al. 2016

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Eicosapentaenoic acid (EPA), a typical kind of n-3 polyunsaturated fatty acids, has been considered to be a potent antitumor adjuvant. However, the mechanism related to EPA-induced SKOV-3 cell apoptosis has not been investigated. In this study, we elucidated the anticancer effect of EPA on SKOV-3 cells and its molecular mechanisms. The results of fluorescence microscopy showed that EPA induced typical apoptotic morphological features in SKOV-3 cells. Flow cytometric analysis indicated that EPA induced apoptosis of SKOV-3 cells through cells arrested at the S phase. Western blotting results showed that EPA could inhibit the phosphorylation of ERK1/2 and Akt, which restrained mammalian target of rapamycin (mTOR) phosphorylated. Simultaneously, EPA downregulated the phosphorylation status of mTOR, which may act as an upstream regulator of EPA-blocked nuclear factor κB (NF-κB) p65 translocation from the cytoplasm into the nucleus; the apoptotic mechanism of SKOV-3 cells induced by EPA was associated with the release of cytochrome c, Bax-to-Bcl-2 expression ratio, and activation of caspase-3 and caspase-9. The results suggested that EPA induced SKOV-3 cell apoptosis through ERK1/2, Akt-mTOR-NF-κB pathways.

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Gardenamide A attenuated cell apoptosis induced by serum deprivation insult via the ERK1/2 and PI3K/AKT signaling pathways

Cited by 32 publications

References 28 publications

Neuropeptide W regulates proliferation and differentiation of ATDC5: Possible involvement of GPR7 activation, PKA and PKC‐dependent signalling cascades

Neuropeptide W regulates proliferation and differentiation of ATDC5: Possible involvement of GPR7 activation, PKA and PKC‐dependent signalling cascades

Sevoflurane Post-conditioning Enhanced Hippocampal Neuron Resistance to Global Cerebral Ischemia Induced by Cardiac Arrest in Rats through PI3K/Akt Survival Pathway

Eicosapentaenoic acid induced SKOV-3 cell apoptosis through ERK1/2–mTOR–NF-κB pathways

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