Involvement of PI 3 kinase/Akt-dependent Bad phosphorylation in Toxoplasma gondii-mediated inhibition of host cell apoptosis

Quan, Juan-Hua; Cha, Guang-Ho; Zhou, Wei; Chu, Jiaqi; Nishikawa, Yoshifumi; Lee, Young-Ha

doi:10.1016/j.exppara.2013.01.005

Cited by 49 publications

(62 citation statements)

References 28 publications

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“…The reduced activation of Akt was found in pancreatic tissues of SAP rats at 3 h and 6 h after treatment with wortmannin. Since the low concentrations of wortmannin used in our studies were generally believed to specifically inhibit PI3K activity, these observations support our conclusion that wortmannin prevents inflammation activation in vivo by inhibiting the PI3K/Akt signaling pathway [19,20]. …”

Section: Discussionsupporting

confidence: 82%

Regulatory Roles of the PI3K/Akt Signaling Pathway in Rats with Severe Acute Pancreatitis

Wang

Yang

et al. 2013

PLoS ONE

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The phosphatidylinositol 3-kinase(PI3K)/protein kinase B (Akt) pathway plays a key role in inflammation. However, the regulatory roles of PI3K/Akt in severe acute pancreatitis (SAP) have not been elucidated. The aim of this study was to investigate the impact of wortmannin, a PI3K/Akt inhibitor, on SAP rats through exposure to sodium taurocholate (STC) after 3 h and 6 h. The SAP group was found to have a significant increase in pancreas Akt expression, along with the activation of serum amylase, TNF-α, IL-1β, and IL-6, and pancreas histological aggravation. The administration of wortmannin in SAP rats reduced Akt expression, attenuated the level of serum amylase and inflammation factor, and alleviated the damage of pancreatic tissue. Furthermore, the administration of wortmannin led to an obvious reduction in NF-κB and p38MAPK expression in SAP rats. These findings showed that the PI3K/Akt inhibitor wortmannin decreases inflammatory cytokines in SAP rats and suggests its regulatory mechanisms may occur through the suppression on NF-κB and p38MAPK activity.

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Section: Discussionsupporting

confidence: 82%

Regulatory Roles of the PI3K/Akt Signaling Pathway in Rats with Severe Acute Pancreatitis

Wang

Yang

et al. 2013

PLoS ONE

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“…These free anti-apoptotic Bcl-2 proteins could then inhibit Bax-triggered apoptosis by maintaining the integrity of the outer mitochondrial membrane (78 -80). Mitochondria play important roles in the regulation and transmission of apoptotic signals, which are regulated by the balance among Bcl-2 family members; therefore, phosphorylation of Bad at Ser 112 promotes cell survival (32,74,81). In the present study, we showed that the PDGF-C-mediated anti-apoptotic signaling pathway was mediated via PI3K/ Akt activation and proapoptotic Bad phosphorylation at Ser 112 , culminating in Bad inactivation of THP-1 macrophages.…”

Section: Discussionmentioning

confidence: 54%

Platelet-derived Growth Factor-C (PDGF-C) Induces Anti-apoptotic Effects on Macrophages through Akt and Bad Phosphorylation

Son¹,

Na²,

Hwang

et al. 2014

Journal of Biological Chemistry

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“…The apoptotic activity of BAD is dependent on its phosphorylation status at Ser112, Ser136, and Ser155 [31]. When BAD is phosphorylated at these sites, it forms a complex with 14-3-3 proteins that cannot induce apoptosis [32]. In our study, BAD expression was greatly down regulated following co-transplantation.…”

Section: Discussionmentioning

confidence: 63%

Co-grafting of neural stem cells with olfactory en sheathing cells promotes neuronal restoration in traumatic brain injury with an anti-inflammatory mechanism

Liu

Zou

Belegu

et al. 2014

J Neuroinflammation

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BackgroundWe sought to investigate the effects of co-grafting neural stem cells (NSCs) with olfactory ensheathing cells (OECs) on neurological behavior in rats subjected to traumatic brain injury (TBI) and explore underlying molecular mechanisms.MethodsTBI was established by percussion device made through a weight drop (50 g) from a 30 cm height. Cultured NSCs and OECs isolated from rats were labeled by Hoechst 33342 (blue) and chloromethyl-benzamidodialkyl carbocyanine (CM-Dil) (red), respectively. Then, NSCs and/or OECs, separately or combined, were transplanted into the area surrounding the injury site. Fourteen days after transplantation, neurological severity score (NSS) were recorded. The brain tissue was harvested and processed for immunocytochemistry, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and reverse transcription-polymerase chain reaction (RT-PCR).ResultsSignificant neurological function improvement was observed in the three transplant groups, compared to the TBI group, and co-transplantation gave rise to the best improvement. Morphological evaluation showed that the number of neurons in cortex from combination implantation was more than for other groups (P <0.05); conversely, the number of apoptotic cells showed a significant decrease by TUNEL staining. Transplanted NSCs and OECs could survive and migrate in the brain, and the number of neurons differentiating from NSCs in the co-transplantation group was significantly greater than in the NSCs group. At the molecular level, the expressions of IL-6 and BAD in the co-graft group were found to be down regulated significantly, when compared to either the NSC or OEC alone groups.ConclusionThe present study demonstrates for the first time the optimal effects of co-grafting NSCs and OECs as a new strategy for the treatment of TBI via an anti-inflammation mechanism.

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Involvement of PI 3 kinase/Akt-dependent Bad phosphorylation in Toxoplasma gondii-mediated inhibition of host cell apoptosis

Cited by 49 publications

References 28 publications

Regulatory Roles of the PI3K/Akt Signaling Pathway in Rats with Severe Acute Pancreatitis

Regulatory Roles of the PI3K/Akt Signaling Pathway in Rats with Severe Acute Pancreatitis

Platelet-derived Growth Factor-C (PDGF-C) Induces Anti-apoptotic Effects on Macrophages through Akt and Bad Phosphorylation

Co-grafting of neural stem cells with olfactory en sheathing cells promotes neuronal restoration in traumatic brain injury with an anti-inflammatory mechanism

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