scholarly journals Exposure to Ionizing Radiation Causes Long-Term Increase in Serum Estradiol and Activation of PI3K-Akt Signaling Pathway in Mouse Mammary Gland

2012 ◽  
Vol 84 (2) ◽  
pp. 500-507 ◽  
Author(s):  
Shubhankar Suman ◽  
Michael D. Johnson ◽  
Albert J. Fornace ◽  
Kamal Datta
Keyword(s):  
Mammary Gland ◽  
Ionizing Radiation ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Mouse Mammary Gland ◽  
Serum Estradiol ◽  
Akt Signaling Pathway

scholarly journals Carbamylated erythropoietin regulates immune responses and promotes long-term kidney allograft survival through activation of PI3K/AKT signaling

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Ning Na ◽  
Daqiang Zhao ◽  
Jinhua Zhang ◽  
Jiaqing Wu ◽  
Bin Miao ◽  
...  
Keyword(s):  
Immune Responses ◽  
Signaling Pathway ◽  
Immune Cells ◽  
Akt Signaling ◽  
Control Group ◽  
Dependent Manner ◽  
Akt Signaling Pathway ◽  
Allograft Survival ◽  
Kidney Allograft

Abstract Modulation of alloimmune responses is critical to improving transplant outcome and promoting long-term graft survival. To determine mechanisms by which a nonhematopoietic erythropoietin (EPO) derivative, carbamylated EPO (CEPO), regulates innate and adaptive immune cells and affects renal allograft survival, we utilized a rat model of fully MHC-mismatched kidney transplantation. CEPO administration markedly extended the survival time of kidney allografts compared with the transplant alone control group. This therapeutic effect was inhibited when the recipients were given LY294002, a selective inhibitor of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway or anti-EPO receptor (EPOR) antibody, in addition to CEPO. In vitro, CEPO inhibited the differentiation and function of dendritic cells and modulated their production of pro-inflammatory and anti-inflammatory cytokines, along with activating the PI3K/AKT signaling pathway and increasing EPOR mRNA and protein expression by these innate immune cells. Moreover, after CD4+ T cells were exposed to CEPO the Th1/Th2 ratio decreased and the regulatory T cell (Treg)/Th17 ratio increased. These effects were abolished by LY294002 or anti-EPOR antibody, suggesting that CEPO regulates immune responses and promotes kidney allograft survival by activating the PI3K/AKT signaling pathway in an EPOR-dependent manner. The immunomodulatory and specific signaling pathway effects of CEPO identified in this study suggest a potential therapeutic approach to promoting kidney transplant survival.

scholarly journals Dexmedetomidine attenuates the propofol-induced long-term neurotoxicity in the developing brain of rats by enhancing the PI3K/Akt signaling pathway

2018 ◽  
Vol Volume 14 ◽  
pp. 2191-2206 ◽  
Author(s):  
Yong Xiao ◽  
Lifang Zhou ◽  
Youbing Tu ◽  
Yuantao Li ◽  
Yubing Liang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Developing Brain ◽  
Akt Signaling Pathway

scholarly journals Administration of rCTRP9 Attenuates Neuronal Apoptosis Through AdipoR1/PI3K/Akt Signaling Pathway after ICH in Mice

2019 ◽  
Vol 28 (6) ◽  
pp. 756-766 ◽  
Author(s):  
Lianhua Zhao ◽  
John H. Zhang ◽  
Prativa Sherchan ◽  
Paul R. Krafft ◽  
Wei Zhao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Western Blots ◽  
Short And Long Term ◽  
Underlying Mechanisms

Targeting neuronal apoptosis after intracerebral hemorrhage (ICH) may be an important therapeutic strategy for ICH patients. Emerging evidence indicates that C1q/TNF-Related Protein 9 (CTRP9), a newly discovered adiponectin receptor agonist, exerts neuroprotection in cerebrovascular disease. The aim of this study was to investigate the anti-apoptotic role of CTRP9 after experimental ICH and to explore the underlying molecular mechanisms. ICH was induced in mice via intrastriatal injection of bacterial collagenase. Recombinant CTRP9 (rCTRP9) was administrated intranasally at 1 h after ICH. To elucidate the underlying mechanisms, adiponectin receptor1 small interfering ribonucleic acid (AdipoR1 siRNA) and selective PI3 K inhibitor LY294002 were administered prior to rCTRP9 treatment. Western blots, neurofunctional assessments, immunofluorescence staining, and Fluoro-Jade C (FJC) staining experiments were performed. Administration of rCTRP9 significantly improved both short- and long-term neurofunctional behavior after ICH. RCTRP9 treatment significantly increased the expression of AdipoR1, PI3 K, p-Akt, and Bcl-2, while at the same time was found to decrease the expression of Bax in the brain, which was reversed by inhibition of AdipoR1 and PI3 K. The neuroprotective effect of rCTRP9 after ICH was mediated by attenuation of neuronal apoptosis via the AdipoR1/PI3K/Akt signaling pathway; therefore, rCTRP9 should be further evaluated as a potential therapeutic agent for ICH patients.

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