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8 results on '"Yao, Yajie"'

4. Resveratrol induces autophagy impeding BAFF-stimulated B-cell proliferation and survival by inhibiting the Akt/mTOR pathway

Author

Yao, Yajie, primary, Zhu, Jiawei, additional, Qin, Shanshan, additional, Zhou, Zhihan, additional, Zeng, Qingyu, additional, Long, Ruyu, additional, Mao, Zun, additional, Dong, Xiaoqing, additional, Zhao, Rui, additional, Zhang, Ruijie, additional, Zhang, Shuangquan, additional, Huang, Shile, additional, and Chen, Long, additional

Published
2022
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6. Rapamycin inhibits B-cell activating factor (BAFF)-stimulated cell proliferation and survival by suppressing Ca2+-CaMKII-dependent PTEN/Akt-Erk1/2 signaling pathway in normal and neoplastic B-lymphoid cells

Author

Zeng, Qingyu, primary, Zhou, Zhihan, additional, Qin, Shanshan, additional, Yao, Yajie, additional, Qin, Jiamin, additional, Zhang, Hai, additional, Zhang, Ruijie, additional, Xu, Chong, additional, Zhang, Shuangquan, additional, Huang, Shile, additional, and Chen, Long, additional

Published
2020
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7. Comparative transcriptome and gut microbiota analysis of Exopalaemon carinicaudawith different growth rates from a full-sib family

Author

Xing, Chaofan, Xiong, Jiayao, Xie, Shumin, Guo, Hanxuan, Hua, Songsong, Yao, Yajie, Zhu, Jiawei, Yan, Binlun, Shen, Xin, Gao, Huan, and Wang, Panpan

Abstract

In the breeding process of Exopalaemon carinicaudafrom the same family, noticeable differences often occur in growth characteristics under the same conditions. To investigate this issue, we performed a comparative transcriptome analysis to identify the critical genes involved in weight gain and compared the intestinal flora to screen for potential intestinal probiotics. In total, we identified 1311 differentially expressed genes (DEGs), of which 735 genes, including troponin C, chitinase, cathepsin B, cathepsin L, and trypsin, were upregulated exclusively in the fast growth group. Several DEGs were validated by quantitative real-time PCR and assigned to the ribosome, phagosome, apoptosis, purine metabolism, and Hippo signaling pathways. The microbiome community richness and diversity of the fast-growing individuals (FGIs) were higher than those of the slow-growing individuals (SGIs). In the current study, the intestinal microflora was mainly distributed in the Proteobacteria, Firmicutes, and Bacteroidota. The species with significant differences (P < 0.05) between the FGI and SGI groups included the iron-reducing bacteria, Nitrospira moscoviensis, Sulfuritalea hydrogenivorans, and Alpha proteobacterium. Our results provided insights towards revealing the mechanism underlying the growth differences in E. carinicauda.

Published
2023
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8. Rapamycin inhibits B-cell activating factor (BAFF)-stimulated cell proliferation and survival by suppressing Ca 2+ -CaMKII-dependent PTEN/Akt-Erk1/2 signaling pathway in normal and neoplastic B-lymphoid cells.

Author

Zeng Q, Zhou Z, Qin S, Yao Y, Qin J, Zhang H, Zhang R, Xu C, Zhang S, Huang S, and Chen L

Subjects
Animals, Apoptosis drug effects, B-Lymphocytes drug effects, B-Lymphocytes pathology, Cell Cycle drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Cell Survival drug effects, Cyclin-Dependent Kinases metabolism, Down-Regulation drug effects, Humans, Lymphoma, B-Cell metabolism, MAP Kinase Signaling System, Mice, Models, Biological, B-Cell Activating Factor metabolism, B-Lymphocytes metabolism, Calcium metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2 metabolism, Lymphoma, B-Cell pathology, PTEN Phosphohydrolase metabolism, Proto-Oncogene Proteins c-akt metabolism, Sirolimus pharmacology
Abstract

B-cell activating factor (BAFF) is a crucial survival factor for B cells, and excess BAFF contributes to development of autoimmune diseases. Recent studies have shown that rapamycin can prevent BAFF-induced B-cell proliferation and survival, but the underlying mechanism remains to be elucidated. Here we found that rapamycin inhibited human soluble BAFF (hsBAFF)-stimulated cell proliferation by inducing G 1 -cell cycle arrest, which was through downregulating the protein levels of CDK2, CDK4, CDK6, cyclin A, cyclin D1, and cyclin E. Rapamycin reduced hsBAFF-stimulated cell survival by downregulating the levels of anti-apoptotic proteins (Mcl-1, Bcl-2, Bcl-xL and survivin) and meanwhile upregulating the levels of pro-apoptotic proteins (BAK and BAX). The cytostatic and cytotoxic effects of rapamycin linked to its attenuation of hsBAFF-elevated intracellular free Ca 2+ ([Ca 2+ ] i ). In addition, rapamycin blocked hsBAFF-stimulated B-cell proliferation and survival by preventing hsBAFF from inactivating PTEN and activating the Akt-Erk1/2 pathway. Overexpression of wild type PTEN or ectopic expression of dominant negative Akt potentiated rapamycin's suppression of hsBAFF-induced Erk1/2 activation and proliferation/viability in Raji cells. Interestingly, PP242 (mTORC1/2 inhibitor) or Akt inhibitor X, like rapamycin (mTORC1 inhibitor), reduced the basal or hsBAFF-induced [Ca 2+ ] i elevations. Chelating [Ca 2+ ] i with BAPTA/AM, preventing [Ca 2+ ] i elevation using EGTA, 2-APB or verapamil, inhibiting CaMKII with KN93, or silencing CaMKII strengthened rapamycin's inhibitory effects. The results indicate that rapamycin inhibits BAFF-stimulated B-cell proliferation and survival by blunting mTORC1/2-mediated [Ca 2+ ] i elevations and suppressing Ca 2+ -CaMKII-dependent PTEN/Akt-Erk1/2 signaling pathway. Our finding underscores that rapamycin may be exploited for prevention of excessive BAFF-induced aggressive B-cell malignancies and autoimmune diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Published
2020
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