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4 results on '"Doudou Tong"'

1. Proteomic profiling analysis reveals that glutathione system plays important roles responding to osmotic stress in wheat (Triticum aestivum L.) roots

Author

Jianhui Ma, Wen Dong, Daijing Zhang, Xiaolong Gao, Lina Jiang, Yun Shao, Doudou Tong, and Chunxi Li

Subjects
Triticum aestivum L., Root, iTRAQ, Osmotic stress, Glutathione, Medicine, Biology (General), QH301-705.5
Abstract

Wheat is one of the most important crops in the world, and osmotic stress has become one of the main factors affecting wheat production. Understanding the mechanism of the response of wheat to osmotic stress would be greatly significant. In the present study, isobaric tag for relative and absolute quantification (iTRAQ) was used to analyze the changes of protein expression in the wheat roots exposed to different osmotic stresses. A total of 2,228 expressed proteins, including 81 differentially expressed proteins, between osmotic stress and control, were found. The comprehensive analysis of these differentially expressed proteins revealed that osmotic stress increased the variety of expressed proteins and suppressed the quantity of expressed proteins in wheat roots. Furthermore, the proteins for detoxifying and reactive oxygen species scavenging, especially the glutathione system, played important roles in maintaining organism balance in response to osmotic stress in wheat roots. Thus, the present study comprehensively describes the protein expression changes in wheat roots in response to osmotic stress, providing firmer foundation to further study the mechanism of osmotic resistance in wheat.

Published
2016
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2. Mutation in NPPA causes atrial fibrillation by activating inflammation and cardiac fibrosis in a knock‐in rat model

Author

Huixia Liu, Chenghui Wang, Chengcheng Tan, Wenxia Si, Doudou Tong, Qiuyun Chen, Chen Cheng, Yimei Du, Lina Liang, Jia Li, Qing Kenneth Wang, Xia Liu, Xiang Ren, Linlin Wang, and Yongxuan Zhao

Subjects
0301 basic medicine, Mutation, business.industry, medicine.drug_class, Cardiac fibrosis, Inflammation, medicine.disease, medicine.disease_cause, Biochemistry, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Atrial natriuretic peptide, Fibrosis, Genetics, medicine, Cancer research, Natriuretic peptide, medicine.symptom, business, Receptor, Molecular Biology, Exome, 030217 neurology & neurosurgery, Biotechnology
Abstract

Atrial fibrillation (AF) affects >30 million individuals worldwide. However, no genetic mutation from human patients with AF has been linked to inflammation. Here, we show that AF-associated human variant p.Ile138Thr in natriuretic peptide A (NPPA) encoding the atrial natriuretic peptide (ANP) causes inflammation, fibroblast activation, atrial fibrosis, and AF in knock-in (KI) rats. Variant p.Ile138Thr inhibits the interaction between ANP and its receptor natriuretic peptide receptor A and reduces intracellular cGMP levels. RNA sequencing and follow-up analyses showed that mutant ANP (mANP) activates multiple innate immunity pathways, including TNF-α, NF-κB, and IL-1β signaling. mANP induces differentiation of cardiac fibroblasts (CFs) to myofibroblasts and promotes CF proliferation and fibrosis. These results suggest that NPPA variant p.Ile138Thr causes AF by activating TNF-α, NF-κB, and IL-1β signaling, inflammation, and fibrosis. Multiple computational programs suggest that p.Ile138Thr is damaging or deleterious. Based on the 2015 American College of Medical Genetics and Genomics Standards and Guidelines, p.Ile138Thr can be classified as a likely pathogenic variant. Variant p.Ile138Thr was found only in Asian people in the Genome Aggregation Database and Exome Aggregation Consortium database at an averaged frequency of 0.026%. An estimated 1.15 million Asian people carry the variant and might be at risk of AF. The KI rats may provide an inflammation-based, genetic animal model for AF valuable for testing anti-inflammation or other therapies for AF.-Cheng, C., Liu, H., Tan, C., Tong, D., Zhao, Y., Liu, X., Si, W., Wang, L., Liang, L., Li, J., Wang, C., Chen, Q., Du, Y., Wang, Q. K., Ren, X. Mutation in NPPA causes atrial fibrillation by activating inflammation and cardiac fibrosis in a knock-in rat model.

Published
2019

3. Mutation in

Author

Chen, Cheng, Huixia, Liu, Chengcheng, Tan, Doudou, Tong, Yongxuan, Zhao, Xia, Liu, Wenxia, Si, Linlin, Wang, Lina, Liang, Jia, Li, Chenghui, Wang, Qiuyun, Chen, Yimei, Du, Qing K, Wang, and Xiang, Ren

Subjects
Male, Tumor Necrosis Factor-alpha, Interleukin-1beta, Mutation, Missense, NF-kappa B, Fibrosis, Immunity, Innate, Rats, Rats, Sprague-Dawley, HEK293 Cells, Atrial Fibrillation, Animals, Humans, Female, Myofibroblasts, Cyclic GMP, Atrial Natriuretic Factor, Cells, Cultured, Signal Transduction
Abstract

Atrial fibrillation (AF) affects30 million individuals worldwide. However, no genetic mutation from human patients with AF has been linked to inflammation. Here, we show that AF-associated human variant p.Ile138Thr in natriuretic peptide A (

Published
2019

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