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43 results on '"Qian, Tianmei"'

16. RSK1 promotes mammalian axon regeneration by inducing the synthesis of regeneration-related proteins

Author

Mao, Susu, Chen, Yuanyuan, Feng, Wei, Zhou, Songlin, Jiang, Chunyi, Zhang, Junjie, Liu, Xiaohong, Qian, Tianmei, Liu, Kai, Wang, Yaxian, Yao, Chun, Gu, Xiaosong, Yu, Bin, Mao, Susu, Chen, Yuanyuan, Feng, Wei, Zhou, Songlin, Jiang, Chunyi, Zhang, Junjie, Liu, Xiaohong, Qian, Tianmei, Liu, Kai, Wang, Yaxian, Yao, Chun, Gu, Xiaosong, and Yu, Bin

Abstract

AU In contrast: Pleaseconfirmthatallheadinglevelsarerepresentedcorrectly to the adult mammalian central nervous system (CNS), : the neurons in the peripheral nervous system (PNS) can regenerate their axons. However, the underlying mechanism dictating the regeneration program after PNS injuries remains poorly understood. Combining chemical inhibitor screening with gain- and loss-of-function analyses, we identified p90 ribosomal S6 kinase 1 (RSK1) as a crucial regulator of axon regeneration in dorsal root ganglion (DRG) neurons after sciatic nerve injury (SNI). Mechanistically, RSK1 was found to preferentially regulate the synthesis of regeneration-related proteins using ribosomal profiling. Interestingly, RSK1 expression was up-regulated in injured DRG neurons, but not retinal ganglion cells (RGCs). Additionally, RSK1 overexpression enhanced phosphatase and tensin homolog (PTEN) deletion-induced axon regeneration in RGCs in the adult CNS. Our findings reveal a critical mechanism in inducing protein synthesis that promotes axon regeneration and further suggest RSK1 as a possible therapeutic target for neuronal injury repair. Copyright: © 2022 Mao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Published
2022

23. Application of stem cells in peripheral nerve regeneration

Author

Yi, Sheng, Zhang, Yu, Gu, Xiaokun, Huang, Li, Zhang, Kairong, Qian, Tianmei, and Gu, Xiaosong

Subjects
Peripheral nerve injury, Seed cells, Tissue-engineered nerve grafts, Peripheral nerve regeneration, Review, Stem cells
Abstract

Traumatic peripheral nerve injury is a worldwide clinical issue with high morbidity. The severity of peripheral nerve injury can be classified as neurapraxia, axonotmesis or neurotmesis, according to Seddon’s classification, or five different degrees according to Sunderland’s classification. Patients with neurotmesis suffer from a complete transection of peripheral nerve stumps and are often in need of surgical repair of nerve defects. The applications of autologous nerve grafts as the golden standard for peripheral nerve transplantation meet some difficulties, including donor nerve sacrifice and nerve mismatch. Attempts have been made to construct tissue-engineered nerve grafts as supplements or even substitutes for autologous nerve grafts to bridge peripheral nerve defects. The incorporation of stem cells as seed cells into the biomaterial-based scaffolds increases the effectiveness of tissue-engineered nerve grafts and largely boosts the regenerative process. Numerous stem cells, including embryonic stem cells, neural stem cells, bone marrow mesenchymal stem cells, adipose stem cells, skin-derived precursor stem cells and induced pluripotent stem cells, have been used in neural tissue engineering. In the current review, recent trials of stem cell-based tissue-engineered nerve grafts have been summarized; potential concerns and perspectives of stem cell therapeutics have also been contemplated., Traumatic peripheral nerve injury is a common clinical issue that leads to nerve dysfunction and chronic pain. Tissue-engineered nerve grafts containing bio-scaffolds, seed cells, and neurotrophic factors can be used as alternatives to substitute autologous nerve grafts for repairing peripheral nerve injury. Stem cells can differentiate into Schwann-like cells, provide a suitable microenvironment for nerve regeneration, and thus are considered as ideal seed cells.

Published
2020

34. Gekko japonicus genome reveals evolution of adhesive toe pads and tail regeneration

Author

Liu, Yan, primary, Zhou, Qian, additional, Wang, Yongjun, additional, Luo, Longhai, additional, Yang, Jian, additional, Yang, Linfeng, additional, Liu, Mei, additional, Li, Yingrui, additional, Qian, Tianmei, additional, Zheng, Yuan, additional, Li, Meiyuan, additional, Li, Jiang, additional, Gu, Yun, additional, Han, Zujing, additional, Xu, Man, additional, Wang, Yingjie, additional, Zhu, Changlai, additional, Yu, Bin, additional, Yang, Yumin, additional, Ding, Fei, additional, Jiang, Jianping, additional, Yang, Huanming, additional, and Gu, Xiaosong, additional

Published
2015
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43. miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injury.

Author

Yu B, Zhou S, Wang Y, Qian T, Ding G, Ding F, and Gu X

Subjects
3' Untranslated Regions genetics, Animals, Base Sequence, Cell Proliferation, Cluster Analysis, Down-Regulation genetics, Gene Expression Profiling, Gene Knockdown Techniques, Gene Silencing, Male, Membrane Proteins genetics, MicroRNAs genetics, Molecular Sequence Data, Oxidoreductases Acting on CH-CH Group Donors, Proteins genetics, RNA Processing, Post-Transcriptional genetics, Rats, Rats, Sprague-Dawley, Schwann Cells metabolism, Sciatic Nerve pathology, Cell Movement genetics, Membrane Proteins metabolism, MicroRNAs metabolism, Proteins metabolism, Schwann Cells pathology, Sciatic Nerve injuries, Sciatic Nerve metabolism
Abstract

microRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level. Their roles in regulating the responses of Schwann cells (SCs) to injury stimuli remain unexplored. Here we report dynamic alteration of miRNA expression following rat sciatic nerve injury using microarray analysis. We harvested the proximal nerve stumps and identified 77 miRNAs that showed significant changes at four time points after nerve transection. Subsequently, we analyzed the expression pattern of miRNA, selected one significant profile, and then integrated putative miRNA targets with differentially expressed mRNA yielding 274 potential targets. The 274 targets were mainly involved in cell proliferation, cell locomotion and cellular homeostasis that were known to play important roles in modulating cell phenotype. The upregulation of the miR-221 and miR-222 cluster (miR-221/222) was found to correlate with the injury-induced SC phenotypic modulation. Enhanced expression of miR-221/222 could promote SC proliferation and migration in vitro, whereas silencing their expression resulted in a reduced proliferation and migration. Further studies revealed that longevity assurance homologue 2 (LASS2) was a direct target of miR-221/222 in SCs because miR-221/222 bound directly to the 3'-untranslated region of LASS2, thus reducing both mRNA and protein levels of LASS2. Silencing of LASS2 recapitulated the effects of miR-221/222 mimics, whereas enforced knockdown of LASS2 reversed the suppressive effects of miR-221/222 inhibitors. Our findings indicate that injury promotes SC proliferation and migration through the regulation of miR-221/222 by targeting LASS2, and provide new insights into the role of miRNAs in nerve regeneration.

Published
2012
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