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Negative regulation by proBDNF signaling of peripheral neurogenesis in the sensory ganglia of adult rats.

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机构： [1]Institute of Neuroscience, Kunming Medical University, Kunming 650500, Yunnan, China [2]Second Department of General Surgery, First People’s Hospital of Yunnan Province, Kunming 650032, Yunnan, China [3]School of Pharmacy and Medical Sciences, Sansom Institute, Faculty of Health Sciences, University of South Australia, Adelaide, SA 5000, Australia [4]Medical college of Panzhihua University, Panzhihua 617000, Sichuan, China [5]Department of Rehabilitation Medicine, Guizhou Medical University, Guiyang 550000, Guizhou, China [6]Department of Neurosurgery, Hospital 12 de Octubre, Instituto de Investigaci´on imas12, Universidad Complutense de Madrid, Madrid, Spain [7]Brain and Mind Centre, Sydney Medical School, The University of Sydney, NSW 2050, Australia [8]The Key Laboratory of Stem Cell and Regenerative Medicine of Yunnan Province, Institute of Molecular and Clinical Medicine, Kunming Medical University, Kunming 650500, Yunnan, China

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Neurogenesis in the adult brain is well recognized and plays a critical role in the maintenance of brain function and homeostasis. However, whether neurogenesis also occurs in the adult peripheral nervous system remains unknown. Here, using sensory ganglia (dorsal root ganglia, DRGs) as a model, we show that neurogenesis also occurs in the peripheral nervous system, but in a manner different from that in the central nervous system. Satellite glial cells (SGCs) express the neuronal precursor markers Nestin, POU domain, class 4, transcription factor 1, and p75 pan-neurotrophin receptor. Following sciatic nerve injury, the suppression of endogenous proBDNF by proBDNF antibodies resulted in the transformation of proliferating SGCs into doublecortin-positive cells in the DRGs. Using purified SGCs migrating out from the DRGs, the inhibition of endogenous proBDNF promoted the conversion of SGCs into neuronal phenotypes in vitro. Our findings suggest that SGCs are neuronal precursors, and that proBDNF maintains the SGC phenotype. Furthermore, the suppression of proBDNF signaling is necessary for neuronal phenotype acquisition by SGCs. Thus, we propose that peripheral neurogenesis may occur via the direct conversion of SGCs into neurons, and that this process is negatively regulated by proBDNF.Copyright © 2021. Published by Elsevier Masson SAS.

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出版当年[2021]版：

大类 | 2 区

医学

小类 | 2 区药学 3 区医学：研究与实验

最新[2023]版：

大类 | 2 区

医学

小类 | 1 区药学 2 区医学：研究与实验

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出版当年[2020]版：

Q1 PHARMACOLOGY & PHARMACY Q1 MEDICINE, RESEARCH & EXPERIMENTAL

最新[2023]版：

Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q1 PHARMACOLOGY & PHARMACY

影响因子： 6.9 最新[2023版] 6.8 最新五年平均 6.53 出版当年[2020版] 5.98 出版当年五年平均 4.545 出版前一年[2019版] 7.419 出版后一年[2021版]

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第一作者机构： [1]Institute of Neuroscience, Kunming Medical University, Kunming 650500, Yunnan, China

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通讯机构： [1]Institute of Neuroscience, Kunming Medical University, Kunming 650500, Yunnan, China [2]Second Department of General Surgery, First People’s Hospital of Yunnan Province, Kunming 650032, Yunnan, China [3]School of Pharmacy and Medical Sciences, Sansom Institute, Faculty of Health Sciences, University of South Australia, Adelaide, SA 5000, Australia [*1]Second Department of General Surgery, First People’s Hospital of Yunnan Province, Kunming, Yunnan, China. [*2]School of Pharmacy and Medical Sciences, Sansom Institute, Faculty of Health Sciences, University of South Australia, Adelaide, Australia [*3]Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China

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