Linguo Pei
Wuhan University
13 Papers
10 Citations
Linguo Pei is an academic researcher from Wuhan University. The author has contributed to research in topics: Offspring & Internal medicine. The author has an hindex of 6, co-authored 10 publications.
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Papers
Decreased H3K9ac level of StAR mediated testicular dysplasia induced by prenatal dexamethasone exposure in male offspring rats
TL;DR: In vivo and in vitro, PDE caused testicular dysplasia before and after birth in male offspring rats, and its mechanism was related to the low-expressional programming of StAR mediated by decreasing H3K9ac level.
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Reduced testicular steroidogenesis in rat offspring by prenatal nicotine exposure: Epigenetic programming and heritability via nAChR/HDAC4.
TL;DR: PNE programmed testicular low steroidogenesis and its heritability in male offspring rats and the underlying mechanism was associated to the low-level programming of StAR/3β-HSD H3K9ac via nAChR/HDAC4.
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Decreased H3K9ac level of AT2R mediates the developmental origin of glomerulosclerosis induced by prenatal dexamethasone exposure in male offspring rats.
Bin Li,Yanan Zhu,Haiyun Chen,Hui Gao,Hangyuan He,Na Zuo,Linguo Pei,Wen Xie,Liaobin Chen,Ying Ao,Hui Wang +10 more
TL;DR: In conclusion, PDE induced the offspring's kidney dysplasia as well as adult glomerulosclerosis, which was mediated by a sustained decrease in renal AT2R expression via decreasing the H3 K9ac level.
25
Prenatal nicotine exposure intergenerationally programs imperfect articular cartilage via histone deacetylation through maternal lineage.
Zhe Xie,Zhe Zhao,Xu Yang,Linguo Pei,Hanwen Luo,Qubo Ni,Bin Li,Yongjian Qi,Kai Tie,Jacques Magdalou,Liaobin Chen,Hui Wang +11 more
TL;DR: Prenatal nicotine exposure impaired the cartilage of the female F1 and F2 generation and reduced the TGF&bgr; signaling in offspring cartilage, which may be helpful to elucidate the developmental variability of articular cartilage quality and useful for the early prevention ofArticular damage.
22
Excitotoxicity and compensatory upregulation of GAD67 in fetal rat hippocampus caused by prenatal nicotine exposure are associated with inhibition of the BDNF pathway.
TL;DR: Results indicated that PNE downregulates the BDNF pathway and mediates the hippocampal excitotoxicity; then, the compensatory upregulation of GAD67 causes the imbalance of signal output in the fetal hippocampus.
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