Key Laboratory of the Ministry of Education for Experimental Teratology

Jinan, China

Key Laboratory of the Ministry of Education for Experimental Teratology

Jinan, China
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Shi W.,Key Laboratory of the Ministry of Education for Experimental Teratology | Chen X.,CAS Hefei Institutes of Physical Science | Wang F.,Key Laboratory of the Ministry of Education for Experimental Teratology | Gao M.,Shandong University | And 6 more authors.
Developmental Neurobiology | Year: 2016

In vertebrates, neural stem/progenitor cells (NSPCs) maintenance is critical for nervous system development and homeostasis. However, the molecular mechanisms underlying the maintenance of NSPCs have not been fully elucidated. Here, we demonstrated that zebrafish ZDHHC16, a DHHC encoding protein, which was related to protein palmitoylation after translation, was expressed in the developing forebrain, and especially in the telencephalon. Loss- and gain-of-function studies showed that ZDHHC16 played a crucial role in the regualtion of NSPCs proliferation during zebrafish telencephalic development, via a mechanism dependent on its palmitoyltransferase activity. Further analyses showed that the inhibition of ZDHHC16 led to inactivation of the FGF/ERK signaling pathway during telencephalic NSPCs proliferation and maintenance. Taken together, our results suggest that ZDHHC16 activity is essential for early NSPCs proliferation where it acts to activate the FGF/ERK network, allowing for the initiation of proliferation –regulated gene expression programs. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1014–1028, 2016. © 2016 Wiley Periodicals, Inc.


Yang S.,Key Laboratory of the Ministry of Education for Experimental Teratology | Gao Q.,Shandong University | Xing S.,Key Laboratory of the Ministry of Education for Experimental Teratology | Feng X.,Key Laboratory of the Ministry of Education for Experimental Teratology | And 9 more authors.
Journal of Ethnopharmacology | Year: 2011

Ethnopharmacological relevance: Buyang Huanwu decoction (BYHWD) is a traditional Chinese medicine and can be used to promote peripheral nerve regeneration. However the regenerative mechanism of BYHWD remains unclear. The objective of this study was to investigate the protective mechanisms of BYHWD in Schwann cells damaged by hydrogen peroxide (H 2O 2). Materials and methods: Schwann cells which were derived from neonatal sciatic nerves of rats were used in subsequent experiments. Schwann cells were injured by various concentrations of H 2O 2 (0.25, 0.5 and 1 mM final concentration). BYHWD (600 μg/ml final concentration) was added to the medium either simultaneously or 1 h later after the addition of H 2O 2. Subsequently, methyl thiazolyl tetrazolium (MTT) assay was performed. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were also examined after 12 h. The expression of Caspase 3 and the concentration of intercellular Ca 2+ ([Ca 2+]i) were also determined. Results: Among three concentrations of H 2O 2, 0.5 mM H 2O 2 induced Schwann cells swelled and neuritis disappeared after 12 h. In the presence of BYHWD, MTT assay showed that more cells were viable in comparison with the H 2O 2 injury group. Moreover, the addition of BYHWD has also increased the SOD activity with decreased in MDA level. Furthermore, the concentration of [Ca 2+]i and expression of Caspase 3 were decreased with the addition of BYHWD in culture. Conclusions: Our results revealed that BYHWD protected Schwann cells from oxidative injury. The mechanism of BYHWD promoting neural regeneration possibly associated with its anti-oxidative activity. © 2011 Elsevier Ireland Ltd. All rights reserved.


Zhang X.,Qilu Hospital | Wu M.,Key Laboratory of the Ministry of Education for Experimental Teratology | Jiang H.,Key Laboratory of the Ministry of Education for Experimental Teratology | Hao J.,Qilu Hospital | And 6 more authors.
PLoS ONE | Year: 2014

Background: Angiotensin II (AngII) participates in endothelial damage and inflammation, and accelerates atherosclerosis. Endothelial lipase (EL) is involved in the metabolism and clearance of high density lipoproteins (HDL), the serum levels of which correlate negatively with the onset of cardiovascular diseases including atherosclerosis. However, the relationship between AngII and EL is not yet fully understood. In this study, we investigated the effects of AngII on the expression of EL and the signaling pathways that mediate its effects in human umbilical vein endothelial cells (HUVECs).Methods and Findings: HUVECs were cultured in vitro with different treatments as follows: 1) The control group without any treatment; 2) AngII treatment for 0 h, 4 h, 8 h, 12 h and 24 h; 3) NF-κB activation inhibitor pyrrolidine dithiocarbamate (PDTC) pretreatment for 1 h before AngII treatment; and 4) mitogen-activated protein kinase (MAPK) p38 inhibitor (SB203580) pretreatment for 1 h before AngII treatment. EL levels in each group were detected by immunocytochemical staining and western blotting. HUVECs proliferation was detected by MTT and proliferating cell nuclear antigen (PCNA) immunofluorescence staining. NF-kappa B (NF-κB) p65, MAPK p38, c-Jun N-terminal kinase (JNK), extracellular signalregulated kinase (ERK) and phosphorylated extracellular signal-regulated kinase (p-ERK) expression levels were assayed by western blotting. The results showed that the protein levels of EL, NF-κB p65, MAPK p38, JNK, and p-ERK protein levels, in addition to the proliferation of HUVECs, were increased by AngII. Both the NF-kB inhibitor (PDTC) and the MAPK p38 inhibitor (SB203580) partially inhibited the effects of AngII on EL expression.Conclusion: AngII may upregulate EL protein expression via the NF-κB and MAPK signaling pathways. © 2014 Zhang et al.

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