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黎明涛, Neng-Wei Hu, Hong-Mei Zhang, Xiao-Dong Hu, Ming-Tao Li, Tong Zhang, Li-Jun Zhou, and Xian-Guo Liu
J Neurophysiol 89: 2354~2359, 2003;,-0001,():
-1年11月30日
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黎明涛, Ming YANG*, Cun-you WAGN, Feng ZHOU, Jing TAO, Tao LIU, Hai-yan WEI, Wei LIU, Ming-tao LI, Xian-song FENG
,-0001,():
-1年11月30日
AIM: A broad-range proteomic approach was applied to investigate the complexity of the mechanisms involved in pancreatic regeneration for identification of new treatment targets and potential markers of pancreatic stem cells. METHODS: A regeneration pancreatic model was induced by partial (90%) pancreatectomy in rats. Changes in protein expression in rat regeneration pancreas at 3 d after partial pancreatectomy, as compared to sham surgery, were analyzed using two-dimensional gel electrophoresis (2-DE), mass spectrometry (MS), and mass fingerprinting. RESULT: Two-DE displayed 91 spots with at least 1.5-fold of differentially expression at the time point of 3 days after pancreatectomy and 53 differentially expressed proteins were identified by peptide mass fingerprinting(PMF). These included embryogenic and cell proliferation-related, lipid and energy metabolism-related, protein and amino acid metabolism-related proteins, signal transduction proteins. CONCLUSION: The proteome profiling technique provided a broad-based and effective approach for the rapid assimilation and identification of adaptive protein changes while pancreas regeneration induced by pancreatectomy. Our data highlight the globe proteome during the pancreatic proliferation and differentiation processes, which is very important and will lead to better understand regulation mechanism of the pancreatic regeneration, and to ultimately reach the target of discovering protein biomarkers of pancreatic stem cells.
Partial pancreatectomy,, Regeneration,, Metabolism,, Stem cell,, Pancreas proteomics
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黎明涛, Xuemin Wang‡§, Xiaoli Tang‡§, Mingtao Li¶, John Marshall, and Zixu Mao‡**
Vol. 280, No.17, Issue of April 29, pp. 16705~16713, 2005,-0001,():
-1年11月30日
The transcription factor myocyte-enhancer factor 2 (MEF2) has been shown to be required for the survival of different types of neurons. However, the death- or survival-inducing second messenger pathways that regulate MEF2 activity remain to be fully elucidated. Membrane depolarization by KCl induces neuronal survival that is dependent upon MEF2-mediated gene transactivation. Here we report that membrane depolarizationinduced activation of MEF2 requires the cAMP-protein kinase A (PKA) pathway. Inhibition of the activity of cAMP-PKA pathway attenuates membrane depolarization-induced activation of MEF2 activity and neuronal survival, whereas enhancing the activity of this pathway prevents KCl withdrawal-induced inhibition of MEF2 and neuronal apoptosis. Moreover, PKA directly phosphorylates MEF2 at Thr-20 in vitro to increase MEF2 DNA binding activity. A mutation of Thr-20 to Ala renders MEF2 resistant to PKA phosphorylation in vitro and reduces its DNA binding activity. Transfection of this T20A mutant blocks survival and induces apoptosis in cultured cortical and cerebellar granule neurons. This study identifies the transcription factor MEF2 as a target of cAMP-PKA pathway and demonstrates that PKA phosphorylation of MEF2 is a key step in modulating its DNA binding activity and ability to promote neuronal survival.
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黎明涛, Wenya Wang a, Leyu Shi a, b, Yuanbin Xie b, Chi Mab, Wenming Li c, Xingwen Su a, Shoujian Huang a, Ruzhu Chen a, Zhenyu Zhu b, Zixu Mao d, Yifan Han c, Mingtao Li a, *
Neuroscience Research 48 (2004) 195~202,-0001,():
-1年11月30日
Increasing evidence suggests that c-Jun N-terminal kinase (JNK) is an important kinase mediating neuronal apoptosis in Parkinson's disease (PD) model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In order to study roles of JNK activity in neuronal apoptosis in this model, we blocked JNK activity in vivo using a specific inhibitor of JNK, SP600125. Our data showed that MPTP-induced phospho-c-Jun of substantial nigral neurons, caused apoptosis of dopaminergic neurons, and decreased the dopamine level in striatal area. We found that inhibiting JNK with SP600125 reduced the levels of c-Jun phosphorylation, protected dopaminergic neurons from apoptosis, and partly restored the level of dopamine in MPTP-induced PD in C57BL/6N mice. These results indicate that JNK pathway is the major mediator of the neurotoxic effects of MPTP in vivo and inhibiting JNK activity may represent a new and effective strategy to treat PD.
1-Methyl-4-phenyl-1,, 2,, 3,, 6-tetrahydropyridine, SP600125, c-Jun N-terminal kinase, Phospho-c-Jun, Dopaminergic neurons, Parkinson, Mouse
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黎明涛, Leyu Shi a, b, Shoufang Gong a, Zhongmin Yuan a, Chi Ma a, Yanling Liu a, Chuanfu Wang a, Wenming Li c, Rongbiao Pi c, Shoujian Huang a, Ruzhu Chen a, Yifan Han c, Zixu Mao d, Mingtao Li a, *
Neuroscience Letters 375 (2005) 7~12,-0001,():
-1年11月30日
Bcl-2-interacting mediator of cell death (Bim), a proapoptotic BH3-only protein, plays a critical role in neuronal apoptosis. Cerebellar granule neurons (CGNs) depend on activity for their survival and undergo apoptosis when deprived of depolarizing concentration of KCl. While it has been proposed that the activation of c-Jun NH2-terminal protein kinase (JNK)/c-Jun pathway contributes to the upregulation of bim gene in neurons subjected to survival signaling withdrawal, here we show that neither inhibition of JNK activity nor expression of dominant-negative c-Jun suppresses the expression of bim gene induced by activity deprivation in CGNs. We conclude that induction of bim gene is independent of the activation of JNK/c-Jun signaling pathway by activity deprivation during apoptosis of CGNs.
Bim, c-Jun NH2-terminal protein kinase, Apoptosis, Cerebellar granule neurons
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