1.The effects of acupuncture on astrocyte proliferation after cerebral ischemia-reperfusion injury in rats
Chinese Journal of Physical Medicine and Rehabilitation 2008;30(4):244-247
Objective To investigate the effects of acupuncture on astrocyte proliferation in hippocampus of rats after cerebral ischemia-reperfusion. Methods Ischemia-reperfusion injury was induced by temporary middle cerebral artery occlusion(MCAO)in 36 Sprague-Dawley rats,who were divided randomly into a control group,a model group and an acupuncture group.The expression level of Cyclin D 1 and glial fibrillary acidic protein(GFAP) was analyzed by immunoreactivity and Western blot. Results It was shown that the expression of Cyclin D1 and GFAP increased significantly(P<0.01)at 2 and 7 days after cerebral ischemia-reperfusion,respectively.It was also shown that application of acupuncture could inhibit Cyclin D1 and GFAP(P<0.01). Conclusion Acupuncture may inhibit glial proliferation by regulating cell cycle factor.
2. Impact of symptom onset to first medical contact time on the prognosis of patients with acute ST-segment elevation myocardial infarction
Tengfei WEI ; Bei ZHAO ; Peilin LIU ; Xueyao FENG ; Zhong ZHANG ; Quanxing SHI ; Tieshan GAO ; Li LIU ; Jingtao ZHAO ; Hongyong SONG ; Lifeng LIU ; Yingqi LIU ; Mengmeng RAO ; Shouli WANG
Chinese Journal of Cardiology 2017;45(5):393-398
Objective:
To investigate the impact of symptom onset to first medical contact (SO-to-FMC)time on the prognosis of patients with acute ST-segment elevation myocardial infarction(STEMI).
Methods:
The clinical data of 341 consecutive STEMI patients, who were hospitalized to our hospital and received primary percutaneous coronary intervention(PCI) from August 2011 to April 2016, were retrospectively analyzed. The patients were divided into ≤90 min group (201 cases) and >90 min group (140 cases) according to the SO-to-FMC time. The treatment time, mortality and incidence of major adverse cardiac and cerebro-vascular events(MACCE) were analyzed. The risk factor of 1-year mortality after PCI and 1-year incidence of MACCE during the post-discharge follow-up period were analyzed by binary logistic regression analysis. The predictor of 4.5-year mortality after PCI was analyzed by multivariate Cox regression analysis. Methods The door to balloon time (104(88, 125) min vs. 111(92, 144)min,
3.Parkin promotes proteasomal degradation of p62: implication of selective vulnerability of neuronal cells in the pathogenesis of Parkinson's disease.
Pingping SONG ; Shanshan LI ; Hao WU ; Ruize GAO ; Guanhua RAO ; Dongmei WANG ; Ziheng CHEN ; Biao MA ; Hongxia WANG ; Nan SUI ; Haiteng DENG ; Zhuohua ZHANG ; Tieshan TANG ; Zheng TAN ; Zehan HAN ; Tieyuan LU ; Yushan ZHU ; Quan CHEN
Protein & Cell 2016;7(2):114-129
Mutations or inactivation of parkin, an E3 ubiquitin ligase, are associated with familial form or sporadic Parkinson's disease (PD), respectively, which manifested with the selective vulnerability of neuronal cells in substantia nigra (SN) and striatum (STR) regions. However, the underlying molecular mechanism linking parkin with the etiology of PD remains elusive. Here we report that p62, a critical regulator for protein quality control, inclusion body formation, selective autophagy and diverse signaling pathways, is a new substrate of parkin. P62 levels were increased in the SN and STR regions, but not in other brain regions in parkin knockout mice. Parkin directly interacts with and ubiquitinates p62 at the K13 to promote proteasomal degradation of p62 even in the absence of ATG5. Pathogenic mutations, knockdown of parkin or mutation of p62 at K13 prevented the degradation of p62. We further showed that parkin deficiency mice have pronounced loss of tyrosine hydroxylase positive neurons and have worse performance in motor test when treated with 6-hydroxydopamine hydrochloride in aged mice. These results suggest that, in addition to their critical role in regulating autophagy, p62 are subjected to parkin mediated proteasomal degradation and implicate that the dysregulation of parkin/p62 axis may involve in the selective vulnerability of neuronal cells during the onset of PD pathogenesis.
Adaptor Proteins, Signal Transducing
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chemistry
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metabolism
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Animals
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HEK293 Cells
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Heat-Shock Proteins
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chemistry
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metabolism
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Humans
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Lysine
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metabolism
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Mice
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Neurons
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metabolism
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pathology
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Oxidopamine
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pharmacology
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Parkinson Disease
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metabolism
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pathology
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Proteasome Endopeptidase Complex
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metabolism
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Protein Stability
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Proteolysis
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drug effects
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Sequestosome-1 Protein
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Ubiquitin-Protein Ligases
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metabolism
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Ubiquitination
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drug effects