Autophagy and tumor / 中国病理生理杂志

Autophagy is a vacuolar process of cytoplasmic degradation by lysosome which ubiquitously occurring in all eukaryotic cells. The researches of autophagy have made great progress with the development of the yeast model and genetic technology. This review will summarize the determination of autophagy, its relationship with apoptosis and its role in the tumor treatment in order to give a comprehensive understanding of the function of autophagy.

Autophagy and myocardial ischemia/reperfusion injury / 中国病理生理杂志

Autophagy is a lysosome-dependent degradative pathway which is characterized by cytoplasmic vacuolization. However, it is not just a simple degradative pathway. Research shows that autophagy is related to many diseases, such as neurodegenerative disease, malignant tumor, ageing, pathogenic microorganism infection, myocardial ischemia/reperfusion injury and so on. Autophagy exactly exists in myocardial ischemia/reperfusion injury, and it becomes a new research hotspot. This review will focus on the occurrence and development of autophagy and its role, signal transduction and research status in myocardial ischemia/reperfusion injury.

Autophagic pathway and probable mechanism in degradation of mutant α-synuclein in PC12 cells / 中华神经科杂志

Objective To observe the effect of mutant α-synuclein(A30P)in autophagic programmed cell death by transfected PC12 cells and explore its probable role and pathway in PD.Methods The definite PC12 cells which were transfected mutant α-synuclein(A30P)were constructed at first and MPP+,Rapamycin and Wortmanin were administrated to transfected PC12 cells with mutant α-synuclein. Not only the proliferative activity of cells was detected with MTT method but also the ultrastructttre changes of cells and expression of α-synuclein in different circumstance were observed by transmission electron microscopy(TEM),Western Blot and the level of SOD.Results (1)The expression of α-synuclein in groups A30P+Wortmannin and A30P+MPP+was higher than that in group A30P(P＜0.01), particularly.there was more significant expression of α-synuclein in group A30P+Wortmannin.The expression of α-synuclein in group A30P+Rapamycin was weaker than that in group A30P(P＜0.01); (2)The results showed that the SOD level(group A30P+MPP+:3 h:97.49±13.8;12 h:102.7±12.7; 24 h:101.5±11.8;48 h:104.3±12.4)was significantly decreased at various time points after MPP+ treatment compared that of group A30P(t=3.7721,P=0.0017).SOD level gradually increased in A30P +Rapamycin 12 h and showed significant difference at 24 h(121.2±13.0),48 h(124.3±14.1)and 72 h(127.7±13.7)after drug treatment compared with that in group A30P+Wortmannin(t:2.9746, P=0.0083);(3)Mutant α-synuclein(A30P)leading to PC12 cells death by means of autophagy involved α-synuclein accumulation,membrane lipid oxidation,and loss of plasma membrane integrity.Mutant α- synuclein(A30P)mediated the toxicity of MPP+.Rapamycin,an inducer of autophagy,reduced the aggregation of α-synuclein in transfected cells.Meanwhile,Wortmanin,an inhibitor of autophagy,promoted the aggregation of α-synuclein in transfected cells and induced cells to die.Conclusions The abnormal aggregation of α-synuclein induces autophagic programmed cell death in PC12 cells and mutant α-synuclein (A30P)mediates the toxicity of MPP+.Meanwhile,Rapamycin may reduce the aggregation of α-synuclein in transfeeted cells by activation of autophagic pathway.

Effects of dust particles on autophagy of macrophages / 中国病理生理杂志

AIM:To investigate the changes of autophagy of macrophages after phagocytizing dust particles and explore the mechanisms of dust particle-induced autophagy of the cells.METHODS:The bronchopulmonary lymph nodes were collected from patients with lung operation.The paraffin sections were prepared and then stained with Wilder's method.The tissue structures were viewed.Peritoneal macrophages were harvested from rats and then treated with carbon particles.Influences of carbon particles in autophagic activities of macrophages were examined.The ultrathin sections of the lymph nodes and the cells phagocytized carbon particles were prepared.The structures and distribution of phagosomes,autophagosomes and lysosomes were viewed.The apoptotic cells in the dust cells of the lymph nodes and the cells having phagocytized carbon particles were examined using transmission electron microscope and TUNEL staining.RESULTS:In adult lymph nodes,dust particles were deposited significantly in macrophages,collagen fibres and density of microvessels increased.There were autophagosome precursors,autophagosomes,autophagolysosomes as well as phagosomes in the dust cells and the cells phagocytized carbon particles.In autophagosomes,mitochondrion,dust particle or carbon particle were usually observed.There were positive cells by TUNEL staining in the dust cells and the cells phagocytized carbon particles.Nuclear condensation or apoptotic body in the apoptotic cells were observed under transmission electron microscope.CONCLUSION:Deposition of dust particles induces enhancement of autophagic activities and apoptosis of macrophages.Autophagy plays an important role in cleaning dust particles and the injured mitochondria.

ROLE OF LYSOSOMES IN THE DEVELOPMENT OF EXPERIMENTAL CARDIAC HYPERTROPHY / 解剖学报

In present study, animal model of cardiac hypertrophy induced by abdominal aortic stenosis was utilized, and the lysosomes were investigated by electron microscopy and ultrastructural cytochemistry. The results showed that while cardiac hypertrophy developed, lysosomes participate in apparent remolding of cardiac muscle cells; in the late stage of cardiac hypertrophy, a great deal of autophagocytoses were viewed in some muscle cells which may result in irreversible cell damage.