Objective To determine the effects of lensspecific overexpression of OSM on the eye development. Methods A truncated mouse OSM c DNA (661 bp) was linked to the αA-crystallin promoter. Transgenic mice were characterized by routine histological and immunohistochemical techiniques. TUNEL assays were used to de tect cell death. The mRNA expression of caspase-3 was detected by in situhybridization, Rabbit anti-cleavage caspase-3 antibody was used to detectactive capase-3. Results At embryonic day (E) 14.5 and 17.5, expression of the OSM transgenic protein was detected specifically in lens fiber cells. The onset of retinal degeneration in the mid portion of the transgenic retinae was observed started from E17.5. By the time of birth 50% or more of the retinal cells were missing. The OSM transgenic retinal cells underwent apoptosis indicated by TUNEL assays. Most strikingly, activation of caspase-3 protein were observed throughout the transgenic retinas. Conclusions Lens-specific overexpression of OSM activate caspase-3, leading to abnormal eye development,apoptosis and widespread retinal degeneration. (Chin J Ocul Fundus Dis，2003，19：201-268)
Objective To demonstrate if apoptosis is one of the mechanisms of siderotic retinopathy. Methods Autoclaved iron particles were implanted in the vitreous cavities of 32 eyes of SD rats.Glass chips were implanted in 10 control eyes.The experimental eyes were enucleated at various time intervals from days 1 to 15.Retinal degeneration was examined using the TdT-mediated,dUTP-biotin nickend labeling(TUNEL)method.Electrophoresis on agarose gel was used to detect internucleosomal DNA fragmentation.Results TUNEL-positive nuclei were observed only in the outer nuclear layer beginning on day 2.The nuclei spread throughout the outer nuclear layer by the end of day 3.No TUNEL-positive nuclei were observed in other layers throughout the experimental perios.Analysis of DNA,extracted from the retinas by electrophoresis on agarose gel,revealed a typical ladder pattern of internucleosoma DNA cleavage in the experimental eyes.ConclusionApoptosis of photoreceptors occurs at the early phase of iron-induced retinopathy in the rats.
ObjectiveTo understand the current progress of programmed cell death in the pathogenesis of acute pancreatitis, and to provide reference for the pathogenesis and treatment of acute pancreatitis.MethodThe research progress of acute pancreatitis and programmed cell death in recent years was reviewed by reading relevant literatures at home and abroad in recent years.ResultsProgrammed cell death was defined as controlled cell death performed by intracellular procedures, including apoptosis, autophagy, programmed necrosis, and coronation. The pattern of death of pancreatic acinar cells mainly includes apoptosis and programmed necrosis. Although the pathogenesis of acute pancreatitis had not yet been fully clarified, it was known that through the study of programmed cell death, it could help us to understand the pathogenesis and pathogenesis of acute pancreatitis and provide more effective treatment methods.ConclusionsProgrammed cell death is very important for acute pancreatitis. The mechanism of programmed cell death in acute pancreatitis is necessary for the treatment and prevention of it.
Objective To observe the effect of visible light on apoptosis of cultured human retinal pigment epithelium (RPE) cells. Methods Being the light source,500lx,(2 000±500)lx and (3 400±200)lx cold white light were used. The duration of exposure was 0,6,12 and 24 hours respectively. Apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling, Annexin V-flunorescein isothiocyanate/Propidium iodium labelling and flow cytometry. Results Apoptosis and necrosis were found in cultured human RPE cells which were exposed to visible light.(1)A significant increase in apoptotic and necrotic percentages was consistent with a higher light intensity.(2)Apoptosis was the main response to shorter (6 h and 12 h) exposure duration,while necrosis was more pronounced correlated to the prolongation of post-exposure culture (P＜0.05),and the longer the post-exposure period was, the more apoptotic necrosis were seen.Thirty-six hours after exposure the necrotic percentages were more pronounced (P＜0.01). Conclusions Visible light (＞500 lx) increases the proportion of apoptosis and necrosis of human RPE cells in vitro.The extent is related to exposure intensity and duration. It demonstrates that the lower intensity and the shorter duration of exposure to light are, the more pronounced apoptotic percentages are observed,otherwise necrosis. (Chin J Ocul Fundus Dis, 2002, 18: 227-230)
Objective To investigate the interference effect of nerve growth factor (NGF) on apoptosis of retinal cells in experimental retinal detac hment (RD). Methods Twenty seven Sprague-Dawely rats were selected, and the left and right eyes were in the experimental control group and NGF group, respectively. After the RD model was set up by subretinal injection with sodium hyaluronate, 5mu;l NGF（1mu;g/mu;l）was injected into the vitreous body of the right eyes which were in the NGF group; 5mu;l PBS was injected into vitreous body of left eyes which were in the experimental control group. The injection was performed once every 4 days till the end of the observation period. The eye balls of the 27 rats were extrafted 1.5, 3, 6, 12 hours, 1 day, 2, 4, 8 , 16, and 32 days after the RD model was established. Another 2 rats were selected as the normal control, which underwent none of the injections but eyeball extraction at the end of the observation period. TUNEL and transmission electron microscopy were used to detect the apoptosis of the retinal cells. Cell counts and statis tical analysis were used to assess results. Results Typical apoptosis cells were observed in the early time of RD. Apoptosis was found in each retinal layers, especially in inner and outer nuclear layers. The number of apoptosis cells increased as the time of RD was prolonged（Plt;0.01）. It was also found that apoptosis cells in NGF group were less than that in the experimenta l control group（Plt;0.01）. Conclusion Intravitreous injection exogenous NGF may inhibit the apoptosis of retinal cells in experimental RD. (Chin J Ocul Fundus Dis, 2006, 22: 333-335)
Objective To investigate the role of anti apoptosis gene bcl-2 in the survival of cultured uveal melanoma UM cells. Methods Antisense oligodeoxynucleotides (AS-ODN) bcl-2 were delivered with cationic lipid to primary cultured UM cells. The inhibitory effect of AS-ODN bcl-2 on proliferation of UM cells was examined by 3,-4,5 Dimethyliazol-2,5 diphenyl tetrazolium bromide (MTT) method. Using DNA ladder to determine if the UM cells had been apoptotic. Bcl-2 expression was detected by RT-PCR and Westernblot technics. Results The effect of AS-ODN bcl-2 in inhibiting the proliferation of cultured UM cells had opposite relation to dosage. It down regulated the mRNA and protein level of bcl-2 gene, and the sense ODN didn′t have this effect. Conclusion AS-ODN bcl-2 can down regulate bcl-2 expression, inhibits UM cells proliferation and induces apoptosis. (Chin J Ocul Fundus Dis, 2002, 18: 38-41)
Cancer is a heterogeneous disease characterized by maladjustment of cell death. The types of cell death were mainly divided into two forms including accidental cell death and regulated cell death (RCD). In recent years, researchers have discovered dozens of RCD modes, among which apoptosis, pyroptosis, necroptosis, and ferroptosis are the most widely studied. Cuproptosis is a new cell death mechanism that first proposed on 17 March 2022. It is recognized as a unique and both copper and mitochondria dependent RCD. The research and development of targeted drugs for regulating different cell death pathways will be hots and difficulties in the treatment of refractory cancer in the future.
Retinal neuronal cells are crucial in the formation of vision. Injury or death of these cells may lead to irreversible damage to visual function due to their low regenerative capacity. The P2X7 receptor is a trimeric adenosine triphosphate (ATP)-gated cation channel. Recent studies have shown that P2X7 receptor plays a role in retinal neuronal death. In a series of animal models, when exposed to conditions of hypoxia or ischemia, elevated ocular pressure, trauma and exogenous agonists, P2X7 receptor activated by extracellular ATP can cause death of retinal neuronal cells such as retinal ganglion cells and photoreceptor cells through direct or indirect pathways. Blocking the expression and function of P2X7 receptor by its specific antagonist and gene knocking-out, the loss of retinal neuronal cells is significantly attenuated. P2X7 receptor may become a potential novel neuroprotective target for diseases related to the loss of retinal neurons.