Cold exposure is an external stress factor that causes skin frostbite as well as a variety of diseases.Estrogen might participate in neuroprotection after cold exposure,but its precise mechanism remains unclear.In thi...Cold exposure is an external stress factor that causes skin frostbite as well as a variety of diseases.Estrogen might participate in neuroprotection after cold exposure,but its precise mechanism remains unclear.In this study,mice were exposed to 10°C for 7 days and 0–4°C for 30 days to induce a model of chronic cold exposure.Results showed that oxidative stress-related c-fos and cyclooxygenase 2 expressions,MAP1LC3-labeled autophagic cells,Iba1-labeled activated microglia,and interleukin-1β-positive pyramidal cells were increased in the hippocampal CA1 area.Chronic cold exposure markedly elevated the levels of estrogen in the blood and the estrogen receptor,G protein-coupled receptor 30.These results indicate that neuroimmunoreactivity is involved in chronic cold exposure-induced pathological alterations,including oxidative stress,neuronal autophagy,and neuroimmunoreactivity.Moreover,estrogen exerts a neuroprotective effect on cold exposure.展开更多
To investigate the pattern of neural differentiation and synaptogenesis in the mouse retina,immunolabeling,Brd U assay and transmission electron microscopy were used.We show that the neuroblastic cell layer is the ger...To investigate the pattern of neural differentiation and synaptogenesis in the mouse retina,immunolabeling,Brd U assay and transmission electron microscopy were used.We show that the neuroblastic cell layer is the germinal zone for neural differentiation and retinal lamination.Ganglion cells differentiated initially at embryonic day 13(E13),and at E18 horizontal cells appeared in the neuroblastic cell layer.Neural stem cells in the outer neuroblastic cell layer differentiated into photoreceptor cells as early as postnatal day 0(P0),and neural stem cells in the inner neuroblastic cell layer differentiated into bipolar cells at P7.Synapses in the retina were mainly located in the outer and inner plexiform layers.At P7,synaptophysin immunostaining appeared in presynaptic terminals in the outer and inner plexiform layers with button-like structures.After P14,presynaptic buttons were concentrated in outer and inner plexiform layers with strong staining.These data indicate that neural differentiation and synaptogenesis in the retina play important roles in the formation of retinal neural circuitry.Our study showed that the period before P14,especially between P0 and P14,represents a critical period during retinal development.Mouse eye opening occurs during that period,suggesting that cell differentiation and synaptic formation lead to the attainment of visual function.展开更多
AIM: To determine whether limb remote ischemic postconditioning(LRIC) protects against high-intraocularpressure(IOP)-induced retinal injur y, and to identify underlying molecular mechanisms. METHODS: In mice, IOP was ...AIM: To determine whether limb remote ischemic postconditioning(LRIC) protects against high-intraocularpressure(IOP)-induced retinal injur y, and to identify underlying molecular mechanisms. METHODS: In mice, IOP was increased to 110 mm Hg for 50 min and LRIC applied to the unilateral leg for three occlusion cycles(5 min/release). Three animal groups(control, high IOP, and high IOP+LRIC) were arranged in this study. Plasma was collected from LRIC treated mice. Retinal histology, oxidative stress were determined by histological section staining and chemical kit. C/EBP homologous protein(CHOP), and Iba-1 parameters were evaluated by immunofluorescent staining and Western blot. RESULTS: The data showed that LRIC treatment alleviated the retinal histological disorganization and ganglion cell loss induced by high IOP. The CHOP, Iba-1 expression and oxidative stress marker also were inhibited by LRIC treatment. To further explore underlying mechanisms, plasma from LRIC treated animals was intravenously transfused into high-IOP animals. The results showed plasma injection decreased caspase 9 expression and DHE staining signals compared with that in high IOP retinas. CONCLUSION: These data suggest that LRIC treatments exert retinal protective effects against high-IOP injury.Endogenous humoral factors release into the circulation by LRIC may contribute to homeostatic protection by reducing monocyte infiltration and/or microglia activation.展开更多
基金supported by the Henan Province Foundation for Key University Teachers in China,No.16A330001,15A180031the Henan Postdoctoral Foundation in China,No.2015051a grant from the Henan Province Research Program of Basic and Advanced Technology in China,No.162300410102
文摘Cold exposure is an external stress factor that causes skin frostbite as well as a variety of diseases.Estrogen might participate in neuroprotection after cold exposure,but its precise mechanism remains unclear.In this study,mice were exposed to 10°C for 7 days and 0–4°C for 30 days to induce a model of chronic cold exposure.Results showed that oxidative stress-related c-fos and cyclooxygenase 2 expressions,MAP1LC3-labeled autophagic cells,Iba1-labeled activated microglia,and interleukin-1β-positive pyramidal cells were increased in the hippocampal CA1 area.Chronic cold exposure markedly elevated the levels of estrogen in the blood and the estrogen receptor,G protein-coupled receptor 30.These results indicate that neuroimmunoreactivity is involved in chronic cold exposure-induced pathological alterations,including oxidative stress,neuronal autophagy,and neuroimmunoreactivity.Moreover,estrogen exerts a neuroprotective effect on cold exposure.
基金supported by the National Natural Science Foundation of China,No.31070952 and U1204311the Scientific Research Foundation of Henan University of China,No.0000A40475 and 0000A40356
文摘To investigate the pattern of neural differentiation and synaptogenesis in the mouse retina,immunolabeling,Brd U assay and transmission electron microscopy were used.We show that the neuroblastic cell layer is the germinal zone for neural differentiation and retinal lamination.Ganglion cells differentiated initially at embryonic day 13(E13),and at E18 horizontal cells appeared in the neuroblastic cell layer.Neural stem cells in the outer neuroblastic cell layer differentiated into photoreceptor cells as early as postnatal day 0(P0),and neural stem cells in the inner neuroblastic cell layer differentiated into bipolar cells at P7.Synapses in the retina were mainly located in the outer and inner plexiform layers.At P7,synaptophysin immunostaining appeared in presynaptic terminals in the outer and inner plexiform layers with button-like structures.After P14,presynaptic buttons were concentrated in outer and inner plexiform layers with strong staining.These data indicate that neural differentiation and synaptogenesis in the retina play important roles in the formation of retinal neural circuitry.Our study showed that the period before P14,especially between P0 and P14,represents a critical period during retinal development.Mouse eye opening occurs during that period,suggesting that cell differentiation and synaptic formation lead to the attainment of visual function.
基金Supported by the National Natural Science Foundation of China(No.31300884No.81803573)。
文摘AIM: To determine whether limb remote ischemic postconditioning(LRIC) protects against high-intraocularpressure(IOP)-induced retinal injur y, and to identify underlying molecular mechanisms. METHODS: In mice, IOP was increased to 110 mm Hg for 50 min and LRIC applied to the unilateral leg for three occlusion cycles(5 min/release). Three animal groups(control, high IOP, and high IOP+LRIC) were arranged in this study. Plasma was collected from LRIC treated mice. Retinal histology, oxidative stress were determined by histological section staining and chemical kit. C/EBP homologous protein(CHOP), and Iba-1 parameters were evaluated by immunofluorescent staining and Western blot. RESULTS: The data showed that LRIC treatment alleviated the retinal histological disorganization and ganglion cell loss induced by high IOP. The CHOP, Iba-1 expression and oxidative stress marker also were inhibited by LRIC treatment. To further explore underlying mechanisms, plasma from LRIC treated animals was intravenously transfused into high-IOP animals. The results showed plasma injection decreased caspase 9 expression and DHE staining signals compared with that in high IOP retinas. CONCLUSION: These data suggest that LRIC treatments exert retinal protective effects against high-IOP injury.Endogenous humoral factors release into the circulation by LRIC may contribute to homeostatic protection by reducing monocyte infiltration and/or microglia activation.
