Purpose:To evaluate the expression patterns of several keratin proteins in pterygial epithelium.Methods:The proteins of K8,K10,K14,K16 and AE3 in the epithelium of 8 pterygia and 4 normal conjunctiva were detected usi...Purpose:To evaluate the expression patterns of several keratin proteins in pterygial epithelium.Methods:The proteins of K8,K10,K14,K16 and AE3 in the epithelium of 8 pterygia and 4 normal conjunctiva were detected using immunofluorescent staining.Results:In pterygial epithelium,the staining patterns of 5 keratin proteins were different with normal conjunctiva.No staining of K8,K10 and K16 was detected in normal conjunctival epithelium,but in pterygial epithelium,K8 and K16 were present in full thickness and K10 was present in superficial cells.In normal conjunctiva, only base layer of epithelium showed positive staining with antibody of K14 and AE3 proteins,but they were present in the full thickness in pterygial epithelium and the antibody of AE3 protein stained the superficial cells heavily comparing with base cells.Conclusion:The abnormal expression of keratin proteins (K8,K10,K14,K16 and AE3) in pterygia indicates that the epithelial cells in pterygia are in the state of hyperproliferation and keratinization,which may be the cause of the abnormal tear function in patients with pterygia.Eye Science 2000;16:48-52.展开更多
Backgroud The JNK3 gene belongs to the c-Jun NH2 -terminal kinases (JNKs) family that is a group of the mitogen - activated protein (MAP) kinases that are activated hy cytokines and other entra-cellular stimuli that r...Backgroud The JNK3 gene belongs to the c-Jun NH2 -terminal kinases (JNKs) family that is a group of the mitogen - activated protein (MAP) kinases that are activated hy cytokines and other entra-cellular stimuli that results in the phosphorylation and activation of the c-Jun protein. Activation of JNK has been shown to be involved in development, proliferation, inflammation and apoptosis. Recent studies on inactivation of the JNK3 gene in mice leads to deficiency in the kainic acid-induced excitotoxicity, resulting in decreased apoptosis in the hippocampus of the JNK3 knockout mice. In the contrast, in context of nerve growth factor -induced differentiation of PC12 cell, JNK3 expression significantly increased the number and length neuritis. JNK3 has a mirrored function. Our report propose to test whether knockout JNK3 genes provide a protection action in spinal cord injuries of mice and the pathology morphology and mechanisms of the JNK3 knockout mice with spinal cord injures will be discussed. Methods Study used adult female C57B mice and JNK3 knockout mice each 20 (17∽21g) were anesthetized and subjected to laminectomy at (T10).Using 35KD force to impact to the expose cord and 0 KD for sham. After surgery 24 h, and 7 days animal were anesthetized, sacrificed. The spinal cords were picked it out.Make paraffin section. 8 micron each section slices. Section were stained with Luxol fast blue and nuclear fast red. Section were analyzed for per mouse. 4 X condenser microscope images of spinal cord were captured using a Sony digital CCD camera attached to a PPC 7100AV computer allowing lesion areas to be outlined with the use of a mouse. The extent of the lesion was demarcated. The total lesion volume was matter its damage area comparison in number or pathology comparison. The recovery behavior following the injury was poorer in the JNK3 knockout mice than in the wild type mice. (2) Using 35KD force for both groups the JNK3 knockout mice's damaged areas are absolutely bigger than that of the wild type C57B mice at 7 day after their surgery. No matter, damage area comparison in number or pathology comparison. Behaviors recovery from paralysis JNK3 knockout mice are worse than wild type mice. (3) The length of time following the injury, the damage area of the JNK3 and wild type mice at 7 day after injury were all larger than the damage area of both groups at 24 h after injury. Conclusion The knockout JNK3 gene does not decrease the damaged area in the knockout JNK3 mice with spinal cord injury, but it has a worse function. So that we propose an interesting hypothesis that JNK3 may play a role in maintenance of normal neuronal function.展开更多
文摘Purpose:To evaluate the expression patterns of several keratin proteins in pterygial epithelium.Methods:The proteins of K8,K10,K14,K16 and AE3 in the epithelium of 8 pterygia and 4 normal conjunctiva were detected using immunofluorescent staining.Results:In pterygial epithelium,the staining patterns of 5 keratin proteins were different with normal conjunctiva.No staining of K8,K10 and K16 was detected in normal conjunctival epithelium,but in pterygial epithelium,K8 and K16 were present in full thickness and K10 was present in superficial cells.In normal conjunctiva, only base layer of epithelium showed positive staining with antibody of K14 and AE3 proteins,but they were present in the full thickness in pterygial epithelium and the antibody of AE3 protein stained the superficial cells heavily comparing with base cells.Conclusion:The abnormal expression of keratin proteins (K8,K10,K14,K16 and AE3) in pterygia indicates that the epithelial cells in pterygia are in the state of hyperproliferation and keratinization,which may be the cause of the abnormal tear function in patients with pterygia.Eye Science 2000;16:48-52.
文摘Backgroud The JNK3 gene belongs to the c-Jun NH2 -terminal kinases (JNKs) family that is a group of the mitogen - activated protein (MAP) kinases that are activated hy cytokines and other entra-cellular stimuli that results in the phosphorylation and activation of the c-Jun protein. Activation of JNK has been shown to be involved in development, proliferation, inflammation and apoptosis. Recent studies on inactivation of the JNK3 gene in mice leads to deficiency in the kainic acid-induced excitotoxicity, resulting in decreased apoptosis in the hippocampus of the JNK3 knockout mice. In the contrast, in context of nerve growth factor -induced differentiation of PC12 cell, JNK3 expression significantly increased the number and length neuritis. JNK3 has a mirrored function. Our report propose to test whether knockout JNK3 genes provide a protection action in spinal cord injuries of mice and the pathology morphology and mechanisms of the JNK3 knockout mice with spinal cord injures will be discussed. Methods Study used adult female C57B mice and JNK3 knockout mice each 20 (17∽21g) were anesthetized and subjected to laminectomy at (T10).Using 35KD force to impact to the expose cord and 0 KD for sham. After surgery 24 h, and 7 days animal were anesthetized, sacrificed. The spinal cords were picked it out.Make paraffin section. 8 micron each section slices. Section were stained with Luxol fast blue and nuclear fast red. Section were analyzed for per mouse. 4 X condenser microscope images of spinal cord were captured using a Sony digital CCD camera attached to a PPC 7100AV computer allowing lesion areas to be outlined with the use of a mouse. The extent of the lesion was demarcated. The total lesion volume was matter its damage area comparison in number or pathology comparison. The recovery behavior following the injury was poorer in the JNK3 knockout mice than in the wild type mice. (2) Using 35KD force for both groups the JNK3 knockout mice's damaged areas are absolutely bigger than that of the wild type C57B mice at 7 day after their surgery. No matter, damage area comparison in number or pathology comparison. Behaviors recovery from paralysis JNK3 knockout mice are worse than wild type mice. (3) The length of time following the injury, the damage area of the JNK3 and wild type mice at 7 day after injury were all larger than the damage area of both groups at 24 h after injury. Conclusion The knockout JNK3 gene does not decrease the damaged area in the knockout JNK3 mice with spinal cord injury, but it has a worse function. So that we propose an interesting hypothesis that JNK3 may play a role in maintenance of normal neuronal function.
