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We began analyzing https://link.springer.com/article/10.1007/s13258-015-0290-5, but it redirected us to https://link.springer.com/article/10.1007/s13258-015-0290-5. The analysis below is for the second page.

Title[redir]:
Genes related with apoptosis by inflammation in diabetic keratocytes | Genes & Genomics
Description:
The goal of this study was to identify the differences in apoptosis-related gene expression between normal and diabetic keratocytes stimulated with IL-1α and TNF-α. Primary cultured normal and diabetic keratocytes were treated with IL-1α and TNF-α. The cDNA from these cells was hybridized to an oligonucleotide microarray. Microarray analysis was used to identify differentially expressed genes, which were further evaluated by real-time polymerase chain reaction. Diabetic keratocytes overexpressed vital components of cell division, migration, and differentiation, including Ppm1a, Ncam1, and Capn9, and under-expressed components related to prevention of apoptosis, including Clu, Ptn, and Mycn. Genes commonly over-expressed in response to IL-1α and TNF-α include Siah1a, Gzmb, and Capn9. Genes underexpressed after treatment with both cytokine include Ets1, Igf1r, and Sgk. Eighteen and eight apoptosis-related genes were newly expressed after treatment with IL-1α and TNF-α, respectively. The genes commonly under-expressed after treatment with both cytokines were Bmp4 and Timp3. Real-time polymerase chain reaction showed results similar to those of the microarray analysis. IL-1α and TNF-α may modulate the expression of genes related to apoptosis in diabetic keratocytes. It may be helpful to suppress newly overexpressed genes or to enhance newly underexpressed genes by IL-1α or TNF-α for the prevention of apoptosis in keratocytes when the cornea is damaged.

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Keywords {🔍}

pubmed, article, google, scholar, cas, genes, diabetic, cell, apoptosis, lee, keratocytes, related, sci, central, ophthalmol, research, gene, expression, ilα, tnfα, pusan, national, university, kim, microarray, corneal, epithelial, privacy, cookies, content, analysis, park, study, cornea, access, invest, vis, publish, search, cells, migration, underexpressed, role, biol, hospital, function, data, including, information, log,

Topics {✒️}

phosphatidylinositol 3-kinase/akt-mediated mechanism noninsulin-dependent diabetes mellitus apoptosis-related gene expression month download article/chapter ppm1a gene-deficient mice electrospun gelatin-fibrinogen constructs ji-eun lee jong soo lee interleukin-6 gene expression tnf-α include siah1a full article pdf biomedical research institute conjunctival clusterin expression privacy choices/manage cookies apoptosis-related genes article park wilson se signature genes related gene microarray expressed components related aldosterone-induced kinase epithelial na+ channels p53-mediated apoptosis cytokine include ets1 corneal epithelial complications corneal epithelial inhibitor related subjects ovarian cancer cells diabetic keratocyte erythroid cell transformation rabbit corneal epithelium european economic area vande geest jp ets oncogene family adult rat tissues avian erythroblastosis virus natural born killer renal collecting duct van horn dl egfr signaling pathways institutional animal care diabetic keratocytes stimulated diabetic olete keratocytes tgf-beta 2 corneal tissue organization gene polymorphisms conditions privacy policy primary cultured normal ischemic tissue regeneration lee js

Schema {🗺️}

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         headline:Genes related with apoptosis by inflammation in diabetic keratocytes
         description:The goal of this study was to identify the differences in apoptosis-related gene expression between normal and diabetic keratocytes stimulated with IL-1α and TNF-α. Primary cultured normal and diabetic keratocytes were treated with IL-1α and TNF-α. The cDNA from these cells was hybridized to an oligonucleotide microarray. Microarray analysis was used to identify differentially expressed genes, which were further evaluated by real-time polymerase chain reaction. Diabetic keratocytes overexpressed vital components of cell division, migration, and differentiation, including Ppm1a, Ncam1, and Capn9, and under-expressed components related to prevention of apoptosis, including Clu, Ptn, and Mycn. Genes commonly over-expressed in response to IL-1α and TNF-α include Siah1a, Gzmb, and Capn9. Genes underexpressed after treatment with both cytokine include Ets1, Igf1r, and Sgk. Eighteen and eight apoptosis-related genes were newly expressed after treatment with IL-1α and TNF-α, respectively. The genes commonly under-expressed after treatment with both cytokines were Bmp4 and Timp3. Real-time polymerase chain reaction showed results similar to those of the microarray analysis. IL-1α and TNF-α may modulate the expression of genes related to apoptosis in diabetic keratocytes. It may be helpful to suppress newly overexpressed genes or to enhance newly underexpressed genes by IL-1α or TNF-α for the prevention of apoptosis in keratocytes when the cornea is damaged.
         datePublished:2015-05-03T00:00:00Z
         dateModified:2015-05-03T00:00:00Z
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            Inflammation
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            Microbial Genetics and Genomics
            Plant Genetics and Genomics
            Animal Genetics and Genomics
            Human Genetics
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      headline:Genes related with apoptosis by inflammation in diabetic keratocytes
      description:The goal of this study was to identify the differences in apoptosis-related gene expression between normal and diabetic keratocytes stimulated with IL-1α and TNF-α. Primary cultured normal and diabetic keratocytes were treated with IL-1α and TNF-α. The cDNA from these cells was hybridized to an oligonucleotide microarray. Microarray analysis was used to identify differentially expressed genes, which were further evaluated by real-time polymerase chain reaction. Diabetic keratocytes overexpressed vital components of cell division, migration, and differentiation, including Ppm1a, Ncam1, and Capn9, and under-expressed components related to prevention of apoptosis, including Clu, Ptn, and Mycn. Genes commonly over-expressed in response to IL-1α and TNF-α include Siah1a, Gzmb, and Capn9. Genes underexpressed after treatment with both cytokine include Ets1, Igf1r, and Sgk. Eighteen and eight apoptosis-related genes were newly expressed after treatment with IL-1α and TNF-α, respectively. The genes commonly under-expressed after treatment with both cytokines were Bmp4 and Timp3. Real-time polymerase chain reaction showed results similar to those of the microarray analysis. IL-1α and TNF-α may modulate the expression of genes related to apoptosis in diabetic keratocytes. It may be helpful to suppress newly overexpressed genes or to enhance newly underexpressed genes by IL-1α or TNF-α for the prevention of apoptosis in keratocytes when the cornea is damaged.
      datePublished:2015-05-03T00:00:00Z
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      pageStart:607
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         Apoptosis
         IL-1α
         Inflammation
         Keratocyte
         Microarray
         TNF-α
         Microbial Genetics and Genomics
         Plant Genetics and Genomics
         Animal Genetics and Genomics
         Human Genetics
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                  name:Pusan National University Yangsan Hospital
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                  name:Pusan National University College of Medicine, and MRC for Ischemic Tissue Regeneration
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                     name:Department of Pharmacology, Pusan National University College of Medicine, and MRC for Ischemic Tissue Regeneration, Yangsan, Republic of Korea
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         name:Department of Ophthalmology, Pusan National University School of Medicine & Medical Research Institute, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea
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               type:PostalAddress
            type:Organization
      name:Chi Dae Kim
      affiliation:
            name:Pusan National University College of Medicine, and MRC for Ischemic Tissue Regeneration
            address:
               name:Department of Pharmacology, Pusan National University College of Medicine, and MRC for Ischemic Tissue Regeneration, Yangsan, Republic of Korea
               type:PostalAddress
            type:Organization
      name:Jong Soo Lee
      affiliation:
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      name:Department of Pharmacology, Pusan National University College of Medicine, and MRC for Ischemic Tissue Regeneration, Yangsan, Republic of Korea
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