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We are analyzing https://link.springer.com/article/10.1007/s00125-007-0768-z.

Title:
Oxidised, glycated LDL selectively influences tissue inhibitor of metalloproteinase-3 gene expression and protein production in human retinal capillary pericytes | Diabetologia
Description:
Aims/hypothesis Matrix metalloproteinases (MMPs) and their natural inhibitors, tissue inhibitor of metalloproteinases (TIMPs), regulate important biological processes including the homeostasis of the extracellular matrix, proteolysis of cell surface proteins, proteinase zymogen activation, angiogenesis and inflammation. Studies have shown that their balance is altered in retinal microvascular tissues in diabetes. Since LDLs modified by oxidation/glycation are implicated in the pathogenesis of diabetic vascular complications, we examined the effects of modified LDL on the gene expression and protein production of MMPs and TIMPs in retinal pericytes. Methods Quiescent human retinal pericytes were exposed to native LDL (N-LDL), glycated LDL (G-LDL) and heavily oxidised and glycated LDL (HOG-LDL) for 24 h. We studied the expression of the genes encoding MMPs and TIMPs mRNAs by analysis of microarray data and quantitative PCR, and protein levels by immunoblotting and ELISA. Results Microarray analysis showed that MMP1, MMP2, MMP11, MMP14 and MMP25 and TIMP1, TIMP2, TIMP3 and TIMP4 were expressed in pericytes. Of these, only TIMP3 mRNA showed altered regulation, being expressed at significantly lower levels in response to HOG– vs N-LDL. Quantitative PCR and immunoblotting of cell/matrix proteins confirmed the reduction in TIMP3 mRNA and protein in response to HOG-LDL. In contrast to cellular TIMP3 protein, analysis of secreted TIMP1, TIMP2, MMP1 and collagenase activity indicated no changes in their production in response to modified LDL. Combined treatment with N– and HOG-LDL restored TIMP3 mRNA expression to a level comparable with that after N-LDL alone. Conclusions/interpretation Among the genes encoding for MMPs and TIMPs expressed in retinal pericytes, TIMP3 is uniquely regulated by HOG-LDL. Reduced TIMP3 expression might contribute to microvascular abnormalities in diabetic retinopathy.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

timp, expression, hogldl, ldl, pericytes, retinal, google, scholar, pubmed, article, human, nldl, cas, modified, diabetic, cells, mmp, mmps, response, retinopathy, diabetes, medium, endothelial, timps, cell, genes, usa, analysis, levels, protein, microarray, matrix, data, vascular, significantly, treatment, treated, proteinml, gldl, reduced, tissue, effects, pericyte, study, experiments, encoding, hog, conditioned, glycated, metalloproteinase,

Topics {✒️}

age-related macular degeneration lipopolysaccharide-stimulated retinal pericytes real-time quantitative pcr modified low-density lipoproteins increased tnf-α low density lipoprotein retinal pigment epithelium stress-induced pericyte loss timp3-deficient animal models pericyte–endothelial cell contacts pericyte-endothelial cell contacts related subjects model-based expression indices blood-retinal barrier /cgi-bin/primer3/primer3 fibroblast growth factor cell/matrix proteins confirmed serum lipoprotein subclasses hog-ldl specifically reduces reduced-serum medium [rsm] privacy choices/manage cookies early-stage pericyte dropout bicinchoninic acid assay concentration-related fashion hypoxia-induced damage blood–retina barrier [7] retinal capillary pericytes bovine retinal pericytes timp3−/− mice leads hog-ldl modulates serum-free medium human retinal pericytes n-ldl response defined separate receptor mechanisms cell–cell contacts epiretinal neovascular membranes jenkins aj increased tnf-alpha retinal vascular patterns metalloproteinase-3 gene expression abnormal tnf activity retinal microvascular tissues retinal diseases retinal hard exudates lower panel shows n-ldl-treated cells human u95av2 genechips reduced serum conditions endothelial cell movement human retinal capillaries

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Oxidised, glycated LDL selectively influences tissue inhibitor of metalloproteinase-3 gene expression and protein production in human retinal capillary pericytes
         description:Matrix metalloproteinases (MMPs) and their natural inhibitors, tissue inhibitor of metalloproteinases (TIMPs), regulate important biological processes including the homeostasis of the extracellular matrix, proteolysis of cell surface proteins, proteinase zymogen activation, angiogenesis and inflammation. Studies have shown that their balance is altered in retinal microvascular tissues in diabetes. Since LDLs modified by oxidation/glycation are implicated in the pathogenesis of diabetic vascular complications, we examined the effects of modified LDL on the gene expression and protein production of MMPs and TIMPs in retinal pericytes. Quiescent human retinal pericytes were exposed to native LDL (N-LDL), glycated LDL (G-LDL) and heavily oxidised and glycated LDL (HOG-LDL) for 24 h. We studied the expression of the genes encoding MMPs and TIMPs mRNAs by analysis of microarray data and quantitative PCR, and protein levels by immunoblotting and ELISA. Microarray analysis showed that MMP1, MMP2, MMP11, MMP14 and MMP25 and TIMP1, TIMP2, TIMP3 and TIMP4 were expressed in pericytes. Of these, only TIMP3 mRNA showed altered regulation, being expressed at significantly lower levels in response to HOG– vs N-LDL. Quantitative PCR and immunoblotting of cell/matrix proteins confirmed the reduction in TIMP3 mRNA and protein in response to HOG-LDL. In contrast to cellular TIMP3 protein, analysis of secreted TIMP1, TIMP2, MMP1 and collagenase activity indicated no changes in their production in response to modified LDL. Combined treatment with N– and HOG-LDL restored TIMP3 mRNA expression to a level comparable with that after N-LDL alone. Among the genes encoding for MMPs and TIMPs expressed in retinal pericytes, TIMP3 is uniquely regulated by HOG-LDL. Reduced TIMP3 expression might contribute to microvascular abnormalities in diabetic retinopathy.
         datePublished:2007-08-04T00:00:00Z
         dateModified:2007-08-04T00:00:00Z
         pageStart:2200
         pageEnd:2208
         sameAs:https://doi.org/10.1007/s00125-007-0768-z
         keywords:
            Diabetic retinopathy
            Gene array
            Glycation
            Lipoprotein
            Metalloproteinase
            Oxidation
            Internal Medicine
            Metabolic Diseases
            Human Physiology
         image:
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         isPartOf:
            name:Diabetologia
            issn:
               1432-0428
               0012-186X
            volumeNumber:50
            type:
               Periodical
               PublicationVolume
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            name:Springer-Verlag
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               name:J. L. Barth
               affiliation:
                     name:Medical University of South Carolina
                     address:
                        name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
                        type:PostalAddress
                     type:Organization
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               name:Y. Yu
               affiliation:
                     name:University of Oklahoma Health Sciences Center, WP1345
                     address:
                        name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:W. Song
               affiliation:
                     name:University of Oklahoma Health Sciences Center, WP1345
                     address:
                        name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                        type:PostalAddress
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               name:K. Lu
               affiliation:
                     name:University of Oklahoma Health Sciences Center, WP1345
                     address:
                        name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                        type:PostalAddress
                     type:Organization
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               name:A. Dashti
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                     name:University of Oklahoma Health Sciences Center, WP1345
                     address:
                        name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Y. Huang
               affiliation:
                     name:Ralph H. Johnson VA Medical Center
                     address:
                        name:Ralph H. Johnson VA Medical Center, Charleston, USA
                        type:PostalAddress
                     type:Organization
                     name:Medical University of South Carolina
                     address:
                        name:Division of Endocrinology, Diabetes and Medical Genetics, Medical University of South Carolina, Charleston, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:W. S. Argraves
               affiliation:
                     name:Medical University of South Carolina
                     address:
                        name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
                        type:PostalAddress
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               type:Person
               name:T. J. Lyons
               affiliation:
                     name:University of Oklahoma Health Sciences Center, WP1345
                     address:
                        name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                        type:PostalAddress
                     type:Organization
                     name:VA Medical Center
                     address:
                        name:VA Medical Center, Oklahoma City, USA
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               email:[email protected]
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      context:https://schema.org
ScholarlyArticle:
      headline:Oxidised, glycated LDL selectively influences tissue inhibitor of metalloproteinase-3 gene expression and protein production in human retinal capillary pericytes
      description:Matrix metalloproteinases (MMPs) and their natural inhibitors, tissue inhibitor of metalloproteinases (TIMPs), regulate important biological processes including the homeostasis of the extracellular matrix, proteolysis of cell surface proteins, proteinase zymogen activation, angiogenesis and inflammation. Studies have shown that their balance is altered in retinal microvascular tissues in diabetes. Since LDLs modified by oxidation/glycation are implicated in the pathogenesis of diabetic vascular complications, we examined the effects of modified LDL on the gene expression and protein production of MMPs and TIMPs in retinal pericytes. Quiescent human retinal pericytes were exposed to native LDL (N-LDL), glycated LDL (G-LDL) and heavily oxidised and glycated LDL (HOG-LDL) for 24 h. We studied the expression of the genes encoding MMPs and TIMPs mRNAs by analysis of microarray data and quantitative PCR, and protein levels by immunoblotting and ELISA. Microarray analysis showed that MMP1, MMP2, MMP11, MMP14 and MMP25 and TIMP1, TIMP2, TIMP3 and TIMP4 were expressed in pericytes. Of these, only TIMP3 mRNA showed altered regulation, being expressed at significantly lower levels in response to HOG– vs N-LDL. Quantitative PCR and immunoblotting of cell/matrix proteins confirmed the reduction in TIMP3 mRNA and protein in response to HOG-LDL. In contrast to cellular TIMP3 protein, analysis of secreted TIMP1, TIMP2, MMP1 and collagenase activity indicated no changes in their production in response to modified LDL. Combined treatment with N– and HOG-LDL restored TIMP3 mRNA expression to a level comparable with that after N-LDL alone. Among the genes encoding for MMPs and TIMPs expressed in retinal pericytes, TIMP3 is uniquely regulated by HOG-LDL. Reduced TIMP3 expression might contribute to microvascular abnormalities in diabetic retinopathy.
      datePublished:2007-08-04T00:00:00Z
      dateModified:2007-08-04T00:00:00Z
      pageStart:2200
      pageEnd:2208
      sameAs:https://doi.org/10.1007/s00125-007-0768-z
      keywords:
         Diabetic retinopathy
         Gene array
         Glycation
         Lipoprotein
         Metalloproteinase
         Oxidation
         Internal Medicine
         Metabolic Diseases
         Human Physiology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-007-0768-z/MediaObjects/125_2007_768_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-007-0768-z/MediaObjects/125_2007_768_Fig2_HTML.gif
      isPartOf:
         name:Diabetologia
         issn:
            1432-0428
            0012-186X
         volumeNumber:50
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:J. L. Barth
            affiliation:
                  name:Medical University of South Carolina
                  address:
                     name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Y. Yu
            affiliation:
                  name:University of Oklahoma Health Sciences Center, WP1345
                  address:
                     name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:W. Song
            affiliation:
                  name:University of Oklahoma Health Sciences Center, WP1345
                  address:
                     name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:K. Lu
            affiliation:
                  name:University of Oklahoma Health Sciences Center, WP1345
                  address:
                     name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:A. Dashti
            affiliation:
                  name:University of Oklahoma Health Sciences Center, WP1345
                  address:
                     name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Y. Huang
            affiliation:
                  name:Ralph H. Johnson VA Medical Center
                  address:
                     name:Ralph H. Johnson VA Medical Center, Charleston, USA
                     type:PostalAddress
                  type:Organization
                  name:Medical University of South Carolina
                  address:
                     name:Division of Endocrinology, Diabetes and Medical Genetics, Medical University of South Carolina, Charleston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:W. S. Argraves
            affiliation:
                  name:Medical University of South Carolina
                  address:
                     name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:T. J. Lyons
            affiliation:
                  name:University of Oklahoma Health Sciences Center, WP1345
                  address:
                     name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
                     type:PostalAddress
                  type:Organization
                  name:VA Medical Center
                  address:
                     name:VA Medical Center, Oklahoma City, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
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      name:Diabetologia
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         1432-0428
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      volumeNumber:50
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      name:Springer-Verlag
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      name:Medical University of South Carolina
      address:
         name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
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         name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
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      name:University of Oklahoma Health Sciences Center, WP1345
      address:
         name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
         type:PostalAddress
      name:Ralph H. Johnson VA Medical Center
      address:
         name:Ralph H. Johnson VA Medical Center, Charleston, USA
         type:PostalAddress
      name:Medical University of South Carolina
      address:
         name:Division of Endocrinology, Diabetes and Medical Genetics, Medical University of South Carolina, Charleston, USA
         type:PostalAddress
      name:Medical University of South Carolina
      address:
         name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
         type:PostalAddress
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      address:
         name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
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      name:VA Medical Center
      address:
         name:VA Medical Center, Oklahoma City, USA
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Person:
      name:J. L. Barth
      affiliation:
            name:Medical University of South Carolina
            address:
               name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
               type:PostalAddress
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      name:Y. Yu
      affiliation:
            name:University of Oklahoma Health Sciences Center, WP1345
            address:
               name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
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            name:University of Oklahoma Health Sciences Center, WP1345
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               name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
               type:PostalAddress
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      affiliation:
            name:University of Oklahoma Health Sciences Center, WP1345
            address:
               name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
               type:PostalAddress
            type:Organization
      name:A. Dashti
      affiliation:
            name:University of Oklahoma Health Sciences Center, WP1345
            address:
               name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
               type:PostalAddress
            type:Organization
      name:Y. Huang
      affiliation:
            name:Ralph H. Johnson VA Medical Center
            address:
               name:Ralph H. Johnson VA Medical Center, Charleston, USA
               type:PostalAddress
            type:Organization
            name:Medical University of South Carolina
            address:
               name:Division of Endocrinology, Diabetes and Medical Genetics, Medical University of South Carolina, Charleston, USA
               type:PostalAddress
            type:Organization
      name:W. S. Argraves
      affiliation:
            name:Medical University of South Carolina
            address:
               name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
               type:PostalAddress
            type:Organization
      name:T. J. Lyons
      affiliation:
            name:University of Oklahoma Health Sciences Center, WP1345
            address:
               name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
               type:PostalAddress
            type:Organization
            name:VA Medical Center
            address:
               name:VA Medical Center, Oklahoma City, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
      name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
      name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
      name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
      name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
      name:Ralph H. Johnson VA Medical Center, Charleston, USA
      name:Division of Endocrinology, Diabetes and Medical Genetics, Medical University of South Carolina, Charleston, USA
      name:Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, USA
      name:Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center, WP1345, Oklahoma City, USA
      name:VA Medical Center, Oklahoma City, USA

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