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We are analyzing https://link.springer.com/article/10.1007/s00418-005-0788-z.

Title:
Characterization of renal interstitial fibroblast-specific protein 1/S100A4-positive cells in healthy and inflamed rodent kidneys | Histochemistry and Cell Biology
Description:
Fibrosis is considered as a central factor in the loss of renal function in chronic kidney diseases. The origin of fibroblasts and myofibroblasts that accumulate in the interstitium of the diseased kidney is still a matter of debate. It has been shown that accumulation of myofibroblasts in inflamed and fibrotic kidneys is associated with upregulation of fibroblast-specific protein 1 (FSP1, S100A4), not only in the renal interstitium but also in the injured renal epithelia. The tubular expression of FSP1 has been taken as evidence of myofibroblast formation by epithelial–mesenchymal transition (EMT). The identity of FSP1/S100A4 cells has not been defined in detail. We originally intended to use FSP1/S100A4 as a marker of putative EMT in a model of distal tubular injury. However, since the immunoreactivity of FSP1 did not seem to fit with the distribution and shape of fibroblasts or myofibroblasts, we undertook the characterization of FSP1/S100A4-expressing cells in the interstitium of rodent kidneys. We performed immunolabeling for FSP1/S100A4 on thin cryostat sections of perfusion-fixed rat and mouse kidneys with peritubular inflammation, induced by thiazides and glomerulonephritis, respectively, in combination with ecto-5â€Č-nucleotidase (5â€ČNT), recognizing local cortical peritubular fibroblasts, with CD45, MHC class II, CD3, CD4 and Thy 1, recognizing mononuclear cells, with alpha smooth muscle actin (αSMA), as marker for myofibroblasts, and vimentin for intracellular intermediate filaments in cells of mesenchymal origin. In the healthy interstitium of rodents the rare FSP1/S100A4+ cells consistently co-expressed CD45 or lymphocyte surface molecules. Around the injured distal tubules of rats treated for 3–4 days with thiazides, FSP1+/S100A4+, 5â€ČNT+, αSMA+, CD45+ and MHC class II+ cells accumulated. FSP1+/S100A4+ cells consistently co-expressed CD45. In the inflamed regions, αSMA was co-expressed by 5â€ČNT+ cells. In glomerulonephritic mice, FSP1+/S100A4+ cells co-expressed Thy 1, CD4 or CD3. Thus, in the inflamed interstitium around distal tubules of rats and of glomerulonephritic mice, the majority of FSP1+ cells express markers of mononuclear cells. Consequently, the usefulness of FSP1/S100A4 as a tool for detection of (myo)fibroblasts in inflamed kidneys and of EMT in vivo is put into question. In the given rat model the consistent co-expression of αSMA and 5â€ČNT suggests that myofibroblasts originate from resident peritubular fibroblasts.
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Keywords {🔍}

google, scholar, renal, kidney, cells, fibrosis, interstitial, cell, hir, fibroblasts, tubular, int, article, kaissling, nephrol, rat, physiol, protein, myofibroblasts, interstitium, expression, neilson, epithelial, transition, fspsa, kidneys, hegyi, distal, access, soc, invest, function, characterization, inflamed, loffing, fsp, myofibroblast, peritubular, rats, privacy, cookies, content, epithelialmesenchymal, injury, mesenchymal, tubulointerstitial, role, clin, yang, liu,

Topics {✒}

transforming growth factor-beta tgf-beta1-mediated induction month download article/chapter fibroblast-specific protein 1 tubular epithelial–myofibroblast transdifferentiation fsp1+/s100a4+ cells consistently epithelial–mesenchymal transition fsp1/s100a4-expressing cells calcium-binding protein s100a4 epithelial–mesenchymal transitions renal interstitial fibrosis renal interstitial fibrogenesis thiazide treatment dominique cueni-loffing molecular profile author information authors tubular epithelial cells related subjects fsp1/s100a4 cells fsp1+/s100a4+ cells mhc class ii tgf-beta signaling mesenchymal transition interstitial cell types privacy choices/manage cookies progressive renal fibrosis full article pdf mediating tubular epithelial recognizing mononuclear cells progressive tubulointerstitial fibrosis check access instant access ischemic renal failure renal damage progresses acute renal failure renal mhc expression collagen-producing cells distal tubule cells renal vascular injury immune renal injury injured renal epithelia myofibroblast transition interstitial cells cell biology aims anti-fsp1 antibodies intercellular adhesion molecules cowley aw jr vaughan ed jr distal tubular damage european economic area

Questions {❓}

  • Herzlinger D (2002) Renal interstitial fibrosis: remembrance of things past?
  • Mazzucchelli L (2002) Protein S100A4: too long overlooked by pathologists?

Schema {đŸ—ș}

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         headline:Characterization of renal interstitial fibroblast-specific protein 1/S100A4-positive cells in healthy and inflamed rodent kidneys
         description:Fibrosis is considered as a central factor in the loss of renal function in chronic kidney diseases. The origin of fibroblasts and myofibroblasts that accumulate in the interstitium of the diseased kidney is still a matter of debate. It has been shown that accumulation of myofibroblasts in inflamed and fibrotic kidneys is associated with upregulation of fibroblast-specific protein 1 (FSP1, S100A4), not only in the renal interstitium but also in the injured renal epithelia. The tubular expression of FSP1 has been taken as evidence of myofibroblast formation by epithelial–mesenchymal transition (EMT). The identity of FSP1/S100A4 cells has not been defined in detail. We originally intended to use FSP1/S100A4 as a marker of putative EMT in a model of distal tubular injury. However, since the immunoreactivity of FSP1 did not seem to fit with the distribution and shape of fibroblasts or myofibroblasts, we undertook the characterization of FSP1/S100A4-expressing cells in the interstitium of rodent kidneys. We performed immunolabeling for FSP1/S100A4 on thin cryostat sections of perfusion-fixed rat and mouse kidneys with peritubular inflammation, induced by thiazides and glomerulonephritis, respectively, in combination with ecto-5â€Č-nucleotidase (5â€ČNT), recognizing local cortical peritubular fibroblasts, with CD45, MHC class II, CD3, CD4 and Thy 1, recognizing mononuclear cells, with alpha smooth muscle actin (αSMA), as marker for myofibroblasts, and vimentin for intracellular intermediate filaments in cells of mesenchymal origin. In the healthy interstitium of rodents the rare FSP1/S100A4+ cells consistently co-expressed CD45 or lymphocyte surface molecules. Around the injured distal tubules of rats treated for 3–4 days with thiazides, FSP1+/S100A4+, 5â€ČNT+, αSMA+, CD45+ and MHC class II+ cells accumulated. FSP1+/S100A4+ cells consistently co-expressed CD45. In the inflamed regions, αSMA was co-expressed by 5â€ČNT+ cells. In glomerulonephritic mice, FSP1+/S100A4+ cells co-expressed Thy 1, CD4 or CD3. Thus, in the inflamed interstitium around distal tubules of rats and of glomerulonephritic mice, the majority of FSP1+ cells express markers of mononuclear cells. Consequently, the usefulness of FSP1/S100A4 as a tool for detection of (myo)fibroblasts in inflamed kidneys and of EMT in vivo is put into question. In the given rat model the consistent co-expression of αSMA and 5â€ČNT suggests that myofibroblasts originate from resident peritubular fibroblasts.
         datePublished:2005-04-26T00:00:00Z
         dateModified:2005-04-26T00:00:00Z
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            Epithelial mesenchymal transition
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            Cell Biology
            Biochemistry
            Developmental Biology
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      headline:Characterization of renal interstitial fibroblast-specific protein 1/S100A4-positive cells in healthy and inflamed rodent kidneys
      description:Fibrosis is considered as a central factor in the loss of renal function in chronic kidney diseases. The origin of fibroblasts and myofibroblasts that accumulate in the interstitium of the diseased kidney is still a matter of debate. It has been shown that accumulation of myofibroblasts in inflamed and fibrotic kidneys is associated with upregulation of fibroblast-specific protein 1 (FSP1, S100A4), not only in the renal interstitium but also in the injured renal epithelia. The tubular expression of FSP1 has been taken as evidence of myofibroblast formation by epithelial–mesenchymal transition (EMT). The identity of FSP1/S100A4 cells has not been defined in detail. We originally intended to use FSP1/S100A4 as a marker of putative EMT in a model of distal tubular injury. However, since the immunoreactivity of FSP1 did not seem to fit with the distribution and shape of fibroblasts or myofibroblasts, we undertook the characterization of FSP1/S100A4-expressing cells in the interstitium of rodent kidneys. We performed immunolabeling for FSP1/S100A4 on thin cryostat sections of perfusion-fixed rat and mouse kidneys with peritubular inflammation, induced by thiazides and glomerulonephritis, respectively, in combination with ecto-5â€Č-nucleotidase (5â€ČNT), recognizing local cortical peritubular fibroblasts, with CD45, MHC class II, CD3, CD4 and Thy 1, recognizing mononuclear cells, with alpha smooth muscle actin (αSMA), as marker for myofibroblasts, and vimentin for intracellular intermediate filaments in cells of mesenchymal origin. In the healthy interstitium of rodents the rare FSP1/S100A4+ cells consistently co-expressed CD45 or lymphocyte surface molecules. Around the injured distal tubules of rats treated for 3–4 days with thiazides, FSP1+/S100A4+, 5â€ČNT+, αSMA+, CD45+ and MHC class II+ cells accumulated. FSP1+/S100A4+ cells consistently co-expressed CD45. In the inflamed regions, αSMA was co-expressed by 5â€ČNT+ cells. In glomerulonephritic mice, FSP1+/S100A4+ cells co-expressed Thy 1, CD4 or CD3. Thus, in the inflamed interstitium around distal tubules of rats and of glomerulonephritic mice, the majority of FSP1+ cells express markers of mononuclear cells. Consequently, the usefulness of FSP1/S100A4 as a tool for detection of (myo)fibroblasts in inflamed kidneys and of EMT in vivo is put into question. In the given rat model the consistent co-expression of αSMA and 5â€ČNT suggests that myofibroblasts originate from resident peritubular fibroblasts.
      datePublished:2005-04-26T00:00:00Z
      dateModified:2005-04-26T00:00:00Z
      pageStart:335
      pageEnd:346
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         Kidney
         Fibroblast
         Myofibroblast
         Epithelial mesenchymal transition
         Thiazide
         FSP1
         S100A4
         Renal interstitium
         Biomedicine
         general
         Cell Biology
         Biochemistry
         Developmental Biology
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            name:Ivan Hegyi
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                  name:Institut fĂŒr Klinische Pathologie, University of ZĂŒrich
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                     type:PostalAddress
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            name:Dominique Cueni-Loffing
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                  name: Division of Vegetative Anatomy, University of Zurich
                  address:
                     name:Anatomical Institute, Division of Vegetative Anatomy, University of Zurich, Zurich, Switzerland
                     type:PostalAddress
                  type:Organization
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            name:Johannes Loffing
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                     name:Institut d‘Anatomie UniversitĂ© de Fribourg, Zurich, Switzerland
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               name:Anatomical Institute, Division of Vegetative Anatomy, University of Zurich, Zurich, Switzerland
               type:PostalAddress
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      name:Ivan Hegyi
      affiliation:
            name:Institut fĂŒr Klinische Pathologie, University of ZĂŒrich
            address:
               name:Department of Pathology, Institut fĂŒr Klinische Pathologie, University of ZĂŒrich, Zurich, Switzerland
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      name:Dominique Cueni-Loffing
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            name: Division of Vegetative Anatomy, University of Zurich
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               name:Anatomical Institute, Division of Vegetative Anatomy, University of Zurich, Zurich, Switzerland
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      name:Johannes Loffing
      affiliation:
            name:Institut d‘Anatomie UniversitĂ© de Fribourg
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      name:Anatomical Institute, Division of Vegetative Anatomy, University of Zurich, Zurich, Switzerland
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      name:Anatomical Institute, Division of Vegetative Anatomy, University of Zurich, Zurich, Switzerland
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