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We are analyzing https://link.springer.com/article/10.1186/1471-213x-11-21.

Title:
The zebrafish heart regenerates after cryoinjury-induced myocardial infarction | BMC Developmental Biology
Description:
Background In humans, myocardial infarction is characterized by irreversible loss of heart tissue, which becomes replaced with a fibrous scar. By contrast, teleost fish and urodele amphibians are capable of heart regeneration after a partial amputation. However, due to the lack of a suitable infarct model, it is not known how these animals respond to myocardial infarction. Results Here, we have established a heart infarct model in zebrafish using cryoinjury. In contrast to the common method of partial resection, cryoinjury results in massive cell death within 20% of the ventricular wall, similar to that observed in mammalian infarcts. As in mammals, the initial stages of the injury response include thrombosis, accumulation of fibroblasts and collagen deposition. However, at later stages, cardiac cells can enter the cell cycle and invade the infarct area in zebrafish. In the subsequent two months, fibrotic scar tissue is progressively eliminated by cell apoptosis and becomes replaced with a new myocardium, resulting in scarless regeneration. We show that tissue remodeling at the myocardial-infarct border zone is associated with accumulation of Vimentin-positive fibroblasts and with expression of an extracellular matrix protein Tenascin-C. Electrocardiogram analysis demonstrated that the reconstitution of the cardiac muscle leads to the restoration of the heart function. Conclusions We developed a new cryoinjury model to induce myocardial infarction in zebrafish. Although the initial stages following cryoinjury resemble typical healing in mammals, the zebrafish heart is capable of structural and functional regeneration. Understanding the key healing processes after myocardial infarction in zebrafish may result in identification of the barriers to efficient cardiac regeneration in mammals.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Fitness & Wellness
  • Education

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

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


Based on our best estimate, this website will receive around 8,280,528 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

heart, pubmed, article, dpci, zebrafish, regeneration, myocardium, cell, figure, google, scholar, cells, cas, cardiomyocytes, tissue, cardiac, myocardial, postinfarct, cryoinjury, infarct, ventricular, infarction, ventricle, scar, wall, area, file, injury, collagen, fibroblasts, hearts, tnc, fish, proliferation, sections, additional, fibrin, apoptosis, zone, blue, central, analysis, resection, matrix, cardiomyocyte, time, size, detected, red, authors,

Topics {✒️}

mcm5/dsred2-nuc-positive nuclei relative open access article brdu-cell-proliferation assay demonstrated goat anti-rabbit cy5 dsred2-nuc/mcm5-positive nuclei van luyn mj article download pdf reveals fibroblast-cardiomyocyte coupling jim jung-ching lin possesses counter-adhesive properties de-adhesive ecm protein cmlc-2 cardiomyocyte-specific promoter anti-digoxigenin fluorescein conjugated protease-rich environment leading tnc counter-adhesive domains cardiac-specific cmlc-2 promoter mcm5/dsred-positive cells massive cell death quadruple-stained cross-sections anti-vimentin antibodies react full size image α-sma-positive cells terminal transferase post-infarct zone extends apical-lateral ventricular wall heart cross-sections stained fibrin-based provisional matrix cryoinjury-induced myocardial infarction digoxigenin-dutp solution article chablais related subjects large disk-shaped damage cardiovascular regeneration damaged tpm-positive myocardium privacy choices/manage cookies anna jaźwińska vim/tnc-expressing cells intermediate filament protein remaining post-infarct region rabbit anti-mcm5 myocardial-infarct border zone post-infarct area decreased authors’ original file rabbit anti-mef-2 enhanced cardiomyocyte proliferation dsred2-positive nuclei complete myocardial regeneration trigger cardiomyocyte proliferation full access cell-cycle entry

Questions {❓}

  • Borchardt T, Braun T: Cardiovascular regeneration in non-mammalian model systems: what are the differences between newts and man?

Schema {🗺️}

WebPage:
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         headline:The zebrafish heart regenerates after cryoinjury-induced myocardial infarction
         description:In humans, myocardial infarction is characterized by irreversible loss of heart tissue, which becomes replaced with a fibrous scar. By contrast, teleost fish and urodele amphibians are capable of heart regeneration after a partial amputation. However, due to the lack of a suitable infarct model, it is not known how these animals respond to myocardial infarction. Here, we have established a heart infarct model in zebrafish using cryoinjury. In contrast to the common method of partial resection, cryoinjury results in massive cell death within 20% of the ventricular wall, similar to that observed in mammalian infarcts. As in mammals, the initial stages of the injury response include thrombosis, accumulation of fibroblasts and collagen deposition. However, at later stages, cardiac cells can enter the cell cycle and invade the infarct area in zebrafish. In the subsequent two months, fibrotic scar tissue is progressively eliminated by cell apoptosis and becomes replaced with a new myocardium, resulting in scarless regeneration. We show that tissue remodeling at the myocardial-infarct border zone is associated with accumulation of Vimentin-positive fibroblasts and with expression of an extracellular matrix protein Tenascin-C. Electrocardiogram analysis demonstrated that the reconstitution of the cardiac muscle leads to the restoration of the heart function. We developed a new cryoinjury model to induce myocardial infarction in zebrafish. Although the initial stages following cryoinjury resemble typical healing in mammals, the zebrafish heart is capable of structural and functional regeneration. Understanding the key healing processes after myocardial infarction in zebrafish may result in identification of the barriers to efficient cardiac regeneration in mammals.
         datePublished:2011-04-07T00:00:00Z
         dateModified:2011-04-07T00:00:00Z
         pageStart:1
         pageEnd:13
         license:https://creativecommons.org/licenses/by/2.0
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            Heart Infarct
            Heart Regeneration
            Cardiomyocyte Proliferation
            Massive Cell Death
            Zebrafish Heart
            Developmental Biology
            Animal Models
            Life Sciences
            general
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                        name:Department of Medicine, Unit of Anatomy, University of Fribourg, Fribourg, Switzerland
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                        name:Department of Biology, Unit of Zoology, University of Fribourg, Fribourg, Switzerland
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ScholarlyArticle:
      headline:The zebrafish heart regenerates after cryoinjury-induced myocardial infarction
      description:In humans, myocardial infarction is characterized by irreversible loss of heart tissue, which becomes replaced with a fibrous scar. By contrast, teleost fish and urodele amphibians are capable of heart regeneration after a partial amputation. However, due to the lack of a suitable infarct model, it is not known how these animals respond to myocardial infarction. Here, we have established a heart infarct model in zebrafish using cryoinjury. In contrast to the common method of partial resection, cryoinjury results in massive cell death within 20% of the ventricular wall, similar to that observed in mammalian infarcts. As in mammals, the initial stages of the injury response include thrombosis, accumulation of fibroblasts and collagen deposition. However, at later stages, cardiac cells can enter the cell cycle and invade the infarct area in zebrafish. In the subsequent two months, fibrotic scar tissue is progressively eliminated by cell apoptosis and becomes replaced with a new myocardium, resulting in scarless regeneration. We show that tissue remodeling at the myocardial-infarct border zone is associated with accumulation of Vimentin-positive fibroblasts and with expression of an extracellular matrix protein Tenascin-C. Electrocardiogram analysis demonstrated that the reconstitution of the cardiac muscle leads to the restoration of the heart function. We developed a new cryoinjury model to induce myocardial infarction in zebrafish. Although the initial stages following cryoinjury resemble typical healing in mammals, the zebrafish heart is capable of structural and functional regeneration. Understanding the key healing processes after myocardial infarction in zebrafish may result in identification of the barriers to efficient cardiac regeneration in mammals.
      datePublished:2011-04-07T00:00:00Z
      dateModified:2011-04-07T00:00:00Z
      pageStart:1
      pageEnd:13
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1471-213X-11-21
      keywords:
         Heart Infarct
         Heart Regeneration
         Cardiomyocyte Proliferation
         Massive Cell Death
         Zebrafish Heart
         Developmental Biology
         Animal Models
         Life Sciences
         general
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                  address:
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                     type:PostalAddress
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                  name:University of Fribourg
                  address:
                     name:Department of Medicine, Unit of Anatomy, University of Fribourg, Fribourg, Switzerland
                     type:PostalAddress
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                  address:
                     name:Department of Biology, Unit of Zoology, University of Fribourg, Fribourg, Switzerland
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      address:
         name:Department of Medicine, Unit of Anatomy, University of Fribourg, Fribourg, Switzerland
         type:PostalAddress
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      address:
         name:Department of Biology, Unit of Zoology, University of Fribourg, Fribourg, Switzerland
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      name:Fabian Chablais
      affiliation:
            name:University of Fribourg
            address:
               name:Department of Medicine, Unit of Anatomy, University of Fribourg, Fribourg, Switzerland
               type:PostalAddress
            type:Organization
            name:University of Fribourg
            address:
               name:Department of Biology, Unit of Zoology, University of Fribourg, Fribourg, Switzerland
               type:PostalAddress
            type:Organization
      name:Julia Veit
      affiliation:
            name:University of Fribourg
            address:
               name:Department of Medicine, Unit of Physiology, University of Fribourg, Fribourg, Switzerland
               type:PostalAddress
            type:Organization
      name:Gregor Rainer
      affiliation:
            name:University of Fribourg
            address:
               name:Department of Medicine, Unit of Physiology, University of Fribourg, Fribourg, Switzerland
               type:PostalAddress
            type:Organization
      name:Anna Jaźwińska
      affiliation:
            name:University of Fribourg
            address:
               name:Department of Medicine, Unit of Anatomy, University of Fribourg, Fribourg, Switzerland
               type:PostalAddress
            type:Organization
            name:University of Fribourg
            address:
               name:Department of Biology, Unit of Zoology, University of Fribourg, Fribourg, Switzerland
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Medicine, Unit of Anatomy, University of Fribourg, Fribourg, Switzerland
      name:Department of Biology, Unit of Zoology, University of Fribourg, Fribourg, Switzerland
      name:Department of Medicine, Unit of Physiology, University of Fribourg, Fribourg, Switzerland
      name:Department of Medicine, Unit of Physiology, University of Fribourg, Fribourg, Switzerland
      name:Department of Medicine, Unit of Anatomy, University of Fribourg, Fribourg, Switzerland
      name:Department of Biology, Unit of Zoology, University of Fribourg, Fribourg, Switzerland

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