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We are analyzing https://link.springer.com/article/10.1186/1471-2121-11-29.

Title:
Mesenchymal stem cells rescue cardiomyoblasts from cell death in an in vitro ischemia model via direct cell-to-cell connections | BMC Molecular and Cell Biology
Description:
Background Bone marrow derived mesenchymal stem cells (MSCs) are promising candidates for cell based therapies in myocardial infarction. However, the exact underlying cellular mechanisms are still not fully understood. Our aim was to explore the possible role of direct cell-to-cell interaction between ischemic H9c2 cardiomyoblasts and normal MSCs. Using an in vitro ischemia model of 150 minutes of oxygen glucose deprivation we investigated cell viability and cell interactions with confocal microscopy and flow cytometry. Results Our model revealed that adding normal MSCs to the ischemic cell population significantly decreased the ratio of dead H9c2 cells (H9c2 only: 0.85 ± 0.086 vs. H9c2+MSCs: 0.16 ± 0.035). This effect was dependent on direct cell-to-cell contact since co-cultivation with MSCs cultured in cell inserts did not exert the same beneficial effect (ratio of dead H9c2 cells: 0.90 ± 0.055). Confocal microscopy revealed that cardiomyoblasts and MSCs frequently formed 200-500 nm wide intercellular connections and cell fusion rarely occurred between these cells. Conclusion Based on these results we hypothesize that mesenchymal stem cells may reduce the number of dead cardiomyoblasts after ischemic damage via direct cell-to-cell interactions and intercellular tubular connections may play an important role in these processes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Telecommunications
  • Education

Content Management System {📝}

What CMS is link.springer.com built with?


Link.springer.com utilizes APACHE LENYA.

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 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We don't see any clear sign of profit-making.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

cells, cell, stem, mscs, article, ogd, google, scholar, pubmed, cardiomyoblasts, figure, mesenchymal, fusion, hours, cas, celltocell, vitro, cardiomyocytes, culture, time, flow, dead, bone, red, double, analysis, direct, connections, microscopy, labeled, cytometry, file, model, number, marrow, damaged, ischemia, effect, heart, added, authors, res, ischemic, minutes, confocal, intercellular, cardiac, tissue, found, paracrine,

Topics {✒️}

levente kiss & zsombor lacza bone-marrow-derived cells oxygen glucose deprivation time-lapse video microscopy article download pdf rescue post-ischemic cardiomyoblasts mesenchymal stem cells hungarian science mesenchymal stem cell bone marrow cells short-lived tubular connections rescue factor time lapse pictures rescuing post-ischemic cardiomyoblasts related subjects modifying ventricular remodeling post-ischemic cardiomyoblasts interact dio-labeled h9c2 cells cardiovascular revascularization medicine stem cell transplantation haematopoietic stem cells labeled stem cell full size image privacy choices/manage cookies stem cell grafting diseases glucose-free dmem brain research protocols stem cells failed clinical experimental research cardiac cell lineages bone marrow complete rightward shift rescue aerobic respiration cardiac myocytes leading garcia-verdugo jm low glucose dmem flow cytometry files authors’ original file preserve heart tissue ischemically damaged cells full access partial cell fusion post-ischemic cardiomyoblasts heart tissue repair healthy cells contacted side scatter plot constantly changing web postinfarcted rat myocardium data represent

Questions {❓}

  • Kaplan LD: The analysis of articular cartilage after thermal exposure: "Is red really dead?
  • Koyanagi M, Brandes RP, Haendeler J, Zeiher AM, Dimmeler S: Cell-to-Cell Connection of Endothelial Progenitor Cells With Cardiac Myocytes by Nanotubes: A Novel Mechanism for Cell Fate Changes?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Mesenchymal stem cells rescue cardiomyoblasts from cell death in an in vitro ischemia model via direct cell-to-cell connections
         description:Bone marrow derived mesenchymal stem cells (MSCs) are promising candidates for cell based therapies in myocardial infarction. However, the exact underlying cellular mechanisms are still not fully understood. Our aim was to explore the possible role of direct cell-to-cell interaction between ischemic H9c2 cardiomyoblasts and normal MSCs. Using an in vitro ischemia model of 150 minutes of oxygen glucose deprivation we investigated cell viability and cell interactions with confocal microscopy and flow cytometry. Our model revealed that adding normal MSCs to the ischemic cell population significantly decreased the ratio of dead H9c2 cells (H9c2 only: 0.85 ± 0.086 vs. H9c2+MSCs: 0.16 ± 0.035). This effect was dependent on direct cell-to-cell contact since co-cultivation with MSCs cultured in cell inserts did not exert the same beneficial effect (ratio of dead H9c2 cells: 0.90 ± 0.055). Confocal microscopy revealed that cardiomyoblasts and MSCs frequently formed 200-500 nm wide intercellular connections and cell fusion rarely occurred between these cells. Based on these results we hypothesize that mesenchymal stem cells may reduce the number of dead cardiomyoblasts after ischemic damage via direct cell-to-cell interactions and intercellular tubular connections may play an important role in these processes.
         datePublished:2010-04-20T00:00:00Z
         dateModified:2010-04-20T00:00:00Z
         pageStart:1
         pageEnd:11
         license:http://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1471-2121-11-29
         keywords:
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            Cell Fusion
            H9c2 Cell
            Oxygen Glucose Deprivation
            Paracrine Factor
            Cell Biology
            Biological Microscopy
            Life Sciences
            general
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            issn:
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         author:
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                        type:PostalAddress
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               name:Levente Kiss
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                     name:Semmelweis University
                     address:
                        name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
                        type:PostalAddress
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               name:Zsombor Lacza
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                     name:Semmelweis University
                     address:
                        name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
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ScholarlyArticle:
      headline:Mesenchymal stem cells rescue cardiomyoblasts from cell death in an in vitro ischemia model via direct cell-to-cell connections
      description:Bone marrow derived mesenchymal stem cells (MSCs) are promising candidates for cell based therapies in myocardial infarction. However, the exact underlying cellular mechanisms are still not fully understood. Our aim was to explore the possible role of direct cell-to-cell interaction between ischemic H9c2 cardiomyoblasts and normal MSCs. Using an in vitro ischemia model of 150 minutes of oxygen glucose deprivation we investigated cell viability and cell interactions with confocal microscopy and flow cytometry. Our model revealed that adding normal MSCs to the ischemic cell population significantly decreased the ratio of dead H9c2 cells (H9c2 only: 0.85 ± 0.086 vs. H9c2+MSCs: 0.16 ± 0.035). This effect was dependent on direct cell-to-cell contact since co-cultivation with MSCs cultured in cell inserts did not exert the same beneficial effect (ratio of dead H9c2 cells: 0.90 ± 0.055). Confocal microscopy revealed that cardiomyoblasts and MSCs frequently formed 200-500 nm wide intercellular connections and cell fusion rarely occurred between these cells. Based on these results we hypothesize that mesenchymal stem cells may reduce the number of dead cardiomyoblasts after ischemic damage via direct cell-to-cell interactions and intercellular tubular connections may play an important role in these processes.
      datePublished:2010-04-20T00:00:00Z
      dateModified:2010-04-20T00:00:00Z
      pageStart:1
      pageEnd:11
      license:http://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1471-2121-11-29
      keywords:
         Mesenchymal Stem Cell
         Cell Fusion
         H9c2 Cell
         Oxygen Glucose Deprivation
         Paracrine Factor
         Cell Biology
         Biological Microscopy
         Life Sciences
         general
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                     name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
                     type:PostalAddress
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            name:Eszter M Horváth
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                  name:Semmelweis University
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                     name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
                     type:PostalAddress
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            name:Levente Kiss
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                  name:Semmelweis University
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            name:Zsombor Lacza
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         name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
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         name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
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            name:Semmelweis University
            address:
               name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Eszter Pankotai
      affiliation:
            name:Semmelweis University
            address:
               name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
               type:PostalAddress
            type:Organization
      name:Eszter M Horváth
      affiliation:
            name:Semmelweis University
            address:
               name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
               type:PostalAddress
            type:Organization
      name:Levente Kiss
      affiliation:
            name:Semmelweis University
            address:
               name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
               type:PostalAddress
            type:Organization
      name:Zsombor Lacza
      affiliation:
            name:Semmelweis University
            address:
               name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
      name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
      name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
      name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
      name:Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary

External Links {🔗}(153)

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