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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00018-024-05570-z.

Title:
Serotonin receptor 5-HT7 modulates inflammatory-associated functions of macrophages | Cellular and Molecular Life Sciences
Description:
The hormone and neurotransmitter serotonin regulates numerous physiological functions within the central nervous system and in the periphery upon binding to specific receptors. In the periphery, the serotonin receptor 7 (5-HT7R) is expressed on different immune cells including monocytes and macrophages. To investigate the impact of 5-HT7R-mediated signaling on macrophage properties, we used human THP-1 cells and differentiated them into pro-inflammatory M1- and anti-inflammatory M2-like macrophages. Pharmacological 5-HT7R activation with the specific agonist LP-211 especially modulates morphology of M1-like macrophages by increasing the number of rounded cells. Furthermore, 5-HT7R stimulation results in significantly reduced phagocytic and migratory ability of M1-like macrophages. Noteworthy, LP-211 treatment leads to changes in secretory properties of all macrophage types with the highest effects obtained for M0- and M2c-like macrophages. Finally, the importance of 5-HT7R for regulation of phagocytosis was confirmed in human primary CD14+ cells. These results indicate that 5-HT7R activation selectively impairs basic functions of macrophages and might thus be a new access point for the modulation of macrophage responses in the future treatment of inflammatory diseases.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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

We can't figure out the monetization strategy.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

macrophages, pubmed, article, cells, google, scholar, mlike, cas, htr, macrophage, cell, fig, phagocytosis, expression, differentiation, signaling, central, thp, treatment, activation, analysis, human, levels, serotonin, subtypes, thpderived, proinflammatory, morphology, mclike, receptor, protein, basal, secretion, mrna, monocytes, immunol, phagocytic, cytokine, day, conditions, data, properties, stimulation, min, reduced, cytokines, dmso, statistical, receptors, htrmediated,

Topics {✒️}

melanie ricke-hoch pe/dazzle 594-anti-human cd105 tumor necrosis factor-α granulocyte-colony-stimulating factor de casas-engel pe/cyanine7-anti-human cd11b apc-anti-human hla-dr cyclic amp-epac1-rap1 pathway macrophage colony-stimulating factor phorbol-12-myristat-13-acetat qrt-pcr anti-inflammatory gene profile goat anti-rabbit igg rabbit anti-goat igg article download pdf pe-anti-human cd200r thp-1-derived pro-inflammatory m1 5-ht7r-pka signaling axis high-affinity serotonin receptor quantitative real-time pcr custom-written matlab script signalboost™immunoreaction enhancer kit anti-human cd14-microbeads fitc-anti-human cd64 denise hilfiker-kleiner texas red-coupled zymosan scavenger receptor-ai/ii evgeni ponimaskin pe-anti-human cd86 ariamx realtime-pcr system human monocyte-derived macrophages anti-5ht7 receptor/htr7 unpaired mann-whitney test ricke-hoch investigating 5-ht7r-mediated signaling g12 protein-mediated activation 5ht7r-mediated signaling plays αmβ2 integrin-mediated adhesion bv421-anti-human cd163 thp-1-derived macrophages represent thp-1-derived macrophages correlated central nervous system view epac-rap1-mediated activation central 5-ht receptors exhibits multiligand-binding properties enhance t-cell activation thp-1-derived macrophage morphology post-golgi trafficking processes 5-ht2br-mediated signaling influence pan-macrophage marker cd11b

Questions {❓}

  • Bahr FS, Ricke-Hoch M, Ponimaskin E, Müller FE (2024) Serotonin receptors in myocardial infarction: friend or foe?
  • Strizova Z, Benesova I, Bartolini R et al (2023) M1/M2 macrophages and their overlaps– myth or reality?
  • Tedesco S, De Majo F, Kim J et al (2018) Convenience versus biological significance: are PMA-Differentiated THP-1 cells a Reliable Substitute for blood-derived macrophages when studying in Vitro polarization?
  • What mechanism could underlie 5-HT7R-mediated regulation of phagocytosis?

Schema {🗺️}

WebPage:
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         headline:Serotonin receptor 5-HT7 modulates inflammatory-associated functions of macrophages
         description:The hormone and neurotransmitter serotonin regulates numerous physiological functions within the central nervous system and in the periphery upon binding to specific receptors. In the periphery, the serotonin receptor 7 (5-HT7R) is expressed on different immune cells including monocytes and macrophages. To investigate the impact of 5-HT7R-mediated signaling on macrophage properties, we used human THP-1 cells and differentiated them into pro-inflammatory M1- and anti-inflammatory M2-like macrophages. Pharmacological 5-HT7R activation with the specific agonist LP-211 especially modulates morphology of M1-like macrophages by increasing the number of rounded cells. Furthermore, 5-HT7R stimulation results in significantly reduced phagocytic and migratory ability of M1-like macrophages. Noteworthy, LP-211 treatment leads to changes in secretory properties of all macrophage types with the highest effects obtained for M0- and M2c-like macrophages. Finally, the importance of 5-HT7R for regulation of phagocytosis was confirmed in human primary CD14+ cells. These results indicate that 5-HT7R activation selectively impairs basic functions of macrophages and might thus be a new access point for the modulation of macrophage responses in the future treatment of inflammatory diseases.
         datePublished:2025-01-21T00:00:00Z
         dateModified:2025-01-21T00:00:00Z
         pageStart:1
         pageEnd:19
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            THP-1 cells
            Serotonin
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            Phagocytosis
            Cell Biology
            Biomedicine
            general
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            Biochemistry
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                        name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
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ScholarlyArticle:
      headline:Serotonin receptor 5-HT7 modulates inflammatory-associated functions of macrophages
      description:The hormone and neurotransmitter serotonin regulates numerous physiological functions within the central nervous system and in the periphery upon binding to specific receptors. In the periphery, the serotonin receptor 7 (5-HT7R) is expressed on different immune cells including monocytes and macrophages. To investigate the impact of 5-HT7R-mediated signaling on macrophage properties, we used human THP-1 cells and differentiated them into pro-inflammatory M1- and anti-inflammatory M2-like macrophages. Pharmacological 5-HT7R activation with the specific agonist LP-211 especially modulates morphology of M1-like macrophages by increasing the number of rounded cells. Furthermore, 5-HT7R stimulation results in significantly reduced phagocytic and migratory ability of M1-like macrophages. Noteworthy, LP-211 treatment leads to changes in secretory properties of all macrophage types with the highest effects obtained for M0- and M2c-like macrophages. Finally, the importance of 5-HT7R for regulation of phagocytosis was confirmed in human primary CD14+ cells. These results indicate that 5-HT7R activation selectively impairs basic functions of macrophages and might thus be a new access point for the modulation of macrophage responses in the future treatment of inflammatory diseases.
      datePublished:2025-01-21T00:00:00Z
      dateModified:2025-01-21T00:00:00Z
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      pageEnd:19
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         Macrophages
         THP-1 cells
         Serotonin
         5-HT7 receptor
         Phagocytosis
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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                  name:Hannover Medical School
                  address:
                     name:Cellular Neurophysiology, Hannover Medical School, Hannover, Germany
                     type:PostalAddress
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                  address:
                     name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
                     type:PostalAddress
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                  name:Hannover Medical School
                  address:
                     name:Centre for Pharmacology and Toxicology, Hannover Medical School, Hannover, Germany
                     type:PostalAddress
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                  name:Hannover Medical School
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                     name:Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany
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                  name:Hannover Medical School
                  address:
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                     type:PostalAddress
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                  name:Medical Faculty of the Philipps-University Marburg, Department of Cardiovascular Complications of Oncologic Therapies
                  address:
                     name:Medical Faculty of the Philipps-University Marburg, Department of Cardiovascular Complications of Oncologic Therapies, Marburg, Germany
                     type:PostalAddress
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            name:Melanie Ricke-Hoch
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                  address:
                     name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
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            name:Evgeni Ponimaskin
            url:http://orcid.org/0000-0002-4570-5130
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                  name:Hannover Medical School
                  address:
                     name:Cellular Neurophysiology, Hannover Medical School, Hannover, Germany
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            name:Hannover Medical School
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               name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
               type:PostalAddress
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            name:Hannover Medical School
            address:
               name:Centre for Pharmacology and Toxicology, Hannover Medical School, Hannover, Germany
               type:PostalAddress
            type:Organization
      name:Michaela Scherr
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            name:Hannover Medical School
            address:
               name:Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany
               type:PostalAddress
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      name:Christine S. Falk
      url:http://orcid.org/0000-0003-1376-7318
      affiliation:
            name:Hannover Medical School
            address:
               name:Institute of Transplant Immunology, Hannover Medical School, Hannover, Germany
               type:PostalAddress
            type:Organization
            name:German Center for Infection Research, DZIF, TTU-IICH
            address:
               name:German Center for Infection Research, DZIF, TTU-IICH, Hannover, Germany
               type:PostalAddress
            type:Organization
      name:Denise Hilfiker-Kleiner
      url:http://orcid.org/0000-0001-6065-9649
      affiliation:
            name:Hannover Medical School
            address:
               name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
               type:PostalAddress
            type:Organization
            name:Medical Faculty of the Philipps-University Marburg, Department of Cardiovascular Complications of Oncologic Therapies
            address:
               name:Medical Faculty of the Philipps-University Marburg, Department of Cardiovascular Complications of Oncologic Therapies, Marburg, Germany
               type:PostalAddress
            type:Organization
      name:Melanie Ricke-Hoch
      url:http://orcid.org/0000-0001-5479-2275
      affiliation:
            name:Hannover Medical School
            address:
               name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
               type:PostalAddress
            type:Organization
      name:Evgeni Ponimaskin
      url:http://orcid.org/0000-0002-4570-5130
      affiliation:
            name:Hannover Medical School
            address:
               name:Cellular Neurophysiology, Hannover Medical School, Hannover, Germany
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Cellular Neurophysiology, Hannover Medical School, Hannover, Germany
      name:Cellular Neurophysiology, Hannover Medical School, Hannover, Germany
      name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
      name:Cellular Neurophysiology, Hannover Medical School, Hannover, Germany
      name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
      name:Centre for Pharmacology and Toxicology, Hannover Medical School, Hannover, Germany
      name:Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany
      name:Institute of Transplant Immunology, Hannover Medical School, Hannover, Germany
      name:German Center for Infection Research, DZIF, TTU-IICH, Hannover, Germany
      name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
      name:Medical Faculty of the Philipps-University Marburg, Department of Cardiovascular Complications of Oncologic Therapies, Marburg, Germany
      name:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
      name:Cellular Neurophysiology, Hannover Medical School, Hannover, Germany

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