We are analyzing https://link.springer.com/article/10.1007/s11605-003-0037-5.

Title:
Induction of MIC-1/growth differentiation factor-15 following bile duct injury | Journal of Gastrointestinal Surgery
Description:
Macrophage inflammatory peptide-1 (MIC-1)/growth/differentiation factor-15 (GDF-15) is a divergent member of the transforming growth factor-β superfamily cloned by others and us. MIC-1/GDF-15 is expressed in the liver, breast, and colon. Studies have demonstrated a growth-inhibiting effect of MIC-1/GDF-15 on colon and breast cancer cell lines in vitro and on tumor growth in vivo. We previously reported that MIC-1 expression is rapidly induced after a wide variety of murine acute and chronic liver injuries including aniline dye administration. I hypothesized, therefore, that MIC-1/GDF-15 may be a mediator of biliary tract injury and could play a role in regulation of bile duct proliferation. C57BL/6 mice underwent surgical ligation of the common bile duct. Northern blot analysis revealed a time-dependent induction of MIC-1/GDF-15 mRNA in the liver. In situ hybridization of liver sections for MIC-1/GDF-15 expression after bile duct ligation demonstrated a zone 1 or periportal expression pattern, consistent with expression of MIC-1 in periductular hepatocytes. Northern blot analysis of liver mRNA from patients with sclerosing cholangitis or cirrhosis also demonstrated enhanced expression of MIC-1/GDF-15. MIC-1/GDF-15 is expressed after bile duct injury in mice and humans. Taken together with the previously demonstrated growth inhibitory effects of MIC-1/GDF-15 on normal and transformed cells, MIC-1/ GDF-15 may play a role in regulation of bile duct proliferation and biliary tumor formation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Science
Social Networks

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 7,626,932 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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 might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

article, google, scholar, cas, pubmed, growth, bile, expression, duct, liver, koniaris, gene, factor, micgdf, tgfbeta, member, superfamily, human, journal, induction, injury, transforming, access, cytokine, privacy, cookies, content, tumor, mic, biliary, mice, inhibitory, baek, publish, search, surgery, macrophage, expressed, demonstrated, tract, cells, characterization, biol, protein, eling, nonsteroidal, antiinflammatory, analysis, data, information,

Topics {✒️}

biliary tract injury nonsteroidal anti-inflammatory drugs month download article/chapter cholestatic liver disease antitumorigenic nsaid-activated gene biliary tumor formation mic-1/growth differentiation factor-15 nested case-control study tgf-beta signaling pathway bile duct injury common bile duct bile duct proliferation /growth/differentiation factor-15 growth-differentiation factor 15 macrophage inhibitory cytokine macrophage inhibitory cytokine-1 tgf-beta family nsaid-activated gene tgf-beta superfamily growth-inhibiting effect full article pdf tgf-beta pathway privacy choices/manage cookies northern blot analysis gene expression regulated p53 target gene human cdna encoding european economic area hsiao ec partial hepa-tectomy systemically administered myostatin alan livingstone chair time-dependent induction tumor suppressor activity baek sj demonstrated enhanced expression glioblastoma cells independently conditions privacy policy periportal expression pattern inhibin-betac expression article koniaris article journal check access instant access accepting optional cookies november 2003 volume 7 related subjects injured rat brain p53-dependent mechanism tgf-beta

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Induction of MIC-1/growth differentiation factor-15 following bile duct injury
         description:Macrophage inflammatory peptide-1 (MIC-1)/growth/differentiation factor-15 (GDF-15) is a divergent member of the transforming growth factor-β superfamily cloned by others and us. MIC-1/GDF-15 is expressed in the liver, breast, and colon. Studies have demonstrated a growth-inhibiting effect of MIC-1/GDF-15 on colon and breast cancer cell lines in vitro and on tumor growth in vivo. We previously reported that MIC-1 expression is rapidly induced after a wide variety of murine acute and chronic liver injuries including aniline dye administration. I hypothesized, therefore, that MIC-1/GDF-15 may be a mediator of biliary tract injury and could play a role in regulation of bile duct proliferation. C57BL/6 mice underwent surgical ligation of the common bile duct. Northern blot analysis revealed a time-dependent induction of MIC-1/GDF-15 mRNA in the liver. In situ hybridization of liver sections for MIC-1/GDF-15 expression after bile duct ligation demonstrated a zone 1 or periportal expression pattern, consistent with expression of MIC-1 in periductular hepatocytes. Northern blot analysis of liver mRNA from patients with sclerosing cholangitis or cirrhosis also demonstrated enhanced expression of MIC-1/GDF-15. MIC-1/GDF-15 is expressed after bile duct injury in mice and humans. Taken together with the previously demonstrated growth inhibitory effects of MIC-1/GDF-15 on normal and transformed cells, MIC-1/ GDF-15 may play a role in regulation of bile duct proliferation and biliary tumor formation.
         datePublished:
         dateModified:
         pageStart:901
         pageEnd:905
         sameAs:https://doi.org/10.1007/s11605-003-0037-5
         keywords:
            Cytokines
            inflammation
            growth substances
            cholangiocarcinoma
            Surgery
            Gastroenterology
         image:
         isPartOf:
            name:Journal of Gastrointestinal Surgery
            issn:
               1873-4626
               1091-255X
            volumeNumber:7
            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:Leonidas G. Koniaris
               affiliation:
                     name:University of Rochester School of Medicine and Dentistry
                     address:
                        name:Department of Surgery, University of Rochester School of Medicine and Dentistry, Rochester
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Induction of MIC-1/growth differentiation factor-15 following bile duct injury
      description:Macrophage inflammatory peptide-1 (MIC-1)/growth/differentiation factor-15 (GDF-15) is a divergent member of the transforming growth factor-β superfamily cloned by others and us. MIC-1/GDF-15 is expressed in the liver, breast, and colon. Studies have demonstrated a growth-inhibiting effect of MIC-1/GDF-15 on colon and breast cancer cell lines in vitro and on tumor growth in vivo. We previously reported that MIC-1 expression is rapidly induced after a wide variety of murine acute and chronic liver injuries including aniline dye administration. I hypothesized, therefore, that MIC-1/GDF-15 may be a mediator of biliary tract injury and could play a role in regulation of bile duct proliferation. C57BL/6 mice underwent surgical ligation of the common bile duct. Northern blot analysis revealed a time-dependent induction of MIC-1/GDF-15 mRNA in the liver. In situ hybridization of liver sections for MIC-1/GDF-15 expression after bile duct ligation demonstrated a zone 1 or periportal expression pattern, consistent with expression of MIC-1 in periductular hepatocytes. Northern blot analysis of liver mRNA from patients with sclerosing cholangitis or cirrhosis also demonstrated enhanced expression of MIC-1/GDF-15. MIC-1/GDF-15 is expressed after bile duct injury in mice and humans. Taken together with the previously demonstrated growth inhibitory effects of MIC-1/GDF-15 on normal and transformed cells, MIC-1/ GDF-15 may play a role in regulation of bile duct proliferation and biliary tumor formation.
      datePublished:
      dateModified:
      pageStart:901
      pageEnd:905
      sameAs:https://doi.org/10.1007/s11605-003-0037-5
      keywords:
         Cytokines
         inflammation
         growth substances
         cholangiocarcinoma
         Surgery
         Gastroenterology
      image:
      isPartOf:
         name:Journal of Gastrointestinal Surgery
         issn:
            1873-4626
            1091-255X
         volumeNumber:7
         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:Leonidas G. Koniaris
            affiliation:
                  name:University of Rochester School of Medicine and Dentistry
                  address:
                     name:Department of Surgery, University of Rochester School of Medicine and Dentistry, Rochester
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Journal of Gastrointestinal Surgery
      issn:
         1873-4626
         1091-255X
      volumeNumber:7
Organization:
      name:Springer-Verlag
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Rochester School of Medicine and Dentistry
      address:
         name:Department of Surgery, University of Rochester School of Medicine and Dentistry, Rochester
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Leonidas G. Koniaris
      affiliation:
            name:University of Rochester School of Medicine and Dentistry
            address:
               name:Department of Surgery, University of Rochester School of Medicine and Dentistry, Rochester
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Surgery, University of Rochester School of Medicine and Dentistry, Rochester
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(89)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.57s.

LINK . SPRINGER . COM {}