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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
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We are analyzing https://link.springer.com/article/10.1007/s13577-017-0163-0.

Title:
MicroRNA-98 inhibits TGF-β1-induced differentiation and collagen production of cardiac fibroblasts by targeting TGFBR1 | Human Cell
Description:
To investigate the effects of miR-98 on TGF-β1-induced cardiac fibrosis in human cardiac fibroblasts (HCFs), and to establish the mechanism underlying these effects, HCFs were transfected with miR-98 inhibitor or mimic, and then treated with or without TGF-β1. The level of miR-98 was determined by qRT-PCR in TGF-β1-induced HCFs. Cell differentiation and collagen accumulation of HCFs were detected by qRT-PCR and Western blot assays, respectively. The mRNA and protein expressions of TGFBR1 were determined by qRT-PCR and Western blotting. In this study, the outcomes showed that TGF-β1 could dramatically decrease the level of miR-98 in a time- and concentration-dependent manner. Upregulation of miR-98 dramatically improved TGF-β1-induced increases in cell differentiation and collagen accumulation of HCFs. Moreover, bioinformatics analysis predicted that the TGFBR1 was a potential target gene of miR-98. Luciferase reporter assay demonstrated that miR-98 could directly target TGFBR1. Inhibition of TGFBR1 had the similar effect as miR-98 overexpression. Downregulation of TGFBR1 in HCFs transfected with miR-98 inhibitor partially reversed the protective effect of miR-98 overexpression on TGF-β1-induced cardiac fibrosis in HCFs. Upregulation of miR-98 ameliorates TGF-β1-induced differentiation and collagen accumulation of HCFs by downregulation of TGFBR1. These results provide further evidence for protective effect of miR-98 overexpression on TGF-β1-induced cardiac fibrosis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Telecommunications
  • Social Networks

Content Management System {šŸ“}

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 {šŸ“ˆ}

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? {šŸ’ø}

We find it hard to spot revenue streams.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {šŸ”}

article, pubmed, cardiac, google, scholar, cas, fibrosis, cell, microrna, fibroblasts, mol, targeting, central, heart, tgfbr, growth, tgfβinduced, differentiation, collagen, hcfs, inhibits, zhou, transforming, wang, human, access, cardiol, res, hebei, privacy, cookies, content, cheng, myofibroblasts, signaling, angiotensin, yang, remodeling, myocardial, function, publish, research, search, ranran, tgfβ, pathway, proliferation, regulates, rats, zhao,

Topics {āœ’ļø}

transforming growth factor-beta targeting tgf-β/smad3 signaling tgf-β1-induced cardiac fibrosis exercise-induced cardiac growth min ding & huikun hua wnt signaling pathway month download article/chapter tgf-β1-induced hcfs cardiac fibrosis tgfβ microrna-15 family inhibits /mapk signal pathway mir-21 promotes fibrosis human cardiac fibroblasts tgf-β1 full article pdf microrna-133a improves microrna expression analysis suppresses fibroblast proliferation targeting pdgfr-β van der made postischemic cardiac fibrosis smad signaling privacy choices/manage cookies tgfbeta-pathway check access instant access acute exhaustive exercise article cheng control interstitial fibrosis pathological cardiac remodeling pressure-overloaded rats extracellular matrix proteins cell mol med cell physiol biochem human cell 30 european economic area concentration-dependent manner potential target gene directly target tgfbr1 related subjects mirna-940 reduction contributes heart failure rats potential therapeutic targets mol cell cardiol mol cell biochem mol genetic metabol article log extracellular matrix remodeling conditions privacy policy bioinformatics analysis predicted

Questions {ā“}

  • Myofibroblasts in diseased hearts: new players in cardiac arrhythmias?

Schema {šŸ—ŗļø}

WebPage:
      mainEntity:
         headline:MicroRNA-98 inhibits TGF-β1-induced differentiation and collagen production of cardiac fibroblasts by targeting TGFBR1
         description:To investigate the effects of miR-98 on TGF-β1-induced cardiac fibrosis in human cardiac fibroblasts (HCFs), and to establish the mechanism underlying these effects, HCFs were transfected with miR-98 inhibitor or mimic, and then treated with or without TGF-β1. The level of miR-98 was determined by qRT-PCR in TGF-β1-induced HCFs. Cell differentiation and collagen accumulation of HCFs were detected by qRT-PCR and Western blot assays, respectively. The mRNA and protein expressions of TGFBR1 were determined by qRT-PCR and Western blotting. In this study, the outcomes showed that TGF-β1 could dramatically decrease the level of miR-98 in a time- and concentration-dependent manner. Upregulation of miR-98 dramatically improved TGF-β1-induced increases in cell differentiation and collagen accumulation of HCFs. Moreover, bioinformatics analysis predicted that the TGFBR1 was a potential target gene of miR-98. Luciferase reporter assay demonstrated that miR-98 could directly target TGFBR1. Inhibition of TGFBR1 had the similar effect as miR-98 overexpression. Downregulation of TGFBR1 in HCFs transfected with miR-98 inhibitor partially reversed the protective effect of miR-98 overexpression on TGF-β1-induced cardiac fibrosis in HCFs. Upregulation of miR-98 ameliorates TGF-β1-induced differentiation and collagen accumulation of HCFs by downregulation of TGFBR1. These results provide further evidence for protective effect of miR-98 overexpression on TGF-β1-induced cardiac fibrosis.
         datePublished:2017-03-01T00:00:00Z
         dateModified:2017-03-01T00:00:00Z
         pageStart:192
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            Cardiac fibrosis
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            Surgery
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      headline:MicroRNA-98 inhibits TGF-β1-induced differentiation and collagen production of cardiac fibroblasts by targeting TGFBR1
      description:To investigate the effects of miR-98 on TGF-β1-induced cardiac fibrosis in human cardiac fibroblasts (HCFs), and to establish the mechanism underlying these effects, HCFs were transfected with miR-98 inhibitor or mimic, and then treated with or without TGF-β1. The level of miR-98 was determined by qRT-PCR in TGF-β1-induced HCFs. Cell differentiation and collagen accumulation of HCFs were detected by qRT-PCR and Western blot assays, respectively. The mRNA and protein expressions of TGFBR1 were determined by qRT-PCR and Western blotting. In this study, the outcomes showed that TGF-β1 could dramatically decrease the level of miR-98 in a time- and concentration-dependent manner. Upregulation of miR-98 dramatically improved TGF-β1-induced increases in cell differentiation and collagen accumulation of HCFs. Moreover, bioinformatics analysis predicted that the TGFBR1 was a potential target gene of miR-98. Luciferase reporter assay demonstrated that miR-98 could directly target TGFBR1. Inhibition of TGFBR1 had the similar effect as miR-98 overexpression. Downregulation of TGFBR1 in HCFs transfected with miR-98 inhibitor partially reversed the protective effect of miR-98 overexpression on TGF-β1-induced cardiac fibrosis in HCFs. Upregulation of miR-98 ameliorates TGF-β1-induced differentiation and collagen accumulation of HCFs by downregulation of TGFBR1. These results provide further evidence for protective effect of miR-98 overexpression on TGF-β1-induced cardiac fibrosis.
      datePublished:2017-03-01T00:00:00Z
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         Cell Biology
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         Gynecology
         Reproductive Medicine
         Stem Cells
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               name:Affiliated Hospital, Medical Department, Hebei University of Engineering, Handan, People’s Republic of China
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      name:Ruiying Dang
      affiliation:
            name:Hebei University of Engineering
            address:
               name:Emergency Department, Affiliated Hospital, Hebei University of Engineering, Handan, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Yan Zhou
      affiliation:
            name:Hebei University of Engineering
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               name:Affiliated Hospital, Medical Department, Hebei University of Engineering, Handan, People’s Republic of China
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            name:Hebei University of Engineering
            address:
               name:College of Medicine, Hebei University of Engineering, Handan, People’s Republic of China
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External Links {šŸ”—}(159)

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