ArticleStem cell research & therapy2017
Upregulation of sodium taurocholate cotransporter polypeptide during hepatogenic differentiation of umbilical cord matrix mesenchymal stem cells facilitates hepatitis B entry.
Article in Stem cell research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Review
- Bona fide receptor for hepatitis B and D viral infections: Mechanism, research models and molecular drug targets.Emerging microbes & infections · 2018Review
- Age-dependent glycosylation of the sodium taurocholate cotransporter polypeptide: From fetal to adult human livers.Hepatology communications · 2018Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatitis B virus (HBV) carriers worldwide number approximately 240 million people and around 780,000 people die every year from HBV infection. HBV entry and uptake are functionally linked to the presence of the human sodium-taurocholate cotransporting peptide (hNTCP) receptor. Recently, our group demonstrated that human umbilical cord matrix stem cells (UCMSCs) become susceptible to HBV after in-vitro hepatogenic differentiation (D-UCMSCs).
methodsIn the present study, we examined the involvement of hNTCP in governing D-UCMSC susceptibility to HBV infection by characterizing the modulation of this transporter expression during hepatogenic differentiation and by appreciating the inhibition of its activity on infection efficacy.
resultsWe show here that in-vitro hepatogenic differentiation upregulated hNTCP mRNA and protein expression as well as its activity in D-UCMSCs. Pre-treatment of D-UCMSCs with taurocholate, a specific NTCP substrate, blocked their infection by HBV which supports the crucial involvement of this transporter in the early steps of the virus entry.
conclusionAltogether, our data support the usefulness of D-UCMSCs as a unique human and non-transformed in-vitro model to study the early stages of HBV infection thanks to its ability to endogenously regulate the expression of hNTCP.
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