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Enhanced Wnt/β-catenin and Notch signalling in the activated canine hepatic progenitor cell niche

Overview of attention for article published in BMC Veterinary Research, December 2014
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Title
Enhanced Wnt/β-catenin and Notch signalling in the activated canine hepatic progenitor cell niche
Published in
BMC Veterinary Research, December 2014
DOI 10.1186/s12917-014-0309-1
Pubmed ID
Authors

Baukje A Schotanus, Hedwig S Kruitwagen, Ted SGAM van den Ingh, Monique E van Wolferen, Jan Rothuizen, Louis C Penning, Bart Spee

Abstract

BackgroundThe liver has a large regenerative capacity. Hepatocytes can replicate and regenerate a diseased liver. However, as is the case in severe liver diseases, this replication may become insufficient or exhausted and hepatic progenitor cells (HPCs) can be activated in an attempt to restore liver function. Due to their bi-potent differentiation capacity, these HPCs have great potential for regenerative approaches yet over-activation does pose potential health risks. Therefore the mechanisms leading to activation must be elucidated prior to safe implementation in the veterinary clinic. Wnt/ß-catenin and Notch signalling have been implicated in the activation of HPCs in mouse models and in humans. Here we assessed the involvement in canine HPC activation. Gene-expression profiles were derived from laser microdissected HPCs niches from lobular dissecting hepatitis (LDH) and normal liver tissue, with a focus on Wnt/ß-catenin and Notch signalling. Immunohistochemical and immunofluorescent studies were combined to assess the role of the pathways in HPCs during LDH.ResultsGene-expression confirmed higher expression of Wnt/ß-catenin and Notch pathway components and target genes in activated HPC niches in diseased liver compared to quiescent HPC niches from normal liver. Immunofluorescence confirmed the activation of these pathways in the HPCs during disease. Immunohistochemistry showed proliferating HPCs during LDH, and double immunofluorescence showed downregulation of Wnt/ß-catenin and Notch in differentiating HPCs. Vimentin, a mesenchymal marker, was expressed on a subset of undifferentiated HPCs.ConclusionsTogether these studies clearly revealed that both Wnt/ß-catenin and Notch signalling pathways are enhanced in undifferentiated, proliferating and potentially migrating HPCs during severe progressive canine liver disease (LDH).

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 22 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 22 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 4 18%
Student > Master 4 18%
Student > Ph. D. Student 3 14%
Student > Bachelor 2 9%
Student > Postgraduate 2 9%
Other 4 18%
Unknown 3 14%
Readers by discipline Count As %
Medicine and Dentistry 5 23%
Biochemistry, Genetics and Molecular Biology 5 23%
Veterinary Science and Veterinary Medicine 3 14%
Agricultural and Biological Sciences 3 14%
Immunology and Microbiology 1 5%
Other 1 5%
Unknown 4 18%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 05 January 2015.
All research outputs
#20,248,338
of 22,776,824 outputs
Outputs from BMC Veterinary Research
#2,415
of 3,045 outputs
Outputs of similar age
#295,049
of 352,205 outputs
Outputs of similar age from BMC Veterinary Research
#87
of 101 outputs
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