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Human fibroblasts display a differential focal adhesion phenotype relative to chimpanzee

It has been documented that there are differences in disease susceptibilities between humans and non-human primates. We investigate one of these differences in fibroblasts to examine differences in cellular adhesion between humans and chimpanzees using microscopy and gene expression and have found s...

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Bibliographic Details
Published in:Evolution, medicine, and public health medicine, and public health, 2016-01, Vol.2016 (1), p.110-116
Main Authors: Advani, Alexander S., Chen, Annie Y., Babbitt, Courtney C.
Format: Article
Language:English
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Summary:It has been documented that there are differences in disease susceptibilities between humans and non-human primates. We investigate one of these differences in fibroblasts to examine differences in cellular adhesion between humans and chimpanzees using microscopy and gene expression and have found significant differences in both datasets. These results suggest that human and chimpanzee fibroblasts may have somewhat different adhesive properties, which could play a role in differential disease phenotypes and responses to external factors.AbstractThere are a number of documented differences between humans and our closest relatives in responses to wound healing and in disease susceptibilities, suggesting a differential cellular response to certain environmental factors. In this study, we sought to look at a specific cell type, fibroblasts, to examine differences in cellular adhesion between humans and chimpanzees in visualized cells and in gene expression. We have found significant differences in the number of focal adhesions between primary human and chimpanzee fibroblasts. Additionally, we see that adhesion related gene ontology categories are some of the most differentially expressed between human and chimpanzee in normal fibroblast cells. These results suggest that human and chimpanzee fibroblasts may have somewhat different adhesive properties, which could play a role in differential disease phenotypes and responses to external factors.
ISSN:2050-6201
2050-6201
DOI:10.1093/emph/eow010