TLR3 activation mediates partial epithelial-to-mesenchymal transition in human keratinocytes

被引:0
|
作者
Schneider, Andrea M. [1 ]
Feehan, Robert P. [1 ]
Sennett, Mackenzie L. [1 ]
Wills, Carson A. [2 ,4 ]
Garner, Charlotte [1 ]
Cong, Zhaoyuan [1 ]
Billingsley, Elizabeth M. [1 ]
Flamm, Alexandra F. [1 ,5 ]
Shantz, Lisa M. [1 ,3 ]
Nelson, Amanda M. [1 ]
机构
[1] Penn State Hlth Hershey Med Ctr, Dept Dermatol, Hershey, PA 17033 USA
[2] Penn State Coll Med, Dept Pediat, Hershey, PA USA
[3] Penn State Coll Med, Dept Cellular & Mol Physiol, Hershey, PA USA
[4] Hosp Univ Penn, Dept Internal Med, Philadelphia, PA USA
[5] NYU Grossman Sch Med, Dept Dermatol, New York, NY USA
关键词
NF-KAPPA-B; INNATE IMMUNITY; RECEPTOR-3; SKIN; GENE; EXPRESSION; CANCER; CELLS; RNA; RECOGNITION;
D O I
10.26508/lsa.202402777
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
TLR3 is expressed in human skin and keratinocytes, and given its varied role in skin inflammation, development, and regeneration, we sought to determine the cellular response in normal human keratinocytes to TLR3 activation. We investigated this mechanism by treating primary human keratinocytes with both UVB, an endogenous and physiologic TLR3 activator, and poly(I:C), a synthetic and selective TLR3 ligand. TLR3 activation with either UVB or poly(I:C) altered keratinocyte morphology, coinciding with the key features of epithelial-to-mesenchymal transition: increased epithelial-to-mesenchymal transition gene expression, enhanced migration, and increased invasion properties. These results confirm and extend previous studies demonstrating that in addition to its classical role in the innate immune response, TLR3 signaling also regulates stem cell-like properties and developmental programs.
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页数:16
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