CAS OpenIR
β1 integrin signaling in asymmetric migration of keratinocytes under mechanical stretch in a co-cultured wound repair model
Lü,Dongyuan1,2,3; Li,Zhan1,2,3; Gao,Yuxin1,2,3; Luo,Chunhua1,2,3; Zhang,Fan1,2,3; Zheng,Lu1,2,3; Wang,Jiawen1,2,3; Sun,Shujin1,2,3; Long,Mian1,2,3
2016-12-28
Source PublicationBioMedical Engineering OnLine
ISSN1475-925X
Volume15Issue:Suppl 2Pages:1-16
Abstract

AbstractBackgroundKeratinocyte (KC) migration in re-epithelization is crucial in repairing injured skin. But the mechanisms of how mechanical stimuli regulate the migration of keratinocytes have been poorly understood.MethodsHuman immortalized keratinocyte HaCaT cells were co-cultured with skin fibroblasts on PDMS membranes and transferred to the static stretch device developed in-house for additional 6?day culture under mechanical stretch to mimic surface tension in skin. To detect the expression of proteins on different position at different time points and the effect of β1 integrin mechanotransduction on HaCaT migration, Immunofluorescence, Reverse transcription-polymerase chain reaction, Flow cytometry, Western blotting assays were applied.ResultsMechanical receptor of β1 integrin that recognizes its ligand of collagen I was found to be strongly associated with migration of HaCaT cells since the knockdown of β1 integrin via RNA silence eliminated the key protein expression dynamically. Here the expression of vinculin was lower but that of Cdc42 was higher for the cells at outward edge than those at inward edge, respectively, supporting that the migration capability of keratinocytes is inversely correlated with the formation of focal adhesion complexes but positively related to the lamellipodia formation. This asymmetric expression feature was further confirmed by high or low expression of PI3K for outward- or inward-migrating cells. And ERK1/2 phosphorylation was up-regulated by mechanical stretch.ConclusionWe reported here, a novel mechanotransduction signaling pathways were β1 integrin-dependent pattern of keratinocytes migration under static stretch in an in vitro co-culture model. These results provided an insight into underlying molecular mechanisms of keratinocyte migration under mechanical stimuli.

KeywordKeratinocyte Mechanical Stretch Fibroblast Β1 Integrin Mechanotransduction
DOI10.1186/s12938-016-0263-1
Language英语
WOS IDBMC:10.1186/s12938-016-0263-1
PublisherBioMed Central
Citation statistics
Document Type期刊论文
Identifierhttp://ir.ipe.ac.cn/handle/122111/24485
Collection中国科学院过程工程研究所
Corresponding AuthorLong,Mian
Affiliation1.Chinese Academy of Sciences; Center of Biomechanics and Bioengineering, Institute of Mechanics
2.Chinese Academy of Sciences; Key Laboratory of Microgravity (National Microgravity Laboratory), Institute of Mechanics
3.Chinese Academy of Sciences; Beijing Key Laboratory of Engineered Construction and Mechanobiology, Institute of Mechanics
Recommended Citation
GB/T 7714
Lü,Dongyuan,Li,Zhan,Gao,Yuxin,et al. β1 integrin signaling in asymmetric migration of keratinocytes under mechanical stretch in a co-cultured wound repair model[J]. BioMedical Engineering OnLine,2016,15(Suppl 2):1-16.
APA Lü,Dongyuan.,Li,Zhan.,Gao,Yuxin.,Luo,Chunhua.,Zhang,Fan.,...&Long,Mian.(2016).β1 integrin signaling in asymmetric migration of keratinocytes under mechanical stretch in a co-cultured wound repair model.BioMedical Engineering OnLine,15(Suppl 2),1-16.
MLA Lü,Dongyuan,et al."β1 integrin signaling in asymmetric migration of keratinocytes under mechanical stretch in a co-cultured wound repair model".BioMedical Engineering OnLine 15.Suppl 2(2016):1-16.
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