Focal adhesion kinase maintains, but not increases the adhesion of dental pulp cells

Focal adhesion kinase (FAK) functions as a key enzyme in the integrin-mediated adhesion-signalling pathway. Here, we aimed to investigate the effects of FAK on adhesion of human dental pulp (HDP) cells. We transfected lentiviral vectors to silence or overexpress FAK in HDP cells ex vivo. Early cell...

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Bibliographic Details
Published in:Human cell : official journal of Human Cell Research Society 2017-04, Vol.30 (2), p.98-105
Main Authors: Qian, Yuyan, Shao, Meiying, Zou, Wenlin, Wang, Linyan, Cheng, Ran, Hu, Tao
Format: Article
Language:English
Subjects:
Adolescent
Adult
Biomedical and Life Sciences
Cell adhesion
Cell adhesion & migration
Cell Adhesion - genetics
Cell Adhesion - physiology
Cell Biology
Cell survival
Cell Survival - genetics
Cells, Cultured
Cytoskeleton
Cytoskeleton - metabolism
Dental pulp
Dental Pulp - cytology
Dental Pulp - metabolism
Focal adhesion kinase
Focal Adhesion Protein-Tyrosine Kinases - physiology
Glycoproteins
Gynecology
Humans
Immunofluorescence
Life Sciences
Oncology
Paxillin
Phosphorylation
Reproductive Medicine
Research Article
Signal transduction
Signal Transduction - genetics
Signal Transduction - physiology
Stem Cells
Surgery
Survival
Young Adult
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Summary:Focal adhesion kinase (FAK) functions as a key enzyme in the integrin-mediated adhesion-signalling pathway. Here, we aimed to investigate the effects of FAK on adhesion of human dental pulp (HDP) cells. We transfected lentiviral vectors to silence or overexpress FAK in HDP cells ex vivo. Early cell adhesion, cell survival and focal contacts (FCs)-related proteins (FAK and paxillin) were examined. By using immunofluorescence, the formation of FCs and cytoskeleton was detected, respectively. We found that both adhesion and survival of HDP cells were suppressed by FAK inhibition. However, FAK overexpression slightly inhibited cell adhesion and exhibited no change in cell survival compared with the control. A thick rim of cytoskeleton accumulated and smaller dot-shaped FCs appeared in FAK knockdown cells. Phosphorylation of paxillin (p-paxillin) was inhibited in FAK knockdown cells, verifying that the adhesion was inhibited. Less cytoskeleton and elongated FCs were observed in FAK-overexpressed cells. However, p-paxillin had no significant difference compared with the control. In conclusion, the data suggest that FAK maintains cell adhesion, survival and cytoskeleton formation, but excessive FAK has no positive effects on these aspects.
ISSN:1749-0774
0914-7470
1749-0774
DOI:10.1007/s13577-017-0159-9