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Open AccessArticle

Deregulated Adhesion Program in Palatal Keratinocytes of Orofacial Cleft Patients

1
Department of Dentistry, Section Orthodontics and Craniofacial Biology, Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University Medical Center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
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Department of Human Genetics, KU Leuven, 3000 Leuven, Belgium
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Department of Oral Health Sciences, KU Leuven, 3000 Leuven, Belgium
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The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan 430079, China
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Department of Human Genetics, Radboud University Medical Center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
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Department of Molecular Developmental Biology, Radboud Institute for Molecular Life Sciences (RIMLS), P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
*
Author to whom correspondence should be addressed.
Genes 2019, 10(11), 836; https://doi.org/10.3390/genes10110836
Received: 23 August 2019 / Revised: 17 October 2019 / Accepted: 19 October 2019 / Published: 23 October 2019
(This article belongs to the Special Issue Molecular Genetics of Facial Traits and Malformations)
Orofacial clefts (OFCs) are the most frequent craniofacial birth defects. An orofacial cleft (OFC) occurs as a result of deviations in palatogenesis. Cell proliferation, differentiation, adhesion, migration and apoptosis are crucial in palatogenesis. We hypothesized that deregulation of these processes in oral keratinocytes contributes to OFC. We performed microarray expression analysis on palatal keratinocytes from OFC and non-OFC individuals. Principal component analysis showed a clear difference in gene expression with 24% and 17% for the first and second component, respectively. In OFC cells, 228 genes were differentially expressed (p < 0.001). Gene ontology analysis showed enrichment of genes involved in β1 integrin-mediated adhesion and migration, as well as in P-cadherin expression. A scratch assay demonstrated reduced migration of OFC keratinocytes (343.6 ± 29.62 μm) vs. non-OFC keratinocytes (503.4 ± 41.81 μm, p < 0.05). Our results indicate that adhesion and migration are deregulated in OFC keratinocytes, which might contribute to OFC pathogenesis. View Full-Text
Keywords: craniofacial anomalies; gene expression; molecular biology; cell biology; craniofacial biology/genetics craniofacial anomalies; gene expression; molecular biology; cell biology; craniofacial biology/genetics
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Mammadova, A.; Carels, C.E.; Zhou, J.; Gilissen, C.; Helmich, M.P.; Bian, Z.; Zhou, H.; Von den Hoff, J.W. Deregulated Adhesion Program in Palatal Keratinocytes of Orofacial Cleft Patients. Genes 2019, 10, 836.

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