NRP1 Activates NF-ÃÂºB Signaling Pathway and Initiates Proliferation in KeratinocytesNikoletta Nagy1,2,3*, Katalin Farkas2, Sarolta Bacsa1, Istvan Balazs Nemeth1, Zsuzsanna Bata-Csorgo1,2, Lajos Kemeny1,2 and Marta Szell2,3
- *Corresponding Author:
- Dr. Nikoletta Nagy
Department of Dermatology and Allergology
University of Szeged, 6 Koranyi fasor, H-6720 Szeged, Hungary
E-mail: [email protected]
Received date: June 05, 2013; Accepted date: June 20, 2013; Published date: June 22, 2013
Citation: Nagy N, Farkas K, Bacsa S, Nemeth IB, Bata-Csorgo Z, et al. (2013) NRP1 Activates NF-κB Signaling Pathway and Initiates Proliferation in Keratinocytes. Int J Genomic Med 1:102. doi:10.4172/2332-0672.1000102
Copyright: © 2013 Nagy N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Neuropilin-1 (NRP1) is a membrane-bound co-receptor of vascular endothelial growth factor receptors (VEGFRs) and type-A plexins. These complexes mediate the effects of ligands such as vascular endothelial growth factor 165 (VEGF165) and semaphorin 3A (SEMA-3A). Aim: Our aims were to elucidate whether the expression of NRP1 is related to the proliferation or differentiation programme of keratinocytes and to identify putative downstream signaling pathways of NRP1 in keratinocytes. Materials and methods: Synchronized HaCaT cells and paraffin-embedded tissue samples of psoriasis were used to modell highly proliferative stages of keratinocytes. Real-time RT-PCR-based expression array was used to analyse downstream signaling pathways in keratinocytes. Results: Synchronized HaCaT cells revealed that the peak expression of NRP1 occurred 24 hours before the cells reached their highest proliferative activity. Immunohistochemical staining of the highly proliferative tissue samples demonstrated that the high level of NRP1 protein expression partially overlapped with the expression of Ki67-positive cells. Real-time RT-PCR-based expression array identified the NF-κB pathway as one putative downstream signaling pathway of NRP1-mediated signaling in HaCaT cells. VEGF165 and SEMA-3A treatment of HaCaT cells stably transformed with a reporter construct for the assessment of NF-κB activation led to upregulation of the NF-κB activity. Conclusion: Our results suggest that the NRP1 might be involved in the regulation of keratinocyte proliferation and might activate NF-κB pathway as a putative downstream signaling pathway in keratinocytes.