- Titel
- Prolyl endopeptidase is involved in the degradation of neural cell adhesion molecules in vitro
- Zitierfähige Url:
- https://nbn-resolving.org/urn:nbn:de:bsz:15-qucosa2-965846
- Quellenangabe
- Journal of Cell Science
Erscheinungsjahr: 2016
Jahrgang: 129
Heft: 20
ISSN: 3792-3802 - Erstveröffentlichung
- 2016
- Abstract (EN)
- Membrane-associated glycoprotein neural cell adhesion molecule (NCAM) and its polysialylated form (PSA-NCAM) play an important role in brain plasticity by regulating cell–cell interactions. Here, we demonstrate that the cytosolic serine protease prolyl endopeptidase (PREP) is able to regulate NCAM and PSA-NCAM. Using a SH-SY5Y neuroblastoma cell line with stable overexpression of PREP, we found a remarkable loss of PSA-NCAM, reduced levels of NCAM180 and NCAM140 protein species, and a significant increase in the NCAM immunoreactive band migrating at an apparent molecular weight of 120 kDa in PREP-overexpressing cells. Moreover, increased levels of NCAM fragments were found in the concentrated medium derived from PREP-overexpressing cells. PREP overexpression selectively induced an activation of matrix metalloproteinase-9 (MMP-9), which could be involved in the observed degradation of NCAM, as MMP-9 neutralization reduced the levels of NCAM fragments in cell culture medium.We propose that increased PREP levels promote epidermal growth factor receptor (EGFR) signaling, which in turn activates MMP-9. In conclusion, our findings provide evidence for newly discovered roles for PREP in mechanisms regulating cellular plasticity through NCAM and PSA-NCAM.
- Andere Ausgabe
- Erstveröffentlichung
DOI: 10.1242/jcs.181891 - Freie Schlagwörter (EN)
- Neural cell adhesion molecule, Prolyl endopeptidase, Neuronal plasticity, Metalloproteinase-9
- Verlag
- The Company of Biologists, Cambridge
- Version / Begutachtungsstatus
- angenommene Version / Postprint / Autorenversion
- URN Qucosa
- urn:nbn:de:bsz:15-qucosa2-965846
- Veröffentlichungsdatum Qucosa
- 10.04.2025
- Dokumenttyp
- Artikel
- Sprache des Dokumentes
- Englisch
- Lizenz / Rechtehinweis
