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001-es BibID:BIBFORM103634
035-os BibID:(WOS)000472082700006 (Scopus)85051646952
Első szerző:Fülöp Balázs Dániel (Orvosi alapkutatások)
Cím:Altered Notch Signaling in Developing Molar Teeth of Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP)-Deficient Mice / B. D. Fulop, B. Sandor, E. Szentleleky, E. Karanyicz, D. Reglodi, B. Gaszner, R. Zakany, H. Hashimoto, T. Juhasz, A. Tamas
Dátum:2019
ISSN:0895-8696
Megjegyzések:Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide with neuroprotective and neurotrophic effects. This suggests its influence on the development of teeth, which are, similarly to the nervous system, ectoderm and neural crest derivatives. Our earlier studies have shown morphological differences between wild-type (WT) and PACAP-deficient mice, with upregulated sonic hedgehog (SHH) signaling in the lack of PACAP. Notch signaling is a key element of proper tooth development by regulating apoptosis and cell proliferation. In this study, our main goal was to evaluate the possible effects of PACAP on Notch signaling pathway. Immunohistochemical staining was performed of Notch receptors (Notch1, 2, 3, 4), their ligands [deltalike protein (DLL)1, 3, 4, Jagged1, 2], and intracellular target molecules [CSL (CBF1 humans/Su (H) Drosophila/LAG1 Caenorhabditis elegans transcription factor); TACE (TNF-? converting enzyme), NUMB] in molar teeth of 5-day-old WT, and homozygous and heterozygous PACAP-deficient mice. We measured immunopositivity in the enamel-producing ameloblasts and dentin-producing odontoblasts. Notch2 receptor and DLL1 expression were elevated in ameloblasts of PACAPdeficient mice compared to those in WT ones. The expression of CSL showed similar results both in the ameloblasts and odontoblasts. Jagged1 ligand expression was elevated in the odontoblasts of homozygous PACAP-deficient mice compared to WT mice. Other Notch pathway elements did not show significant differences between the genotype groups. The lack of PACAP leads to upregulation of Notch pathway elements in the odontoblast and ameloblast cells. The underlying molecular mechanisms are yet to be elucidated; however, we propose SHH-dependent and independent processes. We hypothesize that this compensatory upregulation of Notch signaling by the lack of PACAP could represent a salvage pathway in PACAP-deficient animals.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
PACAP-deficient mice
Notch signaling
DLL1, 3, 4, Jagged1, 2
Notch1, 2, 3, 4
CSL
TACE
NUMB
Development of molar tooth
Megjelenés:Journal of Molecular Neuroscience. - 68 : 3 (2019), p. 377-388. -
További szerzők:Sándor Balázs Szentléleky Eszter (fogászat) Karanyicz Edina Reglődi Dóra (Idegtudományok) Gaszner Balázs (Neuroanatómia) Zákány Róza (1963-) (anatómus-, kötőszövetbiológus) Hashimoto, Hitoshi Juhász Tamás (1976-) (biológus, orvosbiológus) Tamás Andrea (Idegtudomány) (Pécs)
Pályázati támogatás:2.3.2-15-2016-00050 BPEPSYS^
GINOP
3.6.3-VEKOP-16-15 2017-00008
EFOP
3.6.2-16-2017-00008
EFOP
3.6.1- 16.2016.00004
EFOP
4.2.4.A/2-11-1-2012-0001
TAMOP
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