CCL

Összesen 7 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM069485
Első szerző:Farkas József
Cím:Early Neurobehavioral Development of Mice Lacking Endogenous PACAP / Farkas J., Sandor B., Tamas A., Kiss P., Hashimoto H., Nagy A. D., Fulop B. D., Juhasz T., Manavalan S., Reglodi D.
Dátum:2017
Megjegyzések:Pituitary adenylate cyclase activating polypeptide (PACAP) is a multifunctional neuropeptide. In addition to its diverse physiological roles, PACAP has important functions in the embryonic development of various tissues, and it is also considered as a trophic factor during development and in the case of neuronal injuries. Data suggest that the development of the nervous system is severely affected by the lack of endogenous PACAP. Short-term neurofunctional outcome correlates with long-term functional deficits; however, the early neurobehavioral development of PACAP-deficient mice has not yet been evaluated. Therefore, the aim of the present study was to describe the postnatal development of physical signs and neurological reflexes in mice partially or completely lacking PACAP. We examined developmental hallmarks during the first 3 weeks of the postnatal period, during which period most neurological reflexes and motor coordination show most intensive development, and we describe the neurobehavioral development using a complex battery of tests. In the present study, we found that PACAP-deficient mice had slower weight gain throughout the observation period. Interestingly, mice partially lacking PACAP weighed significantly less than homozygous mice. There was no difference between male and female mice during the first 3 weeks. Some other signs were also more severely affected in the heterozygous mice than in the homozygous mice, such as air righting, grasp, and gait initiation reflexes. Interestingly, incisor teeth erupted earlier in mice lacking PACAP. Motor coordination, shown by the number of foot-faults on an elevated grid, was also less developed in PACAP-deficient mice. In summary, our results show that mice lacking endogenous PACAP have slower weight gain during the first weeks of development and slower neurobehavioral development regarding a few developmental hallmarks.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Knockout
Neurodevelopment
Neuropeptide
Reflex
Trophic factor
Megjelenés:Journal of molecular neuroscience. - 61 : 4 (2017), p. 468-478. -
További szerzők:Sándor Balázs Tamás Andrea (Idegtudomány) (Pécs) Kiss Péter (Pécs) Hashimoto, Hitoshi Nagy András Dávid Fülöp Balázs Dániel (Orvosi alapkutatások) Juhász Tamás (1976-) (biológus, orvosbiológus) Manavalan, Sridharan Reglődi Dóra (Idegtudományok)
Pályázati támogatás:K104984
OTKA
K119759
OTKA
GINOP-2.3.2-15-2016-00050
GINOP
TAMOP 4.2.4.A/2-11-1-2012-0001
TÁMOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM076862
035-os BibID:(cikkazonosító)e0211433 (WOS)000457037500170 (Scopus)85060512660
Első szerző:Ivic, Ivan
Cím:VPAC1 receptors play a dominant role in PACAP-induced vasorelaxation in female mice / Ivan Ivic, Marta Balasko, Balazs D. Fulop, Hitoshi Hashimoto, Gabor Toth, Andrea Tamas, Tamas Juhasz, Akos Koller, Dora Reglodi, Margit Solymár
Dátum:2019
ISSN:1932-6203
Megjegyzések:PACAP and VIP are closely related neuropeptides with wide distribution and potent effect in the vasculature. We previously reported vasomotor activity in peripheral vasculature of male wild type (WT) and PACAP-deficient (KO) mice. However, female vascular responses are still unexplored. We hypothesized that PACAP-like activity is maintained in female PACAP KO mice and the mechanism through which it is regulated differs from that of male PACAP KO animals. METHODS: We investigated the vasomotor effects of VIP and PACAP isoforms and their selective blockers in WT and PACAP KO female mice in carotid and femoral arteries. The expression and level of different PACAP receptors in the vessels were measured by RT-PCR and Western blot. RESULTS: In both carotid and femoral arteries of WT mice, PACAP1-38, PACAP1-27 or VIP induced relaxation, without pronounced differences between them. Reduced relaxation was recorded only in the carotid arteries of KO mice as compared to their WT controls. The specific VPAC1R antagonist completely blocked the PACAP/VIP-induced relaxation in both arteries of all mice, while PAC1R antagonist affected relaxation only in their femoral arteries. CONCLUSION: In female WT mice, VPAC1 receptors appear to play a dominant role in PACAP-induced vasorelaxation both in carotid and in femoral arteries. In the PACAP KO group PAC1R activation exerts vasorelaxation in the femoral arteries but in carotid arteries there is no significant effect of the activation of this receptor. In the background of this regional difference, decreased PAC1R and increased VPAC1R availability in the carotid arteries was found.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Plos One. - 14 : 1 (2019), p. e0211433. -
További szerzők:Balaskó Márta Fülöp Balázs Dániel (Orvosi alapkutatások) Hashimoto, Hitoshi Tóth Gábor (Szeged) Tamás Andrea (Idegtudomány) (Pécs) Juhász Tamás (1976-) (biológus, orvosbiológus) Koller Ákos Reglődi Dóra (Idegtudományok) Solymár Margit
Pályázati támogatás:EFOP-3.6.3-VEKOP-16-15 2017-00008
EFOP
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
K115874
OTKA
K104984
OTKA
K119759
OTKA
KTIA_13_NAP-A-III/5
Egyéb
GINOP-2.3.2-15-2016-00050 "PEPSYS"
GINOP
TÁMOP-4.2.4.A/2-11-1-2012-0001
TÁMOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM069486
Első szerző:Ivic, Ivan
Cím:Backup Mechanisms Maintain PACAP/VIP-Induced Arterial Relaxations in Pituitary Adenylate Cyclase-Activating Polypeptide-Deficient Mice / Ivic I., Fulop B. D., Juhasz T., Reglodi D., Toth G., Hashimoto H., Tamas A., Koller A.
Dátum:2017
Megjegyzések:Pituitary adenylate cyclase-activating polypeptide (PACAP) is a multifunctional neuropeptide in the VIP/secretin/glucagon peptide superfamily. Two active forms, PACAP1-38 and PACAP1-27, act through G protein-coupled receptors, the PAC1 and VPAC1/2 receptors. Effects of PACAP include potent vasomotor activity. Vasomotor activity and organ-specific vasomotor effects of PACAP-deficient mice have not yet been investigated; thus, the assessment of its physiological importance in vasomotor functions is still missing. We hypothesized that backup mechanisms exist to maintain PACAP pathway activity in PACAP knockout (KO) mice. Thus, we investigated the vasomotor effects of exogenous vasoactive intestinal peptide (VIP) and PACAP polypeptides in PACAP wild-type (WT) and PACAP-deficient (KO) male mice.METHODS:Carotid and femoral arteries were isolated from 8- to 12-week-old male WT and PACAP-KO mice. Vasomotor responses were measured with isometric myography.RESULTS:In the arteries of WT mice the peptides induced relaxations, which were significantly greater to PACAP1-38 than to PACAP1-27 and VIP. In KO mice, PACAP1-38 did not elicit relaxation, whereas PACAP1-27 and VIP elicited significantly greater relaxation in KO mice than in WT mice. The specific PAC1R and VPAC1R antagonist completely blocked the PACAP-induced relaxations.CONCLUSION:Our data suggest that in PACAP deficiency, backup mechanisms maintain arterial relaxations to polypeptides, indicating an important physiological role for the PACAP pathway in the regulation of vascular tone.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Carotid arteries
Femoral arteries
PAC1 receptor
PACAP-KO mice
Pituitary adenylate cyclase-activating polypeptide
VPAC1/VPAC2 receptors
Vasoactive intestinal peptide
Vasomotor responses
Megjelenés:Journal of Vascular Research 54 : 3 (2017), p. 180-192. -
További szerzők:Fülöp Balázs Dániel (Orvosi alapkutatások) Juhász Tamás (1976-) (biológus, orvosbiológus) Reglődi Dóra (Idegtudományok) Tóth Gábor (Szeged) Hashimoto, Hitoshi Tamás Andrea (Idegtudomány) (Pécs) Koller Ákos
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM107589
035-os BibID:(scopus)85049967047 (wos)000438654600009
Első szerző:Reglődi Dóra (Idegtudományok)
Cím:Accelerated pre-senile systemic amyloidosis in PACAP knockout mice : a protective role of PACAP in age-related degenerative processes / Reglodi Dora, Jungling Adel, Longuespée Rémi, Kriegsmann Joerg, Casadonte Rita, Kriegsmann Mark, Juhasz Tamas, Bardosi Sebastian, Tamas Andrea, Fulop Balazs Daniel, Kovacs Krisztina, Nagy Zsuzsanna, Sparks Jason, Miseta Attila, Mazzucchelli Gabriel, Hashimoto Hitoshi, Bardosi Attila
Dátum:2018
ISSN:0022-3417
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Pathology. - 245 : 4 (2018), p. 478-490. -
További szerzők:Jungling Adél Longuespée, Rémi Kriegsmann, Joerg Casadonte, Rita Kriegsmann, Mark Juhász Tamás (1976-) (biológus, orvosbiológus) Bardosi, Sebastian Tamás Andrea (Idegtudomány) (Pécs) Fülöp Balázs Dániel (Orvosi alapkutatások) Kovács Krisztina Nagy Zsuzsanna Sparks, Jason Miseta Attila Mazzucchelli, Gabriel Hashimoto, Hitoshi Bárdosi Attila
Pályázati támogatás:Szodoray Lajos ösztöndíj
Egyéb
Magyary Zoltán ösztöndíj
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

6.

001-es BibID:BIBFORM072074
035-os BibID:(WoS)000424699400006 (Scopus)85041205300
Első szerző:Reglődi Dóra (Idegtudományok)
Cím:Disturbed spermatogenic signaling in pituitary adenylate cyclase activating polypeptide-deficient mice / Reglodi D., Cseh S., Somoskoi B., Fulop B. D., Szentleleky E., Szegeczki V., Kovacs A., Varga A., Kiss P., Hashimoto H., Tamas A., Bardosi A., Manavalan S., Bako E., Zakany R., Juhasz T.
Dátum:2018
ISSN:1470-1626
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Reproduction. - 155 : 2 (2018), p. 127-137. -
További szerzők:Cseh Sándor (1954-) (állatorvos) Somoskői B. Fülöp Balázs Dániel (Orvosi alapkutatások) Szentléleky Eszter (fogászat) Szegeczki Vince (1992-) Kovács A. (Pécs) Varga A. (anatómia, Pécs) Kiss Péter (Pécs) Hashimoto, Hitoshi Tamás A. (Pécs) Bárdosi Attila Manavalan, Sridharan Bakó Éva (1958-) (biokémikus) Zákány Róza (1963-) (anatómus-, kötőszövetbiológus) Juhász Tamás (1976-) (biológus, orvosbiológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM054231
035-os BibID:PMID: 25112419
Első szerző:Sándor Balázs
Cím:Structural and Morphometric Comparison of the Molar Teeth in Pre-eruptive Developmental Stage of PACAP-Deficient and Wild-Type Mice / B. Sandor, K. Fintor, Sz. Felszeghy, T. Juhasz, D. Reglodi, L. Mark, P. Kiss, A. Jungling, B. D. Fulop, A. D. Nagy, H. Hashimoto, R. Zakany, A. Nagy, A. Tamas
Dátum:2014
ISSN:0895-8696
Megjegyzések:Pituitary adenylate cyclase activating polypeptide (PACAP) is a pleiotropic neuropeptide with widespread distribution. It plays pivotal role in neuronal development. PACAP-immunoreactive fibers have been found in the tooth pulp, and recently, it has been shown that PACAP may also play a role in the regeneration of the periodontium after luxation injuries. However, there is no data about the effect of endogenous PACAP on tooth development. Ectodermal organogenesis including tooth development is regulated by different members of bone morphogenetic protein (BMP), fibroblast growth factor (FGF), hedgehog (HH), and Wnt families. There is also a growing evidence to support the hypothesis that PACAP interacts with sonic hedgehog (SHH) receptor (PTCH1) and its downstream target (Gli1) suggesting its role in tooth development. Therefore, our aim was to study molar tooth development in mice lacking endogenous PACAP. In this study morphometric, immunohistochemical and structural comparison of molar teeth in pre-eruptive developmental stage was performed on histological sections of 7-day-old wild-type and PACAP-deficient mice. Further structural analysis was carried out with Raman microscope. The morphometric comparison of the 7-day-old samples revealed that the dentin was significantly thinner in the molars of PACAP-deficient mice compared to wild-type animals. Raman spectra of the enamel in wild-type mice demonstrated higher diversity in secondary structure of enamel proteins. In the dentin of PACAP-deficient mice higher intracrystalline disordering in the hydroxyapatite molecular structure was found. We also obtained altered SHH, PTCH1 and Gli1 expression level in secretory ameloblasts of PACAP-deficient mice compared to wild-type littermates suggesting that PACAP might play an important role in molar tooth development and matrix mineralization involving influence on SHH signaling cascade.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular Neuroscience. - 54 : 3 (2014), p. 331-334. -
További szerzők:Fintor K. Felszeghy Szabolcs Béla (1972-) (fogorvos, anatómus, kötőszövetbiológus) Juhász Tamás (1976-) (biológus, orvosbiológus) Reglődi Dóra (Idegtudományok) Mark L. Kiss Péter (Pécs) Jungling Adél Fülöp Balázs Dániel (Orvosi alapkutatások) Nagy András Dávid Hashimoto, Hitoshi Zákány Róza (1963-) (anatómus-, kötőszövetbiológus) Nagy Ákos Tamás Andrea (Idegtudomány) (Pécs)
Pályázati támogatás:PTE-MTA Lendület
Egyéb
K104984
OTKA
PD109644
OTKA
4.2.2.A-11/1/KONV-2012-0024
TÁMOP
4.2.4A/2-11-1-2012-0001
TÁMOP
Bolyai Ösztöndíj
Egyéb
Debreceni Egyetem RH/885/2013
Egyéb
Grants-in-Aid for Scientific Research KAKENHI, 26293020, 26670122
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.