@article{MTMT:32704701,
	title = {Examination of pituitary adenylate cyclase-activating polypeptide in Parkinson’s disease focusing on correlations with motor symptom},
	url = {https://m2.mtmt.hu/api/publication/32704701},
	author = {Pham, Dániel and Polgár, Beáta and Tóth, Tünde and Jüngling, Adél and Kovács, Norbert and Balás, István and Pál, Endre and Szabó, Dóra and Fülöp, Balázs Dániel and Reglődi, Dóra and Szántó, Zalán and Herczeg, Róbert and Gyenesei, Attila and Tamás, Andrea},
	doi = {10.1007/s11357-022-00530-6},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {44},
	unique-id = {32704701},
	issn = {2509-2715},
	year = {2022},
	eissn = {2509-2723},
	pages = {785-803},
	orcid-numbers = {Kovács, Norbert/0000-0002-7332-9240; Herczeg, Róbert/0000-0002-5903-0082}
}

@article{MTMT:32012392,
	title = {Congenital Malformation of the Aortic Arch and its Branches With no Documented Clinical Symptoms: A Post-Mortem Case Study},
	url = {https://m2.mtmt.hu/api/publication/32012392},
	author = {Fülöp, Balázs Dániel and Tamás, Andrea and Reglődi, Dóra and Fábián, Eszter},
	journal-iso = {INT J ANAT VAR},
	journal = {INTERNATIONAL JOURNAL OF ANATOMICAL VARIATIONS},
	volume = {14},
	unique-id = {32012392},
	issn = {1308-4038},
	year = {2021},
	pages = {33-34}
}

@article{MTMT:30935538,
	title = {Lack of Pituitary Adenylate Cyclase–Activating Polypeptide (PACAP) Disturbs Callus Formation},
	url = {https://m2.mtmt.hu/api/publication/30935538},
	author = {Józsa, Gergő and Fülöp, Balázs Dániel and Kovács, László Ákos and Czibere, Bernadett and Szegeczki, Vince and Kiss, Tamás and Hajdú, Tibor and Tamás, Andrea and Helyes, Zsuzsanna and Zákány, Róza and Reglődi, Dóra and Juhász, Tamás},
	doi = {10.1007/s12031-019-01448-z},
	journal-iso = {J MOL NEUROSCI},
	journal = {JOURNAL OF MOLECULAR NEUROSCIENCE},
	volume = {71},
	unique-id = {30935538},
	issn = {0895-8696},
	abstract = {Pituitary adenylate cyclase–activating polypeptide (PACAP) is a naturally secreted signaling peptide and has important regulatory roles in the differentiation of the central nervous system and its absence results in disorders in femur development. PACAP has an important function in prevention of oxidative stress or mechanical stress in chondrogenesis but little is known about its function in bone regeneration. A new callus formation model was set to investigate its role in bone remodeling. Fracturing was 5 mm distal from the proximal articular surface of the tibia and the depth was 0.5 mm. Reproducibility of callus formation was investigated with CT 3, 7, and 21 days after the operation. Absence of PACAP did not alter the alkaline phosphatase (ALP) activation in PACAP KO healing process. In developing callus, the expression of collagen type I increased in wild-type (WT) and PACAP KO mice decreased to the end of healing process. Expression of the elements of BMP signaling was disturbed in the callus formation of PACAP KO mice, as bone morphogenic protein 4 (BMP4) and 6 showed an early reduction in bone regeneration. However, elevated Smad1 expression was demonstrated in PACAP KO mice. Our results indicate that PACAP KO mice show various signs of disturbed bone healing and suggest PACAP compensatory and fine tuning effects in proper bone regeneration.},
	year = {2021},
	eissn = {1559-1166},
	pages = {1543-1555}
}

@mastersthesis{MTMT:31662236,
	title = {Az endogén hypophysis adenilát-cikláz aktiváló polipeptid (PACAP) hiányának vizsgálata génkiütött egerek hallórendszerében, érrendszerében és fogfejlődése során},
	url = {https://m2.mtmt.hu/api/publication/31662236},
	author = {Fülöp, Balázs Dániel},
	unique-id = {31662236},
	year = {2020}
}

@article{MTMT:31138433,
	title = {Possible effects of pituitary adenylate cyclase activating polypeptide (PACAP) on early embryo implantation marker HB-EGF in mouse.},
	url = {https://m2.mtmt.hu/api/publication/31138433},
	author = {Somoskői, Bence and Török, Dóra and Reglődi, Dóra and Tamás, Andrea and Fülöp, Balázs Dániel and Cseh, Sándor},
	doi = {10.1016/j.repbio.2020.01.005},
	journal-iso = {REPROD BIOL},
	journal = {REPRODUCTIVE BIOLOGY},
	volume = {20},
	unique-id = {31138433},
	issn = {1642-431X},
	abstract = {Pituitary adenylate cyclase activating polypeptide (PACAP) was originally isolated as a hypothalamic neuropeptide stimulating adenylate cyclase activity. Besides its neuroprotective effects, numerous data proved its role in reproductive processes. However, there are limited data on its role in preimplantation embryo development and implantation. Our aim was to analyse the mRNA expression of Adcyap1 (coding region of PACAP) and Hbegf [coding region of HB-EGF (Heparin-binding EGF-like growth factor)] in embryos and pregnant uterus to investigate the possible correlation between them. Eight-week-old BDF1 mice were superovulated and subsequently mated overnight or left in their cage after hCG treatment. Day4 embryos were flushed from mated females. After morphological analysis, Adcyap1 and Hbegf gene expression of embryos and uterine tissues was assessed with qPCR. Our results showed significantly higher Adcyap1 and Hbegf mRNA levels in females producing embryos compared to non-mated ones. Robust elevation of Adcyap1 and slight elevation of Hbegf were detected in females with blastocyst embryos compared with non-blastocysts. We found low rate of Hbegf mRNA expression in uncompacted embryos, whereas morulae and blastocysts expressed high amounts of Hbegf. However, we did not find detectable Adcyap1 mRNA in embryos. Strong correlation was found between uterine tissue and embryonic Hbegf levels, slight correlation between uterine Adcyap1 and Hbegf levels. Uterine tissue Adcyap1 and embryonic Hbegf showed no correlation. In summary, our present data show, for the first time, the correlation between PACAP and HB-EGF mRNA expression suggesting that PACAP might play a role during the peri-implantation period of early mouse embryo development.},
	keywords = {PACAP; MOUSE; IMPLANTATION; embryo; HB-EGF},
	year = {2020},
	eissn = {2300-732X},
	pages = {9-13}
}

@article{MTMT:30914524,
	title = {Phenotypic characterization of testicular immune cells expressing immune checkpoint molecules in wild-type and pituitary adenylate cyclase-activating polypeptide-deficient mice},
	url = {https://m2.mtmt.hu/api/publication/30914524},
	author = {Meggyes, Mátyás and Lajkó, Adrienn and Fülöp, Balázs Dániel and Reglődi, Dóra and Szereday, László},
	doi = {10.1111/aji.13212},
	journal-iso = {AM J REPROD IMMUNOL},
	journal = {AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY},
	volume = {83},
	unique-id = {30914524},
	issn = {1046-7408},
	abstract = {PACAP is a neuropeptide having several regulatory functions in the nervous system and in peripheral organs including those of the reproductive system. PACAP-deficient male mice have several morphological, biochemical, behavioral defects and show disturbed signaling in spermatogenesis affecting fertility in PACAP KO mice. Reproductive functions such as fertility, mating and maternal behaviors have been widely investigated, but no immune analyses are available regarding the testicular immune-privileged environment in male PACAP-deficient mice.Therefore, we performed detailed immunophenotyping of testicular immune cells and investigated the expression of TIM-3 and PD-1 immune-checkpoint molecules of immune cells together with the detection of Galectin-9 and perforin. We investigated the percentage of numerous immune cell populations in the testis of wild-type and PACAP-deficient mice.We demonstrated a significant increase in the frequency of testicular CD8+ T cells together with the decrease of Treg cell number obtained from PACAP KO mice compared to wild-type mice. Investigating immune-checkpoint receptors, only PD-1 showed a significantly decreased expression in CD8+ T cells in PACAP KO mice compared to wild-type suggesting an impaired PD-1/PD-L1 pathway. Regarding TIM-3 expression, we did not find any significant difference between the investigated groups.We hypothesize that these local changes may result in an immune activation with disturbed testicular immunoregulation in PACAP KO mice, however, determining the exact function requires further investigations. Our data further support the view that besides a systemic immune tolerance, localized active immunosuppression is involved in the regulation of testicular immune privilege.},
	keywords = {NEUROPEPTIDE; PACAP; PD-1; PD-L1; Galectin-9; TIM-3},
	year = {2020},
	eissn = {1600-0897},
	orcid-numbers = {Szereday, László/0000-0002-1208-2969}
}

@article{MTMT:30868332,
	title = {Age-related alterations of articular cartilage in pituitary adenylate cyclase–activating polypeptide (PACAP) gene–deficient mice},
	url = {https://m2.mtmt.hu/api/publication/30868332},
	author = {Szegeczki, Vince and Bauer, Balázs and Jüngling, Adél and Fülöp, Balázs Dániel and Vágó, Judit and Perényi, Helga and Tarantini, Stefano and Tamás, Andrea and Zákány, Róza and Reglődi, Dóra and Juhász, Tamás},
	doi = {10.1007/s11357-019-00097-9},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {41},
	unique-id = {30868332},
	issn = {2509-2715},
	abstract = {Pituitary adenylate cyclase activating polypeptide (PACAP) is an evolutionarly conserved neuropeptide which is produced by various neuronal and non-neuronal cells, including cartilage and bone cells. PACAP has trophic functions in tissue development, and it also plays a role in cellular and tissue aging. PACAP takes part in the regulation of chondrogenesis, which prevents insufficient cartilage formation caused by oxidative and mechanical stress. PACAP knockout (KO) mice have been shown to display early aging signs affecting several organs. In the present work, we investigated articular cartilage of knee joints in young and aged wild-type (WT) and PACAP KO mice. A significant increase in the thickness of articular cartilage was detected in aged PACAP gene–deficient mice. Amongst PACAP receptors, dominantly PAC1 receptor was expressed in WT knee joints and a remarkable decrease was found in aged PACAP KO mice. Expression of PKA-regulated transcription factors, Sox5, Sox9 and CREB, decreased both in young and aged gene deficient mice, while Sox6, collagen type II and aggrecan expressions were elevated in young but were reduced in aged PACAP KO animals. Increased expression of hyaluronan (HA) synthases and HA-binding proteins was detected parallel with an elevated presence of HA in aged PACAP KO mice. Expression of bone related collagens (I and X) was augmented in young and aged animals. These results suggest that loss of PACAP signaling results in dysregulation of cartilage matrix composition and may transform articular cartilage in a way that it becomes more prone to degenerate.},
	year = {2019},
	eissn = {2509-2723},
	pages = {775-793},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430}
}

@article{MTMT:30815894,
	title = {Hearing impairment and associated morphological changes in pituitary adenylate cyclase activating polypeptide (PACAP)-deficient mice},
	url = {https://m2.mtmt.hu/api/publication/30815894},
	author = {Fülöp, Balázs Dániel and Humli, Viktória and Szepesy, Judit and Ott, Virag and Reglődi, Dóra and Gaszner, Balázs and Németh, Adrienn and Szirmai, Ágnes and Tamás, László and Hashimoto, Hitoshi and Zelles, Tibor and Tamás, Andrea},
	doi = {10.1038/s41598-019-50775-z},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {9},
	unique-id = {30815894},
	issn = {2045-2322},
	abstract = {Pituitary adenylate cyclase activating polypeptide (PACAP) is a regulatory and cytoprotective neuropeptide, its deficiency implies accelerated aging in mice. It is present in the auditory system having antiapoptotic effects. Expression of Ca2+-binding proteins and its PAC1 receptor differs in the inner ear of PACAP-deficient (KO) and wild-type (WT) mice. Our aim was to elucidate the functional role of PACAP in the auditory system. Auditory brainstem response (ABR) tests found higher hearing thresholds in KO mice at click and low frequency burst stimuli. Hearing impairment at higher frequencies showed as reduced ABR wave amplitudes and latencies in KO animals. Increase in neuronal activity, demonstrated by c-Fos immunolabeling, was lower in KO mice after noise exposure in the ventral and dorsal cochlear nuclei. Noise induced neuronal activation was similar in further relay nuclei of the auditory pathway of WT and KO mice. Based on the similar inflammatory and angiogenic protein profile data from cochlear duct lysates, neither inflammation nor disturbed angiogenesis, as potential pathological components in sensorineural hearing losses, seem to be involved in the pathomechanism of the presented functional and morphological changes in PACAP KO mice. The hearing impairment is probably concomitant with the markedly accelerated aging processes in these animals.},
	year = {2019},
	eissn = {2045-2322},
	orcid-numbers = {Humli, Viktória/0000-0003-1363-1939; Szepesy, Judit/0000-0003-3870-4882; Gaszner, Balázs/0000-0003-2830-2732; Szirmai, Ágnes/0000-0002-8421-6452; Tamás, László/0000-0003-3723-9149; Zelles, Tibor/0000-0002-0357-0469}
}

@article{MTMT:30413407,
	title = {VPAC1 receptors play a dominant role in PACAP-induced vasorelaxation in female mice},
	url = {https://m2.mtmt.hu/api/publication/30413407},
	author = {Ivic, Ivan and Balaskó, Márta and Fülöp, Balázs Dániel and Hashimoto, Hitoshi and Tóth, Gábor and Tamás, Andrea and Juhász, Tamás and Koller, Ákos and Reglődi, Dóra and Varjú-Solymár, Margit},
	doi = {10.1371/journal.pone.0211433},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {14},
	unique-id = {30413407},
	issn = {1932-6203},
	abstract = {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.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.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.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.},
	year = {2019},
	eissn = {1932-6203},
	orcid-numbers = {Tóth, Gábor/0000-0002-3604-4385; Koller, Ákos/0000-0003-3256-8701; Varjú-Solymár, Margit/0000-0001-6667-6263}
}

@article{MTMT:3402939,
	title = {Altered Notch Signaling in Developing Molar Teeth of Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP)-Deficient Mice},
	url = {https://m2.mtmt.hu/api/publication/3402939},
	author = {Fülöp, Balázs Dániel and Sándor, Balázs Attila and Szentléleky, Eszter and Karanyicz, E and Reglődi, Dóra and Gaszner, Balázs and Zákány, Róza and Hashimoto, H and Juhász, Tamás and Tamás, Andrea},
	doi = {10.1007/s12031-018-1146-7},
	journal-iso = {J MOL NEUROSCI},
	journal = {JOURNAL OF MOLECULAR NEUROSCIENCE},
	volume = {68},
	unique-id = {3402939},
	issn = {0895-8696},
	abstract = {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 [delta-like protein (DLL)1, 3, 4, Jagged1, 2], and intracellular target molecules [CSL (CBF1 humans/Su (H) Drosophila/LAG1 Caenorhabditis elegans transcription factor); TACE (TNF-alpha 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 PACAP-deficient 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.},
	keywords = {Notch signaling; CSL; DLL1, 3, 4, Jagged1, 2; Development of molar tooth; NUMB; Notch1, 2, 3, 4; PACAP-deficient mice; TACE},
	year = {2019},
	eissn = {1559-1166},
	pages = {377-388},
	orcid-numbers = {Gaszner, Balázs/0000-0003-2830-2732}
}