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001-es BibID:	BIBFORM077826
035-os BibID:	(PMID)30345481 (WOS)000453351000002 (Scopus)85055724927
Első szerző:	Reglődi Dóra (Idegtudományok)
Cím:	PACAP deficiency as a model of aging / D. Reglodi, T. Atlasz, E. Szabo, A. Jungling, A. Tamas, T. Juhasz, B. D. Fulop, A. Bardosi
Dátum:	2018
ISSN:	2509-2715 2509-2723
Megjegyzések:	Dysregulation of neuropeptides may play an important role in aging-induced impairments. In the long list of neuropeptides, pituitary adenylate cyclase-activating polypeptide (PACAP) represents a highly effective cytoprotective peptide that provides an endogenous control against a variety of tissue-damaging stimuli. PACAP has neuro- and general cytoprotective effects due to anti-apoptotic, anti-inflammatory, and antioxidant actions. As PACAP is also a part of the endogenous protective machinery, it can be hypothesized that the decreased protective effects in lack of endogenous PACAP would accelerate age-related degeneration and PACAP knockout mice would display age-related degenerative signs earlier. Recent results support this hypothesis showing that PACAP deficiency mimics aspects of age-related pathophysiological changes including increased neuronal vulnerability and systemic degeneration accompanied by increased apoptosis, oxidative stress, and inflammation. Decrease in PACAP expression has been shown in different species from invertebrates to humans. PACAP-deficient mice display numerous pathological alterations mimicking early aging, such as retinal changes, corneal keratinization and blurring, and systemic amyloidosis. In the present review, we summarize these findings and propose that PACAP deficiency could be a good model of premature aging.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Aging Amyloidosis Apoptosis Degeneration PACAP
Megjelenés:	GeroScience. - 40 : 5-6 (2018), p. 437-452. -
További szerzők:	Atlasz Tamás Szabó E. Jungling Adél Tamás A. (Pécs) Juhász Tamás (1976-) (biológus, orvosbiológus) Fülöp Balázs Dániel (Orvosi alapkutatások) Bárdosi Attila
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001-es BibID:	BIBFORM081853
035-os BibID:	(PMID)31655957 (WOS)000492656400002 (Scopus)85074500121
Első szerző:	Szegeczki Vince
Cím:	Age-related alterations of articular cartilage in pituitary adenylate cyclase-activating polypeptide (PACAP) gene-deficient mice / Vince Szegeczki, Balázs Bauer, Adél Jüngling, Balázs Daniel Fülöp, Judit Vágó, Helga Perényi, Stefano Tarantini, Andrea Tamás, Róza Zákány, Dóra Reglődi, Tamás Juhász
Dátum:	2019
ISSN:	2509-2715 2509-2723
Megjegyzések:	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.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Aggrecan Collagen expression Hyaluronic acid Sox5 Sox6 Sox9
Megjelenés:	GeroScience. - 41 : 6 (2019), p. 775-793. -
További szerzők:	Bauer Balázs Jüngling Adél Fülöp Balázs Dániel (Orvosi alapkutatások) Vágó Judit (1990-) (molekuláris biológus) Perényi Helga Tarantini, Stefano Tamás Andrea (Idegtudomány) (Pécs) Zákány Róza (1963-) (anatómus-, kötőszövetbiológus) Reglődi Dóra (Idegtudományok) Juhász Tamás (1976-) (biológus, orvosbiológus)
Pályázati támogatás:	NKFIK115874 Egyéb Bridging Fund OTKA NKFI-HFK129190 Egyéb NKFI-K119759 Egyéb NKFI-K115874 Egyéb GINOP-2.3.2-15-2016-00050 GINOP (UNKP-16-4- IV.), 2017-1.2.1-NKP-2017-00002 UNKP EFOP-3.6.1.-16-2016-00004 EFOP
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