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001-es BibID:	BIBFORM078592
Első szerző:	Balla József (belgyógyász, nephrológus)
Cím:	Role of heme in soft tissue mineralization / Balla József, Zarjou Abolfazl, Agarwal Anupam, Becs Gergely, Kovács Katalin, Nyitrai Mónika, Potor László, Pethő Dávid, Oros Melinda, Zavaczki Erzsébet, Arosio Paolo, Eaton John, Balla György
Dátum:	2016
ISSN:	0891-5849
Megjegyzések:	Infiltration of red blood cells into atherosclerotic lesions is a common event in the progression of atherosclerosis. Recently we have observed that after infiltration and exposure of erythrocytes to plaque material, are lysed, and the liberated hemoglobin is oxidized to ferryl hemoglobin (FeIII/FeIV?O) and ferri (FeIII) hemoglobin. After oxidation of ferro (FeII) hemoglobin heme dissociates from globin then is translocated into resident cells including smooth muscle cells within arteries. Mounting evidence suggests an essential role for the heme oxygenase 1 (HO-1)/ferritin system to maintain homeostasis of vascular function. We examined whether induction of HO-1 and ferritin by heme alters mineralization of human smooth muscle cells provoked by phosphorous and vitamin D3 analogs. Upregulation of the HO-1/ferritin system inhibited human smooth muscle cells calcification and osteoblastic differentiation. Of the products of the system, only ferritin and, to a lesser extent, biliverdin were responsible for the inhibition. Ferritin heavy chain and ceruloplasmin, which both possess ferroxidase activity, inhibited calcification; a site-directed mutant of ferritin heavy chain, which lacked ferroxidase activity, failed to inhibit calcification. In addition, osteoblastic transformation of human smooth muscle cells (assessed by upregulation of core binding factor alpha-1, osteocalcin, and alkaline phosphatase activity) was diminished by ferritin/ferroxidase activity. Furthermore, iron-provoked inhibition of osteoblast activity was also demonstrated to be mediated by ferritin and its ferroxidase activity. We conclude that induction of the HO-1/ferritin system prevents calcification and osteoblastic differentiation of human smooth muscle cells mainly via the ferroxidase activity of ferritin.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idézhető absztrakt heme mineralization
Megjelenés:	Free Radical Biology And Medicine. - 96 (2016), p. S13. -
További szerzők:	Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Becs Gergely Sikura Katalin Éva (1985-) (biológus) Nyitrai Mónika Potor László Pethő Dávid Oros Melinda (1975-) (molekuláris biológus) Zavaczki Erzsébet (1983-) (biotechnológus) Arosio, Paolo Eaton, John W. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
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001-es BibID:	BIBFORM010279
Első szerző:	Zarjou, Abolfazl (kutató orvos)
Cím:	Ferritin ferroxidase activity : a potent inhibitor of osteogenesis / Abolfazl Zarjou, Viktória Jeney, Paolo Arosio, Maura Poli, Erzsébet Zavaczki, György Balla, József Balla
Dátum:	2010
ISSN:	0884-0431
Megjegyzések:	Hemochromatosis is a known cause of osteoporosis, and iron overload has deleterious effects on bone. Although iron overload and its association with osteoporosis has long been recognized, the pathogenesis and exact role of iron have been undefined. Bone is an active tissue with constant remodeling capacity. Osteoblast (OB) development and maturation are under the influence of core binding factor alpha-1 (CBF-alpha1), which induces expression of OB-specific genes, including alkaline phosphatase, an important enzyme in early osteogenesis, and osteocalcin, a noncollagenous protein deposited within the osteoid. This study investigates the mechanism by which iron inhibits human OB activity, which in vivo may lead to decreased mineralization, osteopenia, and osteoporosis. We demonstrate that iron-provoked inhibition of OB activity is mediated by ferritin and its ferroxidase activity. We confirm this notion by using purified ferritin H-chain and ceruloplasmin, both known to possess ferroxidase activity that inhibited calcification, whereas a site-directed mutant of ferritin H-chain lacking ferroxidase activity failed to provide any inhibition. Furthermore, we are reporting that such suppression is not restricted to inhibition of calcification, but OB-specific genes such as alkaline phosphatase, osteocalcin, and CBF-alpha1 are all downregulated by ferritin in a dose-responsive manner. This study corroborates that iron decreases mineralization and demonstrates that this suppression is provided by iron-induced upregulation of ferritin. In addition, we conclude that inhibition of OB activity, mineralization, and specific gene expression is attributed to the ferroxidase activity of ferritin. 2010 American Society for Bone and Mineral Research
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Egészség- és Környezettudomány
Megjelenés:	Journal of Bone and Mineral Research. - 25 : 1 (2010), p. 164-172. -
További szerzők:	Jeney Viktória (1971-) (vegyész, kémia tanár) Arosio, Paolo Poli, Maura Zavaczki Erzsébet (1983-) (biotechnológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Újszülött-, és gyermekkori érbetegségek. A hemoxigenáznak és a ferritinnek, mint protektív stressz fehérjéknek szerepe intenzív ellátást igénylő újszülöttek és gyermekek akut és krónikus betegségeiben OTKA-K75883 OTKA
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