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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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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM083275
035-os BibID:(cikkazonosító)1584 (WoS)000509956400001 (Scopus)85078738706
Első szerző:Nagy Annamária
Cím:Zinc Inhibits HIF-Prolyl Hydroxylase Inhibitor-Aggravated VSMC Calcification Induced by High Phosphate / Annamária Nagy, Dávid Pethő, Tamás Gáll, Erzsébet Zavaczki, Mónika Nyitrai, József Posta, Abolfazl Zarjou, Anupam Agarwal, György Balla, József Balla
Dátum:2020
ISSN:1664-042X
Megjegyzések:Vascular calcification is a life-threatening clinical condition in chronic kidney disease (CKD) and is associated with reduced zinc serum levels. Anemia is another frequent complication of CKD. Hypoxia-inducible factor (HIF) stabilizers, also known as HIF prolyl hydroxylase inhibitors (PHI), are promising candidates to treat CKD-associated anemia by increasing erythropoietin synthesis. Recent evidence suggests that HIFs play a pivotal role in vascular calcification. Our study explored feasible impacts of HIF PHI on phosphate (Pi)-induced calcification of vascular smooth muscle cells (VSMCs) and tested whether zinc might inhibit this mineralization process. Treatment of VSMCs with PHI aggravated Pi-induced calcium deposition and Pi uptake. PHI promoted Pi-induced loss of smooth muscle cell markers (ACTA-2, MYH11, SM22?) and enhanced osteochondrogenic gene expression (Msx-2, BMP-2, Sp7) triggering osteochondrogenic phenotypic switch of VSMCs. These effects of PHI paralleled with increased pyruvate dehydrogenase kinase 4 (PDK4) expression, decreased Runx2 Ser451 phosphorylation, and reduced cell viability. Zinc inhibited Pi-induced mineralization of VSMCs in a dose-dependent manner and also attenuated the pro-calcification effect of PHI in Pi-induced mineralization. Zinc inhibited osteochondrogenic phenotypic switch of VSMCs reflected by lowering Pi uptake, decreasing the expressions of Msx-2, BMP-2, and Sp7 as well as the loss of smooth muscle cell-specific markers. Zinc preserved phosphorylation state of Runx2 Ser451, decreased PDK4 level, and restored cell viability. PHI alone reduced the expression of smooth muscle markers without inducing mineralization, which was also inhibited by zinc. In addition, we observed a significantly lower serum zinc level in CKD as well as in patients undergoing carotid endarterectomy compared to healthy individuals. Conclusion - PHI promoted the loss of smooth muscle markers and augmented Pi-induced osteochondrogenic phenotypic switch leading to VSMCs calcification. This mineralization process was attenuated by zinc. Enhanced vascular calcification is a potential risk factor during PHI therapy in CKD which necessitates the strict follow up of vascular calcification and zinc supplementation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
vascular calcification, PHI
Megjelenés:Frontiers in Physiology. - 10 (2020), p. 1-15. -
További szerzők:Pethő Dávid Gáll Tamás (1982-) (molekuláris biológus, mikrobiológus) Zavaczki Erzsébet (1983-) (biotechnológus) Nyitrai Mónika Posta József (1948-) (vegyész, analitikus) Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:OTKA-112333
OTKA
K132828
OTKA
GINOP-2.3.2-15-2016-00043
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
EFOP-3.6.3-VEKOP16-2017-00009
EFOP
ED-18-1-2019-0028
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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