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001-es BibID:	BIBFORM045939
035-os BibID:	PMID:12839568
Első szerző:	Bakondi Edina (biokémikus, vegyész)
Cím:	Role of Intracellular Calcium Mobilization and Cell-Density-Dependent Signaling in Oxidative-Stress-Induced Cytotoxicity in HaCaT Keratinocytes / Edina Bakondi, Mónika Gönczi, Éva Szabó, Péter Bai, Pál Pacher, Pál Gergely, László Kovács, János Hunyadi, Csaba Szabó, László Csernoch, László Virág
Dátum:	2003
ISSN:	0022-202X
Megjegyzések:	Peroxynitrite is a nitric-oxide-derived cytotoxic mediator produced in a broad range of inflammatory conditions, ranging from sunburn erythema to contact hypersensitivity. Our previous work has shown that in HaCaT cells the cytotoxic activity of peroxynitrite involves both apoptotic and necrotic routes with poly(ADP-ribose) polymerase activation serving as a mol-ecular switch diverting the default apoptotic pathway toward necrosis. Nonetheless, keratinocytes are regarded as highly resistant toward environmental noxa including oxidative stress. We set out to investigate the possible role of two parameters, intracellular calcium mobilization and high cell density, in protecting HaCaT cells from peroxynitrite/oxidative-stress-induced cytotoxicity. First we characterized the effect of peroxynitrite on the calcium homeostasis of HaCaT cells and demonstrated that both authentic peroxynitrite and the peroxynitrite generating compound 3-morpholino-sydnonimine triggered an elevation in intracellular calcium levels. Moreover, we established that treatment of cells with the cell-permeable calcium chelator BAPTA-AM provided significant cytoprotection against peroxynitrite- and hydrogen-peroxide-induced cytotoxicity. Furthermore, when cells reached confluence they were highly resistant to the toxic effects of peroxynitrite, hydrogen peroxide, and superoxide. The resistance to oxidative stress provided by calcium chelation and high cell density involved inhibiting the activation of both poly(ADP-ribose) polymerase and caspases. Our data may provide an explanation for the resistance to oxidative stress of superficial, highly differentiated keratinocytes and indicate that basal proliferative keratinocytes are sensitive in vivo targets of oxidative stress injury.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Journal of Investigative Dermatology. - 121 : 1 (2003), p. 88-95. -
További szerzők:	Gönczi Mónika (1974-) (élettanász) Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Bai Péter (1976-) (biokémikus) Pacher Pál Gergely Pál (1947-) (biokémikus) Kovács László (1939-) (élettanász) Hunyadi János (1943-) (bőrgyógyász, kozmetológus, allergológus) Szabó Csaba (1967-) (orvos) Csernoch László (1961-) (élettanász) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
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001-es BibID:	BIBFORM014289
Első szerző:	Virág László (biokémikus, sejtbiológus, farmakológus)
Cím:	Effects of poly(ADP-ribose) polymerase inhibition on inflammatory cell migration in a murine model of asthma / Virag, L., Bai, P., Bak, I., Pacher, P., Mabley, J. G., Liaudet, L., Bakondi, E., Gergely, P., Kollai, M., Szabo, C.
Dátum:	2004
ISSN:	0891-5849 (Print)
Megjegyzések:	Poly(ADP-ribose) polymerase-1 (PARP-1), a monomeric nuclear enzyme present in eukaryotes, plays a role in cell death, inflammatory mediator expression, and mononuclear cell recruitment in various experimental models of inflammation and reperfusion injury. Part of the molecular mechanism of this function involves the regulation of cytokine and chemokine production. Since chemokines are principal regulators of mononuclear and polymorphonuclear cell trafficking in asthma, we investigated the possibility whether PARP modulates chemokine production and cell recruitment in a murine model of asthma. MATERIAL/METHODS: We studied ovalbumin-sensitized mice challenged with a single dose of ovalbumin. RESULTS: PARP inhibition with the phenanthridinone-based PARP inhibitor PJ34 suppressed inflammatory cell migration. These effects were associated with downregulation of the CC chemokine MIP-1alpha, but not the CXC chemokine MIP-2. The production of TNF- alpha and IL-12, but not IL-5 or IL-13, was also suppressed by PARP inhibition. CONCLUSIONS: Our results demonstrate the pathogenetic role of PARP activation in a murine model of asthma. PARP selectively regulates the production of certain chemokines and cytokines in this experimental model, which may be responsible for some of the observed protective effects seen in the current murine asthma model.Matrix metalloproteinase (MMP) activation contributes to the development of various pathophysiological conditions, including dilated cardiomyopathy, congestive heart failure, and reperfusion injury. Increased oxidative and nitrosative stress have been implicated in the activation of MMPs and also in the cardiotoxicity of doxorubicin (DOX), a commonly used antitumor agent. Thus, we hypothesized that MMP activation occurs in DOX-induced cardiotoxicity. Male Balb/c mice received a single injection of DOX (25 mg/kg i.p.) and were sacrificed 12 h, 1, 2, 3 and 4 days later. Hearts and aortae were harvested for MMP zymography. DOX induced time-dependent activation of MMPs both in the heart and in the aortic tissue with an earlier onset in the latter. These results demonstrate that MMP activation is an early event in DOX-induced cardiotoxicity and raises the possibility that MMP inhibitors may influence the outcome of this severe complication.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Asthma/ drug therapy Bronchoalveolar Lavage Catalysis Cell Death Cell Movement Chemokine CXCL2 Chemokines/metabolism Cytokines/metabolism Disease Models, Animal Down-Regulation Enzyme Inhibitors/ pharmacology Interleukin-10/metabolism Interleukin-12/metabolism Interleukin-13/metabolism Interleukin-5/metabolism Leukocytes, Mononuclear/metabolism Lung/pathology Male Mice Mice, Inbred BALB C Ovalbumin/metabolism/pharmacology Peroxidase/metabolism Poly(ADP-ribose) Polymerases/ antagonists & inhibitors Time Factors Tumor Necrosis Factor-alpha/metabolism Antineoplastic Agents/toxicity Biological Markers/analysis Cardiomyopathy, Dilated/chemically induced/enzymology Doxorubicin/ toxicity Enzyme Activation Heart/ drug effects Heart Failure/chemically induced Matrix Metalloproteinases/ metabolism Models, Animal Myocardium/enzymology/ pathology Reperfusion Injury/chemically induced/enzymology Acute Disease Catalysis/drug effects Chronic Disease Creatine Kinase/blood Enzyme Inhibitors/pharmacology Heart/ drug effects/physiopathology Heart Failure/ chemically induced/physiopathology/prevention & control L-Lactate Dehydrogenase/blood Metalloporphyrins/ pharmacology Mice, Inbred C57BL Mice, Knockout Nitric Oxide Synthase/antagonists & inhibitors/genetics/metabolism Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Oxidative Stress/drug effects/genetics Peroxynitrous Acid/ metabolism Survival Rate Antibiotics, Antineoplastic Creatine Kinase/metabolism Doxorubicin Enzyme Activation/drug effects Heart Failure/ chemically induced/pathology/physiopathology Hemodynamics/drug effects L-Lactate Dehydrogenase/metabolism Metalloendopeptidases/metabolism Poly(ADP-ribose) Polymerases/ genetics/ metabolism Survival Analysis Ventricular Function, Left/genetics Apoptosis Benzamides/ pharmacology Caspases/metabolism Cells, Cultured DNA Damage/drug effects DNA Fragmentation/drug effects Enzyme Activation/drug effects/physiology Mitochondria/ drug effects Nitrates Nitrites/toxicity Nitrogen Oxides/ toxicity Poly(ADP-ribose) Polymerases/ antagonists & inhibitors/metabolism Protective Agents/ pharmacology Thymus Gland/cytology/ drug effects Tyrosine külföldön készült közlemény
Megjelenés:	Medical Science Monitor. - 10 : 3 (2004), p. BR77-83. -
További szerzők:	Bai Péter (1976-) (biokémikus) Bak István (1975-) (vegyész, analitikus, farmakológus) Pacher Pál Mabley, Jon G. Liaudet, Lucas Bakondi Edina (1975-) (biokémikus, vegyész) Gergely Pál (1947-) (biokémikus) Kollai, M. Szabó Csaba
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