Novel N-Phenyl-Substituted Thiazolidinediones Protect Neural Cells against Glutamate- and tBid-Induced Toxicity (822 views)
J Pharmacol Exp Ther (ISSN: 0022-3565, 1521-0103), 2014 Sep; 350(2): 273-289.
Export to BibTeX Export to EndNote
Paper type: Journal Article, Research Support, Non-U. S. Gov'T,
Impact factor: 3.972, 5-year impact factor: 3.819
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84904992419&partnerID=40&md5=c9a7395249ff9b0dd571ca55ae53fb5b
Keywords: Animals, Apoptosis Drug Effects, Bh3 Interacting Domain Death Agonist Protein Toxicity, Cells, Cultured, Glutamic Acid Toxicity, Humans, Membrane Potential, Mitochondrial Drug Effects, Neurons Drug Effects, Neuroprotective Agents Pharmacology, Structure-Activity Relationship, Thiazolidinediones Pharmacology, 4 Thiazolidinedione Derivative, 4 Dimethoxyphenyl)thiazolidine 2, 4 Dione, 4 Dimethylphenyl)thiazolidine 2, 3 (4 Benzylphenyl)thiazolidine 2, 3 (4 Methoxyphenyl)thiazolidine 2, 3 (4 Phenoxyphenyl)thiazolidine 2, 8 Tetrahydronaphthalen 2 Yl)tiazolidine 2, 3 2 Tolylthiazolidine 2, 3 4 Tolylthiazolidine 2, 3 Phenylthiazolidine 2, 3 [4 (methylsulfonyl)phenyl]thiazolidine 2, 5 (2, 4 Dioxothiazolidin 3 Yl) 2 Methylbenzonitrile, Adenosine Triphosphate, Bi 2a1, Bi 6c9, N [3 (2, 4 Dioxothiazolidin 3 Yl)phenyl]acetamide, Protein Bid, Protein Inhibitor, Truncated Protein Bid, Unclassified Drug, [n [4 [(4 Aminophenyl)thio]phenyl] 4 [[(4 Methoxyphenyl)sulfonyl]amino]butanamide], Animal Cell, Animal Experiment, Animal Model, Article, Binding Affinity, Cell Death, Cell Differentiation, Cell Proliferation, Cell Structure, Cell Survival, Cell Viability, Concentration (parameters), Concentration Response, Degenerative Disease, Disorders Of Mitochondrial Functions, Drug Cytotoxicity, Drug Determination, Drug Potency, Drug Screening, Drug Structure, Drug Synthesis, Excitotoxicity, Gene Overexpression, Gene Transfer, Hippocampus, Human Cell, Median Effective Concentration, Mitochondrial Membrane Potential, Mitochondrial Respiration, Mouse, Nerve Cell, Neurotoxicity, Nonhuman, Oxygen Consumption, Plasmid, Priority Journal, Protein Depletion, Structure Activity Relation, 4 Dimethoxyphenyl) Thiazolidine 2, 4 Dimethylphenyl) Thiazolidine 2, 3 (4 Benzylphenyl) Thiazolidine 2, 3 (4 Methoxyphenyl) Thiazolidine 2, 3 (4 Phenoxyphenyl) Thiazolidine 2, 8 Tetrahydronaphthalen 2 Yl) Tiazolidine 2, 3 [4 (methylsulfonyl) Phenyl] Thiazolidine 2, 4 Dioxothiazolidin 3 Yl) Phenyl] Acetamide, [n [4 [(4 Aminophenyl) Thio] Phenyl] 4 [[(4 Methoxyphenyl) Sulfonyl] Amino] Butanamide],
Affiliations:
*** IBB - CNR ***
Institute for Pharmacology and Clinical Pharmacy, Faculty of Pharmacy (S.O., K.E., A.M.D., C.C.) and Institute for Pharmaceutical Chemistry, Faculty of Pharmacy, Philipps University of Marburg, Marburg, Germany (F.C.S., A.L.K., C.W.-G., M.S.)
and Institute of Biostructures and Bioimaging, Naples, Italy (N.D.).
References:
Not available.
J Pharmacol Exp Ther (ISSN: 0022-3565, 1521-0103), 2014 Sep; 350(2): 273-289.
Export to BibTeX Export to EndNote
Paper type: Journal Article, Research Support, Non-U. S. Gov'T,
Impact factor: 3.972, 5-year impact factor: 3.819
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84904992419&partnerID=40&md5=c9a7395249ff9b0dd571ca55ae53fb5b
Keywords: Animals, Apoptosis Drug Effects, Bh3 Interacting Domain Death Agonist Protein Toxicity, Cells, Cultured, Glutamic Acid Toxicity, Humans, Membrane Potential, Mitochondrial Drug Effects, Neurons Drug Effects, Neuroprotective Agents Pharmacology, Structure-Activity Relationship, Thiazolidinediones Pharmacology, 4 Thiazolidinedione Derivative, 4 Dimethoxyphenyl)thiazolidine 2, 4 Dione, 4 Dimethylphenyl)thiazolidine 2, 3 (4 Benzylphenyl)thiazolidine 2, 3 (4 Methoxyphenyl)thiazolidine 2, 3 (4 Phenoxyphenyl)thiazolidine 2, 8 Tetrahydronaphthalen 2 Yl)tiazolidine 2, 3 2 Tolylthiazolidine 2, 3 4 Tolylthiazolidine 2, 3 Phenylthiazolidine 2, 3 [4 (methylsulfonyl)phenyl]thiazolidine 2, 5 (2, 4 Dioxothiazolidin 3 Yl) 2 Methylbenzonitrile, Adenosine Triphosphate, Bi 2a1, Bi 6c9, N [3 (2, 4 Dioxothiazolidin 3 Yl)phenyl]acetamide, Protein Bid, Protein Inhibitor, Truncated Protein Bid, Unclassified Drug, [n [4 [(4 Aminophenyl)thio]phenyl] 4 [[(4 Methoxyphenyl)sulfonyl]amino]butanamide], Animal Cell, Animal Experiment, Animal Model, Article, Binding Affinity, Cell Death, Cell Differentiation, Cell Proliferation, Cell Structure, Cell Survival, Cell Viability, Concentration (parameters), Concentration Response, Degenerative Disease, Disorders Of Mitochondrial Functions, Drug Cytotoxicity, Drug Determination, Drug Potency, Drug Screening, Drug Structure, Drug Synthesis, Excitotoxicity, Gene Overexpression, Gene Transfer, Hippocampus, Human Cell, Median Effective Concentration, Mitochondrial Membrane Potential, Mitochondrial Respiration, Mouse, Nerve Cell, Neurotoxicity, Nonhuman, Oxygen Consumption, Plasmid, Priority Journal, Protein Depletion, Structure Activity Relation, 4 Dimethoxyphenyl) Thiazolidine 2, 4 Dimethylphenyl) Thiazolidine 2, 3 (4 Benzylphenyl) Thiazolidine 2, 3 (4 Methoxyphenyl) Thiazolidine 2, 3 (4 Phenoxyphenyl) Thiazolidine 2, 8 Tetrahydronaphthalen 2 Yl) Tiazolidine 2, 3 [4 (methylsulfonyl) Phenyl] Thiazolidine 2, 4 Dioxothiazolidin 3 Yl) Phenyl] Acetamide, [n [4 [(4 Aminophenyl) Thio] Phenyl] 4 [[(4 Methoxyphenyl) Sulfonyl] Amino] Butanamide],
Affiliations:
*** IBB - CNR ***
Institute for Pharmacology and Clinical Pharmacy, Faculty of Pharmacy (S.O., K.E., A.M.D., C.C.) and Institute for Pharmaceutical Chemistry, Faculty of Pharmacy, Philipps University of Marburg, Marburg, Germany (F.C.S., A.L.K., C.W.-G., M.S.)
and Institute of Biostructures and Bioimaging, Naples, Italy (N.D.).
References:
Not available.
Novel N-Phenyl-Substituted Thiazolidinediones Protect Neural Cells against Glutamate- and tBid-Induced Toxicity
Mitochondrial demise is a key feature of progressive neuronal death contributing to acute and chronic neurological disorders. Recent studies identified a pivotal role for the BH3-only protein B-cell lymphoma-2 interacting domain death antagonist (Bid) for such mitochondrial damage and delayed neuronal death after oxygen-glucose deprivation, glutamate-induced excitotoxicity, or oxidative stress in vitro and after cerebral ischemia in vivo. Therefore, we developed new N-phenyl-substituted thiazolidine-2,4-dione derivatives as potent inhibitors of Bid-dependent neurotoxicity. The new compounds 6, 7, and 16 were identified as highly protective by extensive screening in a model of glutamate toxicity in immortalized mouse hippocampal neurons (HT-22 cells). These compounds significantly prevent truncated Bid-induced toxicity in the neuronal cell line, providing strong evidence that inhibition of Bid was the underlying mechanism of the observed protective effects. Furthermore, Bid-dependent hallmarks of mitochondrial dysfunction, such as loss of mitochondrial membrane potential, ATP depletion, as well as impairments in mitochondrial respiration, are significantly prevented by compounds 6, 7, and 16. Therefore, the present study identifies a class of N-phenyl thiazolidinediones as novel Bid-inhibiting neuroprotective agents that provide promising therapeutic perspectives for neurodegenerative diseases, in which Bid-mediated mitochondrial damage and associated intrinsic death pathways contribute to the underlying progressive loss of neurons.
Mitochondrial demise is a key feature of progressive neuronal death contributing to acute and chronic neurological disorders. Recent studies identified a pivotal role for the BH3-only protein B-cell lymphoma-2 interacting domain death antagonist (Bid) for such mitochondrial damage and delayed neuronal death after oxygen-glucose deprivation, glutamate-induced excitotoxicity, or oxidative stress in vitro and after cerebral ischemia in vivo. Therefore, we developed new N-phenyl-substituted thiazolidine-2,4-dione derivatives as potent inhibitors of Bid-dependent neurotoxicity. The new compounds 6, 7, and 16 were identified as highly protective by extensive screening in a model of glutamate toxicity in immortalized mouse hippocampal neurons (HT-22 cells). These compounds significantly prevent truncated Bid-induced toxicity in the neuronal cell line, providing strong evidence that inhibition of Bid was the underlying mechanism of the observed protective effects. Furthermore, Bid-dependent hallmarks of mitochondrial dysfunction, such as loss of mitochondrial membrane potential, ATP depletion, as well as impairments in mitochondrial respiration, are significantly prevented by compounds 6, 7, and 16. Therefore, the present study identifies a class of N-phenyl thiazolidinediones as novel Bid-inhibiting neuroprotective agents that provide promising therapeutic perspectives for neurodegenerative diseases, in which Bid-mediated mitochondrial damage and associated intrinsic death pathways contribute to the underlying progressive loss of neurons.
Novel N-Phenyl-Substituted Thiazolidinediones Protect Neural Cells against Glutamate- and tBid-Induced Toxicity
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Novel N-Phenyl-Substituted Thiazolidinediones Protect Neural Cells against Glutamate- and tBid-Induced Toxicity
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* Design, Optimization, and Structural Characterization of an Apoptosis-Inducing Factor Peptide Targeting Human Cyclophilin A to Inhibit Apoptosis Inducing Factor-Mediated Cell Death (111 views)
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Impact Factor: 5.207
View Export to BibTeX Export to EndNote
Miceli M, Cutignano A, Conte M, Ummarino R, Romanelli A, Ruvo M, Leone M, Mercurio FA, Doti N, Manzo E, Romano G, Altucci L, Ianora A
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Impact Factor: 3.345
View Export to BibTeX Export to EndNote
Soprano M, Sorriento D, Rusciano MR, Maione AS, Limite G, Forestieri P, D'Angelo D, D'Alessio M, Campiglia P, Formisano P, Iaccarino G, Bianco R, Illario M
* Oxidative Stress Mediates the Antiproliferative Effects of Nelfinavir in Breast Cancer Cells (319 views)
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Impact Factor: 2.806
View Export to BibTeX Export to EndNote
De Rosa V, Iommelli F, Monti M, Fonti R, Votta G, Stoppelli MP, Del Vecchio S
* Reversal of Warburg Effect and Reactivation of Oxidative Phosphorylation by Differential Inhibition of EGFR Signaling Pathways in Non-Small Cell Lung Cancer (764 views)
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Impact Factor: 8.738
View Export to BibTeX Export to EndNote
Hangen E, Féraud O, Lachkar S, Mou H, Doti N, Fimia GM, Lam N-V, Zhu C, Godin I, Muller K, Chatzi A, Nuebel E, Ciccosanti F, Flamant S, Bénit P, Perfettini J-L, Sauvat A, Bennaceur-Griscelli A, Ser-Le Roux K, Gonin P, Tokatlidis K, Rustin P, Piacentini M, Ruvo M, Blomgren K, Kroemer G, Modjtahedi N
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Impact Factor: 13.958
View Export to BibTeX Export to EndNote
Doti N, Reuther C, Scognamiglio PL, Dolga AM, Plesnila N, Ruvo M, Culmsee C
* Inhibition of the AIF/CypA complex protects against intrinsic death pathways induced by oxidative stress (3675 views)
Cell Death & (ISSN: 2041-4889, 2041-4889electronic), 2014 Jan 16; 5(1): e993-e993.
Impact Factor: 5.014
View Export to BibTeX Export to EndNote
Severino V, Alessio N, Farina A, Sandomenico A, Cipollaro M, Peluso G, Galderisi U, Chambery A
* Insulin-like growth factor binding proteins 4 and 7 released by senescent cells promote premature senescence in mesenchymal stem cells (3871 views)
Cell Death & (ISSN: 2041-4889, 2041-4889electronic), 2013 Nov 7; 4(11): e911-e911.
Impact Factor: 5.177
View Export to BibTeX Export to EndNote
Perrino C, Schiattarella GG, Sannino A, Pironti G, Petretta MP, Cannavo A, Gargiulo G, Ilardi F, Magliulo F, Franzone A, Carotenuto G, Serino F, Altobelli GG, Cimini V, Cuocolo A, Lombardi A, Goglia F, Indolfi C, Trimarco B, Esposito G
* Genetic deletion of uncoupling protein 3 exaggerates apoptotic cell death in the ischemic heart leading to heart failure (638 views)
J Am Heart Assoc Journal Of The American Heart Association (ISSN: 2047-9980), 2013 May 20; 2(3): e000086-e000086.
Impact Factor: 2.882
View Export to BibTeX Export to EndNote
Dolga AM, Netter MF, Perocchi F, Doti N, Meissner L, Tobaben S, Grohm J, Zischka H, Plesnila N, Decher N, Culmsee C
* Mitochondrial Small Conductance SK2 Channels Prevent Glutamate-induced Oxytosis and Mitochondrial Dysfunction (719 views)
Jbc Papers (ISSN: 0021-9258, 1083-351x, 0021-9258linking), 2013 Apr 12; 288(15): 10792-10804.
Impact Factor: 4.6
View Export to BibTeX Export to EndNote
Sandomenico A, Russo A, Palmieri G, Bergamo P, Gogliettino M, Falcigno L, Ruvo M
* Small peptide inhibitors of acetyl-peptide hydrolase having an uncommon mechanism of inhibition and a stable bent conformation (724 views)
J Med Chem (ISSN: 0022-2623, 1520-4804, 0022-2623print), 2012 Mar 8; 55(5): 2102-2111.
Impact Factor: 5.614
View Export to BibTeX Export to EndNote
Zannetti A, Iommelli F, Speranza A, Salvatore M, Del Vecchio S
* 3'-deoxy-3'-18F-fluorothymidine (FLT) PET/CT to guide therapy with epidermal growth factor receptor (EGFR) antagonists and Bcl-xL inhibitors in non-small cell lung cancer (779 views)
J Nucl Med (ISSN: 0161-5505, 1535-5667, 1535-5667electronic), 2012 Mar 1; 53(3): 443-450.
Impact Factor: 5.774
View Export to BibTeX Export to EndNote
Zannetti A, Iommelli F, Speranza A, Salvatore M, Del Vecchio S
* 3'-deoxy-3'-18F-fluorothymidine PET/CT to guide therapy with epidermal growth factor receptor antagonists and Bcl-xL inhibitors in non-small cell lung cancer (720 views)
J Nucl Med (ISSN: 1535-5667, 0161-5505, 1535-5667electronic), 2012 Mar 1; 53(3): 443-450.
Impact Factor: 5.774
View Export to BibTeX Export to EndNote
Zannetti A, Iommelli F, Fonti R, Papaccioli A, Sommella J, Lettieri A, Pirozzi G, Bianco R, Tortora G, Salvatore M, Del Vecchio S
* Gefitinib induction of in vivo detectable signals by Bcl-2/Bcl-xL modulation of inositol trisphosphate receptor type (701 views)
Clin Cancer Res (ISSN: 1078-0432, 1078-0432linking, 1078-0432print), 2008 Aug 15; 14(16): 5209-5219.
Impact Factor: 6.488
View Export to BibTeX Export to EndNote
Atlante A, Amadoro G, Bobba A, de Bari L, Corsetti V, Pappalardo G, Marra E, Calissano P, Passarella S
* A peptide containing residues 26-44 of tau protein impairs mitochondrial oxidative phosphorylation acting at the level of the adenine nucleotide translocator (783 views)
Bba-Gen Subjects (ISSN: 0005-2728, 0006-3002print, 0006-3002linking), 2008; 1777(10): 1289-1300.
Impact Factor: 4.447
View Export to BibTeX Export to EndNote
Russo M, Palumbo R, Tedesco I, Mazzarella G, Russo P, Iacomino G, Russo GL
Quercetin and anti-CD95(Fas/Apo1) enhance apoptosis in HPB-ALL cell line (551 views)
Febs Lett (ISSN: 0014-5793, 0014-5793print, 1873-3468electronic), 1999 Dec 3; 462(3): 322-328.
Impact Factor: 3.72
View Export to BibTeX Export to EndNote
15 Records (12 excluding Abstracts).
Total impact factor: 83.544 (70.471 excluding Abstracts).
Total 5 year impact factor: 86.773 (73.24 excluding Abstracts).
Total impact factor: 83.544 (70.471 excluding Abstracts).
Total 5 year impact factor: 86.773 (73.24 excluding Abstracts).
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