18 results on '"Petrazzuolo, M."'
Search Results
2. Does High Speed Rail compete fairly with other transportation modes? Madrid-Barcelona case study
- Author
-
Petrazzuolo M., Ortega Horte A., Vassallo J., PAGLIARA, FRANCESCA, Petrazzuolo, M., Ortega Horte, A., Pagliara, Francesca, and Vassallo, J.
- Published
- 2013
3. Captopril modulates acetylcholinesterase in human keratinocytes
- Author
-
BARONI, Adone, BUOMMINO, Elisabetta, RUOCCO, Eleonora, PETRAZZUOLO M, DE FILIPPIS A, SATRIANO RA, RUOCCO, Vincenzo, COZZA V, TUFANO MA, DE FILIPPIS, Anna, Baroni, Adone, Buommino, Elisabetta, Ruocco, Eleonora, Petrazzuolo, M, DE FILIPPIS, A, Satriano, Ra, Ruocco, Vincenzo, Cozza, V, Tufano, Ma, and DE FILIPPIS, Anna
- Published
- 2011
4. 3OMETHYLFUNICONE, A METABOLITE FROM PENICILLIUM PINOPHYLUM, INHIBITS PROLIFERATION OF HUMAN MELANOMA CELLS BY CAUSING G2/M ARREST AND INDUCING APOPTOSIS
- Author
-
Baroni A, De Luca A, De Filippis A, Petrazzuolo M, Manente L, Nicoletti R, Tufano MA, Buommino E, Baroni, A, De Luca, A, De Filippis, A, Petrazzuolo, M, Manente, L, Nicoletti, R, Tufano, Ma, and Buommino, E
- Published
- 2009
5. BIOPROSPECTING FOR ANTAGONIST PENICILLIUM STRAINS AS A RESOURCE AF A NEW ANTITUMOR COMPOUNDS
- Author
-
Nicoletti R, Buommino E, De Filippis A, Lopez-Gresa M P, Manzo E, Carella A, Petrazzuolo M, Tufano M A, Nicoletti, R, Buommino, E, De Filippis, A, Lopez-Gresa, M P, Manzo, E, Carella, A, Petrazzuolo, M, and Tufano, M A
- Published
- 2008
6. Artemisinin reduces human melanoma cell migration by down-regulating alphaVbeta3 integrin and reducing metalloproteinase 2 production
- Author
-
BUOMMINO, Elisabetta, BARONI, Adone, CANOZO N., PETRAZZUOLO M., NICOLETTI R., VOZZA A., TUFANO M. A., Buommino, Elisabetta, Baroni, Adone, Canozo, N., Petrazzuolo, M., Nicoletti, R., Vozza, A., and Tufano, M. A.
- Subjects
parasitic diseases ,metalloproteinase 2 ,Artemisinin reduces human melanoma ,alphaVbeta3 integrin - Abstract
Summary Artemisinin and its derivatives are well known antimalarial drugs, particularly useful after resistance to traditional antimalarial pharmaceuticals has started to occur in Plasmodium falciparum. In recent years, anticancer activity of artemisinin has been reported both in vitro and in vivo. Artemisinin has inhibitory effects on cancer cell growth and anti-angiogenetic activity. In the present investigation, we analyzed the inhibitory effects of artemisinin on migratory ability of melanoma cell lines (A375P and A375M, low and medium metastatic properties, respectively). We demonstrate that artemisinin induces cell growth arrest in A375M, and affects A375P cells viability with cytotoxic and growth inhibitory effects, while it was not effective in contrasting proliferation of other tumor cell lines (MCF7 and MKN). In addition, artemisinin affected the migratory ability of A375M cells by reducing metalloproteinase 2 (MMP-2) production and down-regulating αvβ3 integrin expression. These findings introduce a potential of artemisinin as a chemotherapeutic agent in melanoma treatment.
- Published
- 2008
7. Il 3-O-methylfunicone, prodotto da Penicillium Pinophilum, inibisce la motilità delle cellule MCF-7 riducendo l’espressione dell’integrina αVβ5
- Author
-
BUOMMINO, Elisabetta, Orlando M, De Filippis A, Cozza V, Petrazzuolo M, Boccellino M, Nicoletti R, Tufano M. A., QUAGLIUOLO, Lucio, Buommino, Elisabetta, Orlando, M, De Filippis, A, Cozza, V, Petrazzuolo, M, Boccellino, M, Quagliuolo, Lucio, Nicoletti, R, and Tufano, M. A.
- Published
- 2005
8. The immunomodulatory protein SV-IV protects serum-deprived cells againstapoptosis but not against G0/G1 arrest: possible implications for the survival ofimplanting embryo
- Author
-
Morelli, F, Peluso, G, Petillo, O, Giannattasio, A, Filosa, S, Motta, Cm, Tammaro, S, Zatterale, A, Calzone, R, Budillon, A, Cartenì, M, DE MARIA, S, Costanza, Mr, Nigro, A, Petrazzuolo, M, Buommino, E, Rizzo, M, Capasso, G, Baiano, S, Moscatiello, F, Ravagnan, G, Fuggetta, Mp, Tajana, Gianfranco, Stiuso, P, Metafora, Bm, Metafora, V, and Metafora, S.
- Published
- 2007
9. 3- O-methylfunicone, a metabolite of Penicillium pinophilum, inhibits proliferation of human melanoma cells by causing G2 + M arrest and inducing apoptosis.
- Author
-
Baroni, A., De Luca, A., De Filippis, A., Petrazzuolo, M., Manente, L., Nicoletti, R., Tufano, M. A., and Buommino, E.
- Subjects
RESEARCH ,CELL proliferation ,MELANOMA ,NEUROENDOCRINE tumors ,CELL death ,PENICILLIUM ,APOPTOSIS - Abstract
Objectives: Melanoma cells take advantage of impaired ability to undergo programmed cell death in response to different external stimuli and chemotherapeutic drugs; this makes prevention of tumour progression very difficult. The aim of this study was to demonstrate whether 3- O-methylfunicone (OMF), a metabolite of Penicillium pinophilum, has the ability to arrest cell population growth and to induce apoptosis in A375P (parental) and A375M (metastasis derivatived) melanoma cell lines. Materials and methods: Cell proliferation and apoptosis were analysed by flow cytometry, DNA fragmentation, caspase-3 and caspase-9 activation, and PARP-1 cleavage. Results: We demonstrated that OMF affected cell proliferation in a time- and dose-dependent manner, reaching the best effect at concentration of 80 µg/ml for 24 h. Flow cytometry revealed that OMF caused significant G
2 phase arrest, which was associated with marked decrease in cyclin B1/p34cdc2 complex and p21 induction. OMF also induced marked decrease of survivin expression. Reduced levels of apoptosis were evident after silencing p21 expression in both cell lines. Finally, the effect exercised by OMF on hTERT and TEP-1 gene expression confirmed the ability of this molecule to interfere with replicative ability of cells. Conclusions: The results reported here seem to suggest that OMF as a promising molecule to include in strategies for treatment of melanoma. [ABSTRACT FROM AUTHOR]- Published
- 2009
- Full Text
- View/download PDF
10. 3-O-METHYLFUNICONE, A METABOLITE FROM PENICILLIUM PINOPHILUM, INHIBITS PROLIFERATION OF HUMAN MELANOMA CELLS BY CAUSING G2/M ARREST AND INDUCING APOPTOSIS
- Author
-
Adone Baroni, Lucrezia Manente, Marcella Petrazzuolo, A. De Filippis, A. De Luca, Rosario Nicoletti, Elisabetta Buommino, Maria Antonietta Tufano, Baroni, Adone, DE LUCA, Antonio, DE FILIPPIS, A., Petrazzuolo, M., Manente, L., Nicoletti, R., Tufano, M. A., Buommino, Elisabetta, Baroni, A, De Luca, A, De Filippis, A, Petrazzuolo, M, Manente, L, Nicoletti, R, and Tufano, M. A
- Subjects
rho GTP-Binding Proteins ,Programmed cell death ,Cell ,Poly (ADP-Ribose) Polymerase-1 ,Apoptosis ,Biology ,Flow cytometry ,Cell Line, Tumor ,Survivin ,medicine ,Humans ,RNA, Small Interfering ,Cyclin B1 ,Poly(ADP-ribose) Polymerase ,Melanoma ,Pyrone ,Cell Proliferation ,medicine.diagnostic_test ,Caspase 3 ,Cell growth ,Cell Cycle ,Penicillium ,Apoptosi ,Original Articles ,Cell Biology ,General Medicine ,Caspase 9 ,Cell biology ,Gene Expression Regulation, Neoplastic ,medicine.anatomical_structure ,Pyrones ,Cell culture ,Cancer research ,Poly(ADP-ribose) Polymerases ,Human - Abstract
Objectives: Melanoma cells take advantage of impaired ability to undergo programmed cell death in response to different external stimuli and chemotherapeutic drugs; this makes prevention of tumour progression very difficult. The aim of this study was to demonstrate whether 3-O-methylfunicone (OMF), a metabolite of Penicillium pinophilum, has the ability to arrest cell population growth and to induce apoptosis in A375P (parental) and A375M (metastasis derivatived) melanoma cell lines. Materials and methods: Cell proliferation and apoptosis were analysed by flow cytometry, DNA fragmentation, caspase-3 and caspase-9 activation, and PARP-1 cleavage. Results: We demonstrated that OMF affected cell proliferation in a time- and dose-dependent manner, reaching the best effect at concentration of 80 g/ml for 24 h. Flow cytometry revealed that OMF caused significant G2 phase arrest, which was associated with marked decrease in cyclin B1/p34cdc2 complex and p21 induction. OMF also induced marked decrease of survivin expression. Reduced levels of apoptosis were evident after silencing p21 expression in both cell lines. Finally, the effect exercised by OMF on hTERT and TEP-1 gene expression confirmed the ability of this molecule to interfere with replicative ability of cells. Conclusions: The results reported here seem to suggest that OMF as a promising molecule to include in strategies for treatment of melanoma. © 2009 Blackwell Publishing Ltd.
- Published
- 2009
11. BIOPROSPECTING FOR ANTAGONISTIC PENICILLIUM STRAINS AS A RESOURCE OF NEW ANTITUMOR COMPOUNDS
- Author
-
R. NICOLETTI, A. DE FILIPPIS, M. P. LOPEZ GRESA, M. PETRAZZUOLO, M. A. TUFANO, BUOMMINO, Elisabetta, Nicoletti, R, Buommino, Elisabetta, FILIPPIS A, De, LOPEZ GRESA, Mp, Petrazzuolo, M, Tufano, Ma, Nicoletti, R., DE FILIPPIS, A., LOPEZ GRESA, M. P., Petrazzuolo, M., and Tufano, M. A.
- Published
- 2008
12. 3-O-methylfunicone produced by penicillium pinophilum affects cell motility of breast cancer cells, downregulating alphavbeta5 integrin and inhibiting metalloproteinase-9 secretion
- Author
-
Maria Antonietta Tufano, Valentina Cozza, Elisabetta Buommino, Mariarosaria Boccellino, Marcella Petrazzuolo, Maria Letizia Ciavatta, Anna De Filippis, Rosario Nicoletti, Lucio Quagliuolo, Buommino, Elisabetta, Boccellino, M., DE FILIPPIS, A., Petrazzuolo, M., Cozza, V., Nicoletti, R., Ciavatta, M., Quagliuolo, Lucio, Tufano, M. A., Boccellino, M, FILIPPIS A, De, Petrazzuolo, M, Cozza, V, Nicoletti, R, Ciavatta, M, Quagliuolo, L, and Tufano, Ma
- Subjects
Cancer Research ,Integrins ,Integrin ,Motility ,Down-Regulation ,Breast Neoplasms ,Matrix metalloproteinase ,cell motility ,metalloproteinases ,Cell Movement ,Tubulin ,Cell Line, Tumor ,Survivin ,Humans ,Secretion ,Receptors, Vitronectin ,OMF ,Molecular Biology ,Cell Shape ,Metalloproteinase ,Cell Proliferation ,OMF,cell motility,integrins,metalloproteinases ,Fibrin ,biology ,Cell growth ,Penicillium ,Cell biology ,Matrix Metalloproteinase 9 ,Cell culture ,Tumor progression ,Pyrones ,biology.protein ,Drug Evaluation ,Female - Abstract
Recent evidence assigns integrins and metalloproteinases (MMPs) an important role in regulating tumor cell progression. Here, we demonstrate that 3-O-methylfunicone (OMF), a secondary metabolite produced by Penicillium pinophilum, affects cell proliferation and motility of breast cancer MCF-7 cells, downregulating avb5 integrin, and inhibiting MMP-9 secretion. This effect was absent when the non-tumoral MCF-10 cell line was used. Inhibition of cell motility was also associated to modifications in cell shape and in the distribution of tubulin fibers of OMF-treated MCF- 7 cells. In addition, a possible effect on survivin and hTERT was also investigated. We found that OMF strongly inhibits survivin and hTERT gene expression. The results of this study indicate that OMF-induced inhibition of cell motility may be mediated through the modulation of avb5 integrin and MMP-9secretion. In addition, the inhibition of typical markers of tumor progression such as hTERT and survivin in MCF-7 and their inactivity towards MCF10 provide strong evidence for a potential use of OMF in anticancer therapy Recent evidence assigns integrins and metalloproteinases (MMPs) an important role in regulating tumor cell progression. Here, we demonstrate that 3-O-methylfunicone (OMF), a secondary metabolite produced by Penicillium pinophilum, affects cell proliferation and motility of breast cancer MCF-7 cells, downregulating αvβ5 integrin, and inhibiting MMP-9 secretion. This effect was absent when the non-tumoral MCF-10 cell line was used. Inhibition of cell motility was also associated to modifications in cell shape and in the distribution of tubulin fibers of OMF-treated MCF-7 cells. In addition, a possible effect on survivin and hTERT was also investigated. We found that OMF strongly inhibits survivin and hTERT gene expression. The results of this study indicate that OMF-induced inhibition of cell motility may be mediated through the modulation of αvβ5 integrin and MMP-9 secretion. In addition, the inhibition of typical markers of tumor progression such as hTERT and survivin in MCF-7 and their inactivity towards MCF10 provide strong evidence for a potential use of OMF in anticancer therapy. © 2007 Wiley-Liss, Inc.
- Published
- 2007
13. Captopril modulates acetylcholinesterase in human keratinocytes
- Author
-
Maria Antonietta Tufano, Eleonora Ruocco, Vincenzo Ruocco, Valentina Cozza, R. A. Satriano, Elisabetta Buommino, Anna De Filippis, Marcella Petrazzuolo, Adone Baroni, Baroni, A, Buommino, Elisabetta, Ruocco, E, Petrazzuolo, M, DE FILIPPIS, A, Satriano, R, Ruocco, V, Cozza, V, and Tufano, M.
- Subjects
Keratinocytes ,medicine.medical_specialty ,Captopril ,Blotting, Western ,Angiotensin-Converting Enzyme Inhibitors ,Dermatology ,Cell Communication ,Cell Line ,chemistry.chemical_compound ,Acetylcholine secretion ,Internal medicine ,medicine ,Humans ,Secretion ,Cell adhesion ,Acetylcholine receptor ,Reverse Transcriptase Polymerase Chain Reaction ,General Medicine ,Acetylcholinesterase ,Acetylcholine ,Cell biology ,Up-Regulation ,HaCaT ,medicine.anatomical_structure ,Endocrinology ,Acantholysis ,Intercellular Junctions ,chemistry ,Keratinocyte ,medicine.drug - Abstract
Human keratinocytes synthesize and secrete non-neuronal acetylcholine, which acts as a local cell signaling molecule, regulating functions like proliferation, cell adhesion, motility, desmosomal cell contact, and glandular activity. The keratinocyte acetylcholine axis is composed of the enzymes mediating acetylcholine synthesis (acetyltransferase) and degradation (acetylcholinesterase), and two classes of acetylcholine receptors. In this study we investigated the effect of captopril, an ACE-inhibitor, on acetylcholinesterase and acetylcholine secretion in human keratinocytes. We analyzed the level of acetylcholinesterase in HaCat and NHEK cells by RT-PCR and Western blotting analysis. In addition, the effect of captopril on AChE activity was evaluated. We found that captopril induces a strong AChE up-regulation leading to ACh degradation and reduced secretion. Our results suggest that acantholysis induced by ACE-inhibitors might be linked to altered level of Ach.
- Published
- 2010
14. Polydatin, a natural precursor of resveratrol, induces β-defensin production and reduces inflammatory response.
- Author
-
Ravagnan G, De Filippis A, Cartenì M, De Maria S, Cozza V, Petrazzuolo M, Tufano MA, and Donnarumma G
- Subjects
- Cell Line, Cytoprotection drug effects, Enzyme-Linked Immunosorbent Assay, Gene Expression drug effects, HSP70 Heat-Shock Proteins biosynthesis, HSP70 Heat-Shock Proteins metabolism, Heat-Shock Response, Humans, Interleukin-6 biosynthesis, Interleukin-6 metabolism, Interleukin-8 biosynthesis, Interleukin-8 metabolism, Resveratrol, Reverse Transcriptase Polymerase Chain Reaction, Tumor Necrosis Factor-alpha biosynthesis, Tumor Necrosis Factor-alpha metabolism, beta-Defensins metabolism, Glucosides pharmacology, Inflammation drug therapy, Keratinocytes metabolism, Stilbenes pharmacology, beta-Defensins biosynthesis
- Abstract
It is well known that human keratinocytes produce the anti-microbial peptide β-defensin 2. Its production is enhanced by pathogenic microorganisms or other environmental stressors. In this study, we evaluated the effect of resveratrol, a polyphenol found in several dietary source as grape seed, and its natural precursor, polydatin on heat-stressed human keratinocytes. By reverse transcription-polymerase chain reaction and enzyme-linked immunoadsorbent assay, we demonstrated that resveratrol used in combination with polydatin was able to modulate interleukin (IL)-6, IL-8 and tumor necrosis factor-alpha gene expression. In addition, our data show that resveratrol and polydatin increased the heat shock protein (Hsp)70B' gene expression, a Hsp that plays an important role in the cytoprotection and repair of cells and tissues. Worthy of note, polydatin used alone or in combination with resveratrol, increased the release of human β-defensin 2. These results highlighted the ability of polydatin and resveratrol to reinforce cytoprotective response in stress conditions and suggest their use in cosmetic or pharmaceutical preparations.
- Published
- 2013
- Full Text
- View/download PDF
15. Captopril modulates acetylcholinesterase in human keratinocytes.
- Author
-
Baroni A, Buommino E, Ruocco E, Petrazzuolo M, De Filippis A, Satriano RA, Ruocco V, Cozza V, and Tufano MA
- Subjects
- Acantholysis physiopathology, Acetylcholine metabolism, Acetylcholinesterase genetics, Blotting, Western, Cell Communication, Cell Line, Humans, Intercellular Junctions, Keratinocytes metabolism, Keratinocytes pathology, Reverse Transcriptase Polymerase Chain Reaction, Up-Regulation, Acantholysis metabolism, Acetylcholinesterase metabolism, Angiotensin-Converting Enzyme Inhibitors pharmacology, Captopril pharmacology, Keratinocytes drug effects
- Abstract
Human keratinocytes synthesize and secrete non-neuronal acetylcholine, which acts as a local cell signaling molecule, regulating functions like proliferation, cell adhesion, motility, desmosomal cell contact, and glandular activity. The keratinocyte acetylcholine axis is composed of the enzymes mediating acetylcholine synthesis (acetyltransferase) and degradation (acetylcholinesterase), and two classes of acetylcholine receptors. In this study we investigated the effect of captopril, an ACE-inhibitor, on acetylcholinesterase and acetylcholine secretion in human keratinocytes. We analyzed the level of acetylcholinesterase in HaCat and NHEK cells by RT-PCR and Western blotting analysis. In addition, the effect of captopril on AChE activity was evaluated. We found that captopril induces a strong AChE up-regulation leading to ACh degradation and reduced secretion. Our results suggest that acantholysis induced by ACE-inhibitors might be linked to altered level of Ach.
- Published
- 2011
- Full Text
- View/download PDF
16. Artemisinin reduces human melanoma cell migration by down-regulating alpha V beta 3 integrin and reducing metalloproteinase 2 production.
- Author
-
Buommino E, Baroni A, Canozo N, Petrazzuolo M, Nicoletti R, Vozza A, and Tufano MA
- Subjects
- Artemisia chemistry, Blotting, Western, Humans, Melanoma metabolism, Melanoma pathology, RNA, Messenger genetics, RNA, Messenger metabolism, Reverse Transcriptase Polymerase Chain Reaction, Tumor Cells, Cultured, Anti-Infective Agents pharmacology, Artemisinins pharmacology, Cell Movement drug effects, Cell Proliferation drug effects, Integrin alphaVbeta3 metabolism, Matrix Metalloproteinase 2 metabolism, Melanoma drug therapy
- Abstract
Artemisinin and its derivatives are well known antimalarial drugs, particularly useful after resistance to traditional antimalarial pharmaceuticals has started to occur in Plasmodium falciparum. In recent years, anticancer activity of artemisinin has been reported both in vitro and in vivo. Artemisinin has inhibitory effects on cancer cell growth and anti-angiogenetic activity. In the present investigation, we analyzed the inhibitory effects of artemisinin on migratory ability of melanoma cell lines (A375P and A375M, low and medium metastatic properties, respectively). We demonstrate that artemisinin induces cell growth arrest in A375M, and affects A375P cells viability with cytotoxic and growth inhibitory effects, while it was not effective in contrasting proliferation of other tumor cell lines (MCF7 and MKN). In addition, artemisinin affected the migratory ability of A375M cells by reducing metalloproteinase 2 (MMP-2) production and down-regulating alpha v beta 3 integrin expression. These findings introduce a potential of artemisinin as a chemotherapeutic agent in melanoma treatment.
- Published
- 2009
- Full Text
- View/download PDF
17. 3-O-methylfunicone produced by penicillium pinophilum affects cell motility of breast cancer cells, downregulating alphavbeta5 integrin and inhibiting metalloproteinase-9 secretion.
- Author
-
Buommino E, Boccellino M, De Filippis A, Petrazzuolo M, Cozza V, Nicoletti R, Ciavatta ML, Quagliuolo L, and Tufano MA
- Subjects
- Breast Neoplasms, Cell Line, Tumor, Cell Proliferation drug effects, Cell Shape drug effects, Down-Regulation, Drug Evaluation, Female, Fibrin metabolism, Humans, Penicillium metabolism, Pyrones chemistry, Tubulin metabolism, Cell Movement drug effects, Integrins metabolism, Matrix Metalloproteinase 9 metabolism, Pyrones pharmacology, Receptors, Vitronectin metabolism
- Abstract
Recent evidence assigns integrins and metalloproteinases (MMPs) an important role in regulating tumor cell progression. Here, we demonstrate that 3-O-methylfunicone (OMF), a secondary metabolite produced by Penicillium pinophilum, affects cell proliferation and motility of breast cancer MCF-7 cells, downregulating alphavbeta5 integrin, and inhibiting MMP-9 secretion. This effect was absent when the non-tumoral MCF-10 cell line was used. Inhibition of cell motility was also associated to modifications in cell shape and in the distribution of tubulin fibers of OMF-treated MCF-7 cells. In addition, a possible effect on survivin and hTERT was also investigated. We found that OMF strongly inhibits survivin and hTERT gene expression. The results of this study indicate that OMF-induced inhibition of cell motility may be mediated through the modulation of alphavbeta5 integrin and MMP-9 secretion. In addition, the inhibition of typical markers of tumor progression such as hTERT and survivin in MCF-7 and their inactivity towards MCF10 provide strong evidence for a potential use of OMF in anticancer therapy., (Copyright (c) 2007 Wiley-Liss, Inc.)
- Published
- 2007
- Full Text
- View/download PDF
18. The immunomodulatory protein SV-IV protects serum-deprived cells against apoptosis but not against G0/G1 arrest: possible implications for the survival of implanting embryo.
- Author
-
Morelli F, Peluso G, Petillo O, Giannattasio A, Filosa S, Motta CM, Tammaro S, Zatterale A, Calzone R, Budillon A, Cartenì M, de Maria S, Costanza MR, Nigro A, Petrazzuolo M, Buommino E, Rizzo M, Capasso G, Baiano S, Moscatiello F, Ravagnan G, Fuggetta MP, Tajana G, Stiuso P, Metafora BM, Metafora V, and Metafora S
- Subjects
- Animals, Antioxidants pharmacology, Apoptosis Regulatory Proteins genetics, Apoptosis Regulatory Proteins metabolism, Catalase genetics, Catalase metabolism, Cell Line, Tumor, Culture Media, Serum-Free metabolism, Cyclin-Dependent Kinases metabolism, Cyclins metabolism, Cytotoxicity, Immunologic, DNA Fragmentation, Embryo Culture Techniques, Embryonic Development, Genomic Instability, Glucosephosphate Dehydrogenase genetics, Glucosephosphate Dehydrogenase metabolism, Humans, Killer Cells, Natural immunology, Killer Cells, Natural metabolism, Leukocytes, Mononuclear drug effects, Leukocytes, Mononuclear enzymology, Leukocytes, Mononuclear immunology, Mice, Mice, Inbred BALB C, Oxidative Stress, Phosphorylation, Protein-Tyrosine Kinases metabolism, RNA, Messenger metabolism, Rats, Rats, Wistar, Reactive Oxygen Species metabolism, Retinoblastoma Protein metabolism, Seminal Vesicle Secretory Proteins pharmacology, Serum metabolism, Signal Transduction, Time Factors, Antioxidants metabolism, Apoptosis drug effects, Cell Proliferation drug effects, Embryo Implantation drug effects, G1 Phase drug effects, Leukocytes, Mononuclear metabolism, Resting Phase, Cell Cycle drug effects, Seminal Vesicle Secretory Proteins metabolism
- Abstract
Serum deprivation induced in human lymphoblastoid Raji cells oxidative stress-associated apoptotic death and G0/G1 cell cycle arrest. Addition into culture medium of the immunomodulatory protein Seminal vesicle protein 4 (SV-IV) protected these cells against apoptosis but not against cycle arrest. The antiapoptotic activity was related to: (1) decrease of endocellular reactive Oxygen species (ROS) (2) increase of mRNAs encoding anti-oxidant enzymes (catalase, G6PD) and antiapoptotic proteins (survivin, cox-1, Hsp70, c-Fos); (3) decrease of mRNAs encoding proapoptotic proteins (c-myc, Bax, caspase-3, Apaf-1). The biochemical changes underlaying these effects were probably induced by a protein tyrosine kinase (PTK) activity triggered by the binding of SV-IV to its putative plasma membrane receptors. The ineffectiveness of SV-IV to abrogate the cycle arrest was accounted for by its downregulating effects on D1,3/E G1-cyclins and CdK2/4 gene expression, ppRb/pRb ratio, and intracellular ROS concentration. In conclusion, these experiments: (1) prove that SV-IV acts as a cell survival factor; (2) suggest the involvement of a PTK in SV-IV signaling; (3) point to cell cycle-linked enzyme inhibition as responsible for cycle arrest; (4) provide a model to dissect the cycle arrest and apoptosis induced by serum withdrawal; (5) imply a possible role of SV-IV in the survival of hemiallogenic implanting embryos.
- Published
- 2007
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.