Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands
Introduction: The role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction is currently explored in Sjogren's syndrome patients and in the nonobese diabetic (NOD) mouse model. Vasoactive intestinal peptide (VIP) has anti-inflammatory effects in vari...
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2009
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14786354_v11_n2_p_Calafat http://hdl.handle.net/20.500.12110/paper_14786354_v11_n2_p_Calafat |
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paper:paper_14786354_v11_n2_p_Calafat |
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dspace |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
amylase caspase 3 cyclic AMP dependent protein kinase nuclear protein protein Bax tumor necrosis factor alpha tumor necrosis factor alpha receptor tumor protein 53 induced nuclear protein 1 alpha unclassified drug vasoactive intestinal polypeptide vasoactive intestinal polypeptide receptor 1 cyclic AMP dependent protein kinase acinar cell animal cell animal experiment animal model animal tissue apoptosis article controlled study enzyme activity enzyme substrate female mouse nonhuman nonobese diabetic mouse protein expression protein function protein protein interaction salivary gland disease salivation submandibular gland animal Bagg albino mouse disease model metabolism pathology physiology reverse transcription polymerase chain reaction signal transduction Sjoegren syndrome Western blotting Animals Apoptosis Blotting, Western Cyclic AMP-Dependent Protein Kinases Disease Models, Animal Female Mice Mice, Inbred BALB C Mice, Inbred NOD Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Sjogren's Syndrome Submandibular Gland Tumor Necrosis Factor-alpha Vasoactive Intestinal Peptide |
| spellingShingle |
amylase caspase 3 cyclic AMP dependent protein kinase nuclear protein protein Bax tumor necrosis factor alpha tumor necrosis factor alpha receptor tumor protein 53 induced nuclear protein 1 alpha unclassified drug vasoactive intestinal polypeptide vasoactive intestinal polypeptide receptor 1 cyclic AMP dependent protein kinase acinar cell animal cell animal experiment animal model animal tissue apoptosis article controlled study enzyme activity enzyme substrate female mouse nonhuman nonobese diabetic mouse protein expression protein function protein protein interaction salivary gland disease salivation submandibular gland animal Bagg albino mouse disease model metabolism pathology physiology reverse transcription polymerase chain reaction signal transduction Sjoegren syndrome Western blotting Animals Apoptosis Blotting, Western Cyclic AMP-Dependent Protein Kinases Disease Models, Animal Female Mice Mice, Inbred BALB C Mice, Inbred NOD Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Sjogren's Syndrome Submandibular Gland Tumor Necrosis Factor-alpha Vasoactive Intestinal Peptide Calafat, Mario José Larocca, Luciana Roca, Valeria Inés Hauk, Vanesa Cintia Pregi, Nicolás Nesse, Alcira Beatriz Pérez Leirós, Claudia Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands |
| topic_facet |
amylase caspase 3 cyclic AMP dependent protein kinase nuclear protein protein Bax tumor necrosis factor alpha tumor necrosis factor alpha receptor tumor protein 53 induced nuclear protein 1 alpha unclassified drug vasoactive intestinal polypeptide vasoactive intestinal polypeptide receptor 1 cyclic AMP dependent protein kinase acinar cell animal cell animal experiment animal model animal tissue apoptosis article controlled study enzyme activity enzyme substrate female mouse nonhuman nonobese diabetic mouse protein expression protein function protein protein interaction salivary gland disease salivation submandibular gland animal Bagg albino mouse disease model metabolism pathology physiology reverse transcription polymerase chain reaction signal transduction Sjoegren syndrome Western blotting Animals Apoptosis Blotting, Western Cyclic AMP-Dependent Protein Kinases Disease Models, Animal Female Mice Mice, Inbred BALB C Mice, Inbred NOD Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Sjogren's Syndrome Submandibular Gland Tumor Necrosis Factor-alpha Vasoactive Intestinal Peptide |
| description |
Introduction: The role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction is currently explored in Sjogren's syndrome patients and in the nonobese diabetic (NOD) mouse model. Vasoactive intestinal peptide (VIP) has anti-inflammatory effects in various models of chronic inflammation. Our goal was to analyse the effect of TNF-α on apoptotic mediators in isolated acinar cells from NOD submandibular gland and their modulation by VIP. Methods: Acinar cells were isolated from submandibular glands of 16-week-old NOD females with salivary flow decline. Age-matched BALB/c females or eight-week-old NOD females were used as controls. Apoptotic mediators and TNF-α receptor expression were assessed by immunoblotting and RT-PCR, caspase 3 activity was assessed by optical density at 405 nm with Ac-DEVD-pNA as a substrate and chromatin condensation by Hoechst stain. They were evaluated in resting conditions and after a 3.5 or 6 hours of culture with TNF-α. VIP effects in acinar cells were assessed at 100 nM in TNF-α-treated cultures and VIP receptor functional assays by radio immunoassay (cAMP) or enzymatic detection (amylase). Results: NOD acinar cells at 16 weeks present an increased expression of TNF-α receptor1 together with increased Bax, tumour protein 53-induced nuclear protein1α (TP53INP1α), caspase 3 activity and chromatin condensation. Acini from NOD mice were more sensitive to TNF-α-induced increases of apoptotic mediators than control cells. VIP inhibited TNF-α-induced apoptotic events through functional VPAC1 receptors coupled to the protein kinase A (PKA) signalling pathway. Conclusions: Our results indicate that acinar cells isolated from submandibular glands of NOD mice with salivary dysfunction are more sensitive to apoptosis induced by TNF-α which could be prevented by VIP through a PKA-mediated pathway. © 2009 Calafat et al.; licensee BioMed Central Ltd. |
| author |
Calafat, Mario José Larocca, Luciana Roca, Valeria Inés Hauk, Vanesa Cintia Pregi, Nicolás Nesse, Alcira Beatriz Pérez Leirós, Claudia |
| author_facet |
Calafat, Mario José Larocca, Luciana Roca, Valeria Inés Hauk, Vanesa Cintia Pregi, Nicolás Nesse, Alcira Beatriz Pérez Leirós, Claudia |
| author_sort |
Calafat, Mario José |
| title |
Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands |
| title_short |
Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands |
| title_full |
Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands |
| title_fullStr |
Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands |
| title_full_unstemmed |
Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands |
| title_sort |
vasoactive intestinal peptide inhibits tnf-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands |
| publishDate |
2009 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14786354_v11_n2_p_Calafat http://hdl.handle.net/20.500.12110/paper_14786354_v11_n2_p_Calafat |
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AT calafatmariojose vasoactiveintestinalpeptideinhibitstnfainducedapoptoticeventsinacinarcellsfromnonobesediabeticmicesubmandibularglands AT laroccaluciana vasoactiveintestinalpeptideinhibitstnfainducedapoptoticeventsinacinarcellsfromnonobesediabeticmicesubmandibularglands AT rocavaleriaines vasoactiveintestinalpeptideinhibitstnfainducedapoptoticeventsinacinarcellsfromnonobesediabeticmicesubmandibularglands AT haukvanesacintia vasoactiveintestinalpeptideinhibitstnfainducedapoptoticeventsinacinarcellsfromnonobesediabeticmicesubmandibularglands AT preginicolas vasoactiveintestinalpeptideinhibitstnfainducedapoptoticeventsinacinarcellsfromnonobesediabeticmicesubmandibularglands AT nessealcirabeatriz vasoactiveintestinalpeptideinhibitstnfainducedapoptoticeventsinacinarcellsfromnonobesediabeticmicesubmandibularglands AT perezleirosclaudia vasoactiveintestinalpeptideinhibitstnfainducedapoptoticeventsinacinarcellsfromnonobesediabeticmicesubmandibularglands |
| _version_ |
1768545433137709056 |
| spelling |
paper:paper_14786354_v11_n2_p_Calafat2023-06-08T16:18:21Z Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands Calafat, Mario José Larocca, Luciana Roca, Valeria Inés Hauk, Vanesa Cintia Pregi, Nicolás Nesse, Alcira Beatriz Pérez Leirós, Claudia amylase caspase 3 cyclic AMP dependent protein kinase nuclear protein protein Bax tumor necrosis factor alpha tumor necrosis factor alpha receptor tumor protein 53 induced nuclear protein 1 alpha unclassified drug vasoactive intestinal polypeptide vasoactive intestinal polypeptide receptor 1 cyclic AMP dependent protein kinase acinar cell animal cell animal experiment animal model animal tissue apoptosis article controlled study enzyme activity enzyme substrate female mouse nonhuman nonobese diabetic mouse protein expression protein function protein protein interaction salivary gland disease salivation submandibular gland animal Bagg albino mouse disease model metabolism pathology physiology reverse transcription polymerase chain reaction signal transduction Sjoegren syndrome Western blotting Animals Apoptosis Blotting, Western Cyclic AMP-Dependent Protein Kinases Disease Models, Animal Female Mice Mice, Inbred BALB C Mice, Inbred NOD Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Sjogren's Syndrome Submandibular Gland Tumor Necrosis Factor-alpha Vasoactive Intestinal Peptide Introduction: The role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction is currently explored in Sjogren's syndrome patients and in the nonobese diabetic (NOD) mouse model. Vasoactive intestinal peptide (VIP) has anti-inflammatory effects in various models of chronic inflammation. Our goal was to analyse the effect of TNF-α on apoptotic mediators in isolated acinar cells from NOD submandibular gland and their modulation by VIP. Methods: Acinar cells were isolated from submandibular glands of 16-week-old NOD females with salivary flow decline. Age-matched BALB/c females or eight-week-old NOD females were used as controls. Apoptotic mediators and TNF-α receptor expression were assessed by immunoblotting and RT-PCR, caspase 3 activity was assessed by optical density at 405 nm with Ac-DEVD-pNA as a substrate and chromatin condensation by Hoechst stain. They were evaluated in resting conditions and after a 3.5 or 6 hours of culture with TNF-α. VIP effects in acinar cells were assessed at 100 nM in TNF-α-treated cultures and VIP receptor functional assays by radio immunoassay (cAMP) or enzymatic detection (amylase). Results: NOD acinar cells at 16 weeks present an increased expression of TNF-α receptor1 together with increased Bax, tumour protein 53-induced nuclear protein1α (TP53INP1α), caspase 3 activity and chromatin condensation. Acini from NOD mice were more sensitive to TNF-α-induced increases of apoptotic mediators than control cells. VIP inhibited TNF-α-induced apoptotic events through functional VPAC1 receptors coupled to the protein kinase A (PKA) signalling pathway. Conclusions: Our results indicate that acinar cells isolated from submandibular glands of NOD mice with salivary dysfunction are more sensitive to apoptosis induced by TNF-α which could be prevented by VIP through a PKA-mediated pathway. © 2009 Calafat et al.; licensee BioMed Central Ltd. Fil:Calafat, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Larocca, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Roca, V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Hauk, V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pregi, N. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Nesse, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pérez Leirós, C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2009 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14786354_v11_n2_p_Calafat http://hdl.handle.net/20.500.12110/paper_14786354_v11_n2_p_Calafat |