LIVIVO - Suchergebnisse -

Suchergebnis

Treffer 1 - 9 von insgesamt 9

Suchoptionen

Artikel ; Online: Genetics of Sjögren's syndrome.

Teos, Leyla Y / Alevizos, Ilias

2017 Band 182, Seite(n) 41–47

Abstract: The pathogenesis of Sjögren's syndrome has not been elucidated. There has been evidence that genetics play an important role in the development of this disease from earlier studies. However, till now only a number of genes have been identified to be ... ...

Abstract	The pathogenesis of Sjögren's syndrome has not been elucidated. There has been evidence that genetics play an important role in the development of this disease from earlier studies. However, till now only a number of genes have been identified to be associated with SS, and these have only a weak or moderate effect. In this review we summarize the findings of the genetics studies and emphasize the need of large multicenter projects that will increase the sample sizes to provide more meaningful associations, as is the case in other common autoimmune diseases.
Mesh-Begriff(e)	B-Cell Activating Factor/genetics ; Chemokine CCL11/genetics ; DNA-Binding Proteins/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; HLA Antigens/genetics ; Humans ; Interferon Regulatory Factors/genetics ; Interleukin-12 Subunit p35/genetics ; Lymphotoxin-alpha/genetics ; Natural Cytotoxicity Triggering Receptor 3/genetics ; OX40 Ligand/genetics ; Receptors, CXCR5/genetics ; STAT4 Transcription Factor/genetics ; Serotonin Plasma Membrane Transport Proteins/genetics ; Sjogren's Syndrome/genetics ; Trans-Activators/genetics ; Transcription Factors, TFII/genetics ; Tumor Necrosis Factor alpha-Induced Protein 3/genetics ; src-Family Kinases/genetics
Chemische Substanzen	B-Cell Activating Factor ; CCL11 protein, human ; CXCR5 protein, human ; Chemokine CCL11 ; DNA-Binding Proteins ; EBF1 protein, human ; GTF2I protein, human ; HLA Antigens ; IL12A protein, human ; IRF5 protein, human ; Interferon Regulatory Factors ; Interleukin-12 Subunit p35 ; Lymphotoxin-alpha ; NCR3 protein, human ; Natural Cytotoxicity Triggering Receptor 3 ; OX40 Ligand ; Receptors, CXCR5 ; STAT4 Transcription Factor ; STAT4 protein, human ; Serotonin Plasma Membrane Transport Proteins ; TNFSF13B protein, human ; TNFSF4 protein, human ; TNIP1 protein, human ; Trans-Activators ; Transcription Factors, TFII ; BLK protein, human (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; TNFAIP3 protein, human (EC 3.4.19.12) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12)
Sprache	Englisch
Erscheinungsdatum	2017-05-03
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2017.04.018
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Volltext online

Zugriff für angemeldete ZB MED Nutzerinnen und Nutzer

Zusatzmaterialien

Verfügbar in ZB MED Köln/Königswinter

Zs.A 880: Hefte anzeigen

Standort:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Über subito bestellen

Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

Details ▾

Artikel ; Online: Autoantibodies against the Immunoglobulin-Binding Region of Ro52 Link its Autoantigenicity with Pathogen Neutralization.

Burbelo, Peter D / Teos, Leyla Y / Herche, Jesse L / Iadarola, Michael J / Alevizos, Ilias

Scientific reports

2018 Band 8, Heft 1, Seite(n) 3345

Abstract: Ro52/TRIM21 plays a key role in antibody-dependent pathogen neutralization and is a major autoantigen in systemic lupus erythematosus, Sjögren's syndrome (SS), and other autoimmune diseases. Here we evaluated immunoreactivity against Ro52-related ... ...

Abstract	Ro52/TRIM21 plays a key role in antibody-dependent pathogen neutralization and is a major autoantigen in systemic lupus erythematosus, Sjögren's syndrome (SS), and other autoimmune diseases. Here we evaluated immunoreactivity against Ro52-related molecules in SS and healthy volunteers. Although most proteins examined were not antigenic, several TRIM paralogs, including TRIM22, and TRIM38, showed sporadic immunoreactivity in SS. In contrast, the murine Ro52 ortholog with limited linear homology demonstrated high levels of autoantibodies implicating the importance of shared conformational epitopes. To further explore the autoantigencity of Ro52, deletion and point mutant analyses were employed revealing previously hidden, robust autoantibodies directed against its C-terminal immunoglobulin-binding domain. Another autoantibody, rheumatoid factor, targeting the Fc region of IgG, strongly overlapped with Ro52 seropositivity (odds ratio 14; P < 0.0001). These convergent mechanistic findings support a model whereby intracellular Ro52-bound antibody-coated pathogen complexes, released or misprocessed from infected cells, drive autoantigenicity against Ro52 and the Fc region of IgG.
Mesh-Begriff(e)	Animals ; Autoantibodies/immunology ; DNA Mutational Analysis ; Humans ; Immunoglobulin Fc Fragments/immunology ; Immunoglobulin G/immunology ; Mice ; Point Mutation ; Ribonucleoproteins/genetics ; Ribonucleoproteins/immunology ; Sequence Deletion ; Sjogren's Syndrome/pathology
Chemische Substanzen	Autoantibodies ; Immunoglobulin Fc Fragments ; Immunoglobulin G ; Ribonucleoproteins ; SS-A antigen
Sprache	Englisch
Erscheinungsdatum	2018-02-20
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-21522-7
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Details ▾
- Kostenpflichtig bestellen

Artikel ; Online: Autoantibodies against the Immunoglobulin-Binding Region of Ro52 Link its Autoantigenicity with Pathogen Neutralization

Peter D. Burbelo / Leyla Y. Teos / Jesse L. Herche / Michael J. Iadarola / Ilias Alevizos

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Band 12

Abstract: Abstract Ro52/TRIM21 plays a key role in antibody-dependent pathogen neutralization and is a major autoantigen in systemic lupus erythematosus, Sjögren’s syndrome (SS), and other autoimmune diseases. Here we evaluated immunoreactivity against Ro52- ... ...

Abstract	Abstract Ro52/TRIM21 plays a key role in antibody-dependent pathogen neutralization and is a major autoantigen in systemic lupus erythematosus, Sjögren’s syndrome (SS), and other autoimmune diseases. Here we evaluated immunoreactivity against Ro52-related molecules in SS and healthy volunteers. Although most proteins examined were not antigenic, several TRIM paralogs, including TRIM22, and TRIM38, showed sporadic immunoreactivity in SS. In contrast, the murine Ro52 ortholog with limited linear homology demonstrated high levels of autoantibodies implicating the importance of shared conformational epitopes. To further explore the autoantigencity of Ro52, deletion and point mutant analyses were employed revealing previously hidden, robust autoantibodies directed against its C-terminal immunoglobulin-binding domain. Another autoantibody, rheumatoid factor, targeting the Fc region of IgG, strongly overlapped with Ro52 seropositivity (odds ratio 14; P < 0.0001). These convergent mechanistic findings support a model whereby intracellular Ro52-bound antibody-coated pathogen complexes, released or misprocessed from infected cells, drive autoantigenicity against Ro52 and the Fc region of IgG.
Schlagwörter	Medicine ; R ; Science ; Q
Thema/Rubrik (Code)	570
Sprache	Englisch
Erscheinungsdatum	2018-02-01T00:00:00Z
Verlag	Nature Publishing Group
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

Volltext online

Volltext online

Zusatzmaterialien

Fernleihe an ZB MED

Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Artikel ; Online: GATA6 coordinates cross-talk between BMP10 and oxidative stress axis in pulmonary arterial hypertension.

Toyama, Tetsuo / Kudryashova, Tatiana V / Ichihara, Asako / Lenna, Stefania / Looney, Agnieszka / Shen, Yuanjun / Jiang, Lifeng / Teos, Leyla / Avolio, Theodore / Lin, Derek / Kaplan, Ulas / Marden, Grace / Dambal, Vrinda / Goncharov, Dmitry / Delisser, Horace / Lafyatis, Robert / Seta, Francesca / Goncharova, Elena A / Trojanowska, Maria

Scientific reports

2023 Band 13, Heft 1, Seite(n) 6593

Abstract: Pulmonary arterial hypertension (PAH) is a life-threatening condition characterized by a progressive increase in pulmonary vascular resistance leading to right ventricular failure and often death. Here we report that deficiency of transcription factor ... ...

Abstract	Pulmonary arterial hypertension (PAH) is a life-threatening condition characterized by a progressive increase in pulmonary vascular resistance leading to right ventricular failure and often death. Here we report that deficiency of transcription factor GATA6 is a shared pathological feature of PA endothelial (PAEC) and smooth muscle cells (PASMC) in human PAH and experimental PH, which is responsible for maintenance of hyper-proliferative cellular phenotypes, pulmonary vascular remodeling and pulmonary hypertension. We further show that GATA6 acts as a transcription factor and direct positive regulator of anti-oxidant enzymes, and its deficiency in PAH/PH pulmonary vascular cells induces oxidative stress and mitochondrial dysfunction. We demonstrate that GATA6 is regulated by the BMP10/BMP receptors axis and its loss in PAECs and PASMC in PAH supports BMPR deficiency. In addition, we have established that GATA6-deficient PAEC, acting in a paracrine manner, increase proliferation and induce other pathological changes in PASMC, supporting the importance of GATA6 in pulmonary vascular cell communication. Treatment with dimethyl fumarate resolved oxidative stress and BMPR deficiency, reversed hemodynamic changes caused by endothelial Gata6 loss in mice, and inhibited proliferation and induced apoptosis in human PAH PASMC, strongly suggesting that targeting GATA6 deficiency may provide a therapeutic advance for patients with PAH.
Mesh-Begriff(e)	Animals ; Mice ; Bone Morphogenetic Proteins/genetics ; Bone Morphogenetic Proteins/metabolism ; Cell Proliferation ; Cells, Cultured ; Familial Primary Pulmonary Hypertension/pathology ; GATA6 Transcription Factor/genetics ; GATA6 Transcription Factor/metabolism ; Myocytes, Smooth Muscle/metabolism ; Oxidative Stress ; Pulmonary Arterial Hypertension/genetics ; Pulmonary Arterial Hypertension/metabolism ; Pulmonary Arterial Hypertension/pathology ; Pulmonary Artery/pathology ; Vascular Remodeling
Chemische Substanzen	Bone Morphogenetic Proteins ; GATA6 Transcription Factor ; Bmp10 protein, mouse ; Gata6 protein, mouse
Sprache	Englisch
Erscheinungsdatum	2023-04-22
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-33779-8
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Details ▾
- Kostenpflichtig bestellen

Artikel ; Online: Unique atrial myocyte Ca2+ signaling.

Dobrev, D / Teos, Leyla Y / Lederer, W J

Journal of molecular and cellular cardiology

2008 Band 46, Heft 4, Seite(n) 448–451

Mesh-Begriff(e)	Animals ; Arrhythmias, Cardiac/metabolism ; Calcium Signaling ; Heart Atria/cytology ; Heart Atria/metabolism ; Heart Ventricles/cytology ; Heart Ventricles/metabolism ; Homeostasis ; Humans ; Myocytes, Cardiac/metabolism
Sprache	Englisch
Erscheinungsdatum	2008-12-25
Erscheinungsland	England
Dokumenttyp	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2008.12.004
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Volltext online

Zugriff für angemeldete ZB MED Nutzerinnen und Nutzer

Zusatzmaterialien

Verfügbar in ZB MED Köln/Königswinter

Zs.A 426: Hefte anzeigen

Standort:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Über subito bestellen

Details ▾

Artikel ; Online: The Chemokine Receptor CXCR3 Promotes CD8

Caldeira-Dantas, Sofia / Furmanak, Thomas / Smith, Corinne / Quinn, Michael / Teos, Leyla Y / Ertel, Adam / Kurup, Drishya / Tandon, Mayank / Alevizos, Ilias / Snyder, Christopher M

Journal of immunology (Baltimore, Md. : 1950)

2017 Band 200, Heft 3, Seite(n) 1133–1145

Abstract: Recent work indicates that salivary glands are able to constitutively recruit ... ...

Abstract	Recent work indicates that salivary glands are able to constitutively recruit CD8
Mesh-Begriff(e)	Animals ; CD8-Positive T-Lymphocytes/immunology ; Cell Movement/immunology ; Cells, Cultured ; Chemokines/metabolism ; Herpesviridae Infections/immunology ; Herpesviridae Infections/virology ; Immunologic Memory/immunology ; Integrin alpha4/genetics ; Interferon-gamma/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muromegalovirus/immunology ; Receptors, CCR5/genetics ; Receptors, CXCR3/genetics ; Salivary Glands/immunology ; Salivary Glands/virology
Chemische Substanzen	CCR5 protein, mouse ; Chemokines ; Cxcr3 protein, mouse ; IFNG protein, mouse ; Receptors, CCR5 ; Receptors, CXCR3 ; Integrin alpha4 (143198-26-9) ; Interferon-gamma (82115-62-6)
Sprache	Englisch
Erscheinungsdatum	2017-12-29
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1701272
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Verfügbar in ZB MED Köln/Königswinter

Ud II Zs.37: Hefte anzeigen			Standort: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Hefte anzeigen

Über subito bestellen

Details ▾
- Im ZB MED-Bestand
- Kostenpflichtig bestellen

Artikel ; Online: IP3R deficit underlies loss of salivary fluid secretion in Sjögren's Syndrome.

Teos, Leyla Y / Zhang, Yu / Cotrim, Ana P / Swaim, William / Won, Jon H / Ambrus, Julian / Shen, Long / Bebris, Lolita / Grisius, Margaret / Jang, Shyh-Ing / Yule, David I / Ambudkar, Indu S / Alevizos, Ilias

Scientific reports

2015 Band 5, Seite(n) 13953

Abstract: The autoimmune exocrinopathy, Sjögren's syndrome (SS), is associated with secretory defects in patients, including individuals with mild lymphocytic infiltration and minimal glandular damage. The mechanism(s) underlying the secretory dysfunction is not ... ...

Abstract	The autoimmune exocrinopathy, Sjögren's syndrome (SS), is associated with secretory defects in patients, including individuals with mild lymphocytic infiltration and minimal glandular damage. The mechanism(s) underlying the secretory dysfunction is not known. We have used minor salivary gland biopsies from SS patients and healthy individuals to assess acinar cell function in morphologically intact glandular areas. We report that agonist-regulated intracellular Ca(2+) release, critically required for Ca(2+) entry and fluid secretion, is defective in acini from SS patients. Importantly, these acini displayed reduction in IP3R2 and IP3R3, but not AQP5 or STIM1. Similar decreases in IP3R and carbachol (CCh)-stimulated [Ca(2+)]i elevation were detected in acinar cells from lymphotoxin-alpha (LTα) transgenic (TG) mice, a model for (SS). Treatment of salivary glands from healthy individuals with LT α, a cytokine linked to disease progression in SS and IL14α mice, reduced Ca(2+) signaling. Together, our findings reveal novel IP3R deficits in acinar cells that underlie secretory dysfunction in SS patients.
Mesh-Begriff(e)	Acinar Cells/cytology ; Acinar Cells/drug effects ; Acinar Cells/metabolism ; Animals ; Calcium/metabolism ; Calcium Signaling/drug effects ; Carbachol/pharmacology ; Case-Control Studies ; Cell Size/drug effects ; Cells, Cultured ; Disease Models, Animal ; Female ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Interleukins/deficiency ; Interleukins/genetics ; Lymphotoxin-alpha/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Fluorescence, Multiphoton ; Salivary Glands/metabolism ; Salivary Glands/pathology ; Salivary Glands/secretion ; Sjogren's Syndrome/metabolism ; Sjogren's Syndrome/pathology
Chemische Substanzen	Inositol 1,4,5-Trisphosphate Receptors ; Interleukins ; Lymphotoxin-alpha ; TXLNA protein, mouse ; Carbachol (8Y164V895Y) ; Calcium (SY7Q814VUP)
Sprache	Englisch
Erscheinungsdatum	2015-09-14
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep13953
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Volltext online

Volltext online

Zusatzmaterialien

Über subito bestellen

Details ▾
- Volltext online
- Kostenpflichtig bestellen

Artikel: Basal and IGF-I-dependent regulation of potassium channels by MAP kinases and PI3-kinase during eccentric cardiac hypertrophy.

Teos, Leyla Y / Zhao, Aiqiu / Alvin, Zikiar / Laurence, Graham G / Li, Chuanfu / Haddad, Georges E

American journal of physiology. Heart and circulatory physiology

2008 Band 295, Heft 5, Seite(n) H1834–45

Abstract: The potassium channels I(K) and I(K1), responsible for the action potential repolarization and resting potential respectively, are altered during cardiac hypertrophy. The activation of insulin-like growth factor-I (IGF-I) during hypertrophy may affect ... ...

Abstract	The potassium channels I(K) and I(K1), responsible for the action potential repolarization and resting potential respectively, are altered during cardiac hypertrophy. The activation of insulin-like growth factor-I (IGF-I) during hypertrophy may affect channel activity. The aim was to examine the modulatory effects of IGF-I on I(K) and I(K1) through mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways during hypertrophy. With the use of specific inhibitors for ERK1/2 (PD98059), p38 MAPK (SB203580) and PI3K/Akt (LY294002), Western blot and whole cell patch-clamp were conducted on sham and aorto-caval shunt-induced hypertrophy adult rat myocytes. Basal activation levels of MAPKs and Akt were increased during hypertrophy. Acute IGF-I (10(-8) M) enhanced basal activation levels of these kinases in normal hearts but only those of Akt in hypertrophied ones. I(K) and I(K1) activities were lowered by IGF-I. Inhibition of ERK1/2, p38 MAPK, or Akt reduced basal I(K) activity by 70, 32, or 50%, respectively, in normal cardiomyocytes vs. 53, 34, or 52% in hypertrophied ones. However, basal activity of I(K1) was reduced by 45, 48, or 45% in the former vs. 63, 43, or 24% in the latter. The inhibition of either MAPKs or Akt alleviated IGF-I effects on I(K) and I(K1). We conclude that basal I(K) and I(K1) are positively maintained by steady-state Akt and ERK activities. K+ channels seem to be regulated in a dichotomic manner by acutely stimulated MAPKs and Akt. Eccentric cardiac hypertrophy may be associated with a change in the regulation of the steady-state basal activities of K+ channels towards MAPKs, while that of the acute IGF-I-stimulated ones toward Akt.
Mesh-Begriff(e)	Animals ; Cardiomegaly/enzymology ; Disease Models, Animal ; Insulin-Like Growth Factor I/metabolism ; Male ; Membrane Potentials ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Mitogen-Activated Protein Kinases/metabolism ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/enzymology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Phosphorylation ; Potassium Channels/metabolism ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Time Factors ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemische Substanzen	Phosphoinositide-3 Kinase Inhibitors ; Potassium Channels ; Protein Kinase Inhibitors ; Insulin-Like Growth Factor I (67763-96-6) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Sprache	Englisch
Erscheinungsdatum	2008-08-29
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.321.2008
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Verfügbar in ZB MED Köln/Königswinter

Uc I Zs.89: Hefte anzeigen

Standort:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Über subito bestellen

Details ▾
- Im ZB MED-Bestand
- Kostenpflichtig bestellen

Artikel ; Online: Loss of TRPM2 function protects against irradiation-induced salivary gland dysfunction.

Liu, Xibao / Cotrim, Ana / Teos, Leyla / Zheng, Changyu / Swaim, William / Mitchell, James / Mori, Yasuo / Ambudkar, Indu

Nature communications

2012 Band 4, Seite(n) 1515

Abstract: Xerostomia as a result of salivary gland damage is a permanent and debilitating side effect of radiotherapy for head and neck cancers. Effective treatments for protecting, or restoring, salivary gland function are not available. Here we report that ... ...

Abstract	Xerostomia as a result of salivary gland damage is a permanent and debilitating side effect of radiotherapy for head and neck cancers. Effective treatments for protecting, or restoring, salivary gland function are not available. Here we report that irradiation treatment leads to activation of the calcium-permeable channel, transient potential melastatin-like 2 (TRPM2), via stimulation of poly-ADP-ribose polymerase. Importantly, irradiation induced an irreversible loss of salivary gland fluid secretion in TRPM2+/+ mice while a transient loss was seen in TRPM2-/- mice with >60% recovery by 30 days after irradiation. Treatment of TRPM2+/+ mice with the free radical scavenger Tempol or the PARP1 inhibitor 3-aminobenzamide attenuated irradiation-induced activation of TRPM2 and induced significant recovery of salivary fluid secretion. Furthermore, TPL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) induced complete recovery of function in irradiated TRPM2-/- mice. These novel data demonstrate that TRPM2 is activated by irradiation, via PARP1 activation, and contributes to irreversible loss of salivary gland function.
Mesh-Begriff(e)	Acinar Cells/drug effects ; Acinar Cells/metabolism ; Acinar Cells/pathology ; Acinar Cells/radiation effects ; Animals ; Benzamides/pharmacology ; Calcium/metabolism ; Carbachol/pharmacology ; Cell Line ; Cell Survival/drug effects ; Cell Survival/radiation effects ; Enzyme Inhibitors/pharmacology ; Humans ; Hydrogen Peroxide/pharmacology ; Ion Channel Gating/drug effects ; Ion Channel Gating/radiation effects ; Mice ; Mice, Inbred C57BL ; Piperidines/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/metabolism ; Radiation Injuries/pathology ; Radiation Injuries/physiopathology ; Radiation Injuries/prevention & control ; Saliva/drug effects ; Saliva/metabolism ; Saliva/radiation effects ; Salivary Glands/metabolism ; Salivary Glands/pathology ; Salivary Glands/physiopathology ; Salivary Glands/radiation effects ; Salivation/drug effects ; Salivation/radiation effects ; Submandibular Gland/metabolism ; Submandibular Gland/pathology ; Submandibular Gland/physiopathology ; Submandibular Gland/radiation effects ; TRPM Cation Channels/deficiency ; TRPM Cation Channels/metabolism ; X-Rays
Chemische Substanzen	4-hydroxy-2,2,6,6--tetramethylpiperidine-1-N-hydroxyl ; Benzamides ; Enzyme Inhibitors ; Piperidines ; Poly(ADP-ribose) Polymerase Inhibitors ; TRPM Cation Channels ; TRPM2 protein, human ; TRPM2 protein, mouse ; 3-aminobenzamide (8J365YF1YH) ; Carbachol (8Y164V895Y) ; Hydrogen Peroxide (BBX060AN9V) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; Calcium (SY7Q814VUP)
Sprache	Englisch
Erscheinungsdatum	2012-12-28
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms2526
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Details ▾
- Kostenpflichtig bestellen

Zum Seitenanfang

Ihre letzten Suchen

Volltext online

Zusatzmaterialien

Kategorien

Verfügbar in ZB MED Köln/Königswinter

Über subito bestellen

Zusatzmaterialien

Kategorien

Über subito bestellen

Volltext online

Zusatzmaterialien

Kategorien

Fernleihe an ZB MED

Zusatzmaterialien

Kategorien

Über subito bestellen

Volltext online

Zusatzmaterialien

Kategorien

Verfügbar in ZB MED Köln/Königswinter

Über subito bestellen

Zusatzmaterialien

Kategorien

Verfügbar in ZB MED Köln/Königswinter

Über subito bestellen

Volltext online

Zusatzmaterialien

Kategorien

Über subito bestellen

Zusatzmaterialien

Kategorien

Verfügbar in ZB MED Köln/Königswinter

Über subito bestellen

Zusatzmaterialien

Kategorien

Über subito bestellen