Дисертації з теми "TRPM2 channel"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся з топ-50 дисертацій для дослідження на тему "TRPM2 channel".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Переглядайте дисертації для різних дисциплін та оформлюйте правильно вашу бібліографію.
Li, Xin. "TRPM2 channel-mediated signalling mechanisms for neuronal cell death." Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/18576/.
Повний текст джерелаLange, Ingo. "The TRPM2 ion channel in nucleotide-gated calcium signaling." kostenfrei, 2008. http://d-nb.info/989951200/34.
Повний текст джерелаXia, Rong. "TRPM2 Channel : Assembly, Ion permeability, and regulation by interacting proteins." Thesis, University of Leeds, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511157.
Повний текст джерелаSyed, Mortadza Sharifah Alawieyah. "Microglial TRPM2 channel activation and its relationship to neurodegenerative diseases." Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/19281/.
Повний текст джерелаAbuarab, Nada Khaled S. "TRPM2 ion channel trafficking and its role in mitochondrial fragmentation and cell death." Thesis, University of Leeds, 2015. http://etheses.whiterose.ac.uk/12490/.
Повний текст джерелаKouzai, Daisuke. "Chemical biological studies on oxidation status-sensitive calcium channels." 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/188546.
Повний текст джерелаFerioli, Silvia [Verfasser], and Barbara [Akademischer Betreuer] Conradt. "Cellular functions of the kinase-coupled TRPM6/TRPM7 channels / Silvia Ferioli ; Betreuer: Barbara Conradt." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1162840501/34.
Повний текст джерелаMassullo, Pam. "Aberrant subcellular targeting of the G185R neutrophil elastase mutant associated with severe congenital neutropenia induces premature apoptosis of differentiating promyelocytes & expression and function of the transient receptor potential 2 (TRPM2) ion channel in dendritic cells." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1172865905.
Повний текст джерелаZou, Jie. "Function and modulation of TRPM2 channels." Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/5902/.
Повний текст джерелаNaylor, Jacqueline. "Function and pharmacology of TRPM3 ion channel." Thesis, University of Leeds, 2008. http://etheses.whiterose.ac.uk/330/.
Повний текст джерелаFernandez, Jose A. "Gating mechanisms of the TRPM* ion channel." Thesis, Queen's University Belfast, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534741.
Повний текст джерелаTajino, Koji. "Cutaneous TRPM8 channels are thermostats against cooling." 京都大学 (Kyoto University), 2011. http://hdl.handle.net/2433/142123.
Повний текст джерелаStraub, Isabelle. "Identification and application of novel and selective blockers for the heat-activated cation channel TRPM3." Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-149321.
Повний текст джерелаGeorgiev, Plamen. "Functional analysis of Drosophila TRPM." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611931.
Повний текст джерелаCao, Tuoxin. "Hydrogen Peroxide and Pharmacological Agent Modulation of TRPV2 Channel Gating." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4848.
Повний текст джерелаKaiser, Simone. "Identification and characterization of the ion channel TRPM8 in prostate cancer." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972610359.
Повний текст джерелаMelanaphy, D. "Expression and function of the TRPMB ion channel in the vasculature." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558085.
Повний текст джерелаLuu, Charles T. "TRPM7 channels as a bioassay of internal and external Mg2+." Wright State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright1572015043215704.
Повний текст джерелаMajeed, Yasser. "Chemical modulation of human TRPC and TRPM ion channels." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515551.
Повний текст джерелаViñuela-Fernández, Ignacio. "Equine laminitis pain and modulatory mechanisms at a potential analgesic target, the TRPM8 ion channel." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/8728.
Повний текст джерелаMak, Stephanie Wai Yin. "Modulation of temperature sensitive ion channels TRPV1 and TRPM8 by Bradykinin." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611520.
Повний текст джерелаWu, Yu [Verfasser], and Peter [Akademischer Betreuer] Heisig. "Ion channel TRPM4 activity and cardiac conduction disease / Yu Wu. Betreuer: Peter Heisig." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/1030365644/34.
Повний текст джерелаLiu, Pin. "Fat Taste Transduction in Mouse Taste Cells: The Role of Transient Receptor Potential Channel Type M5." DigitalCommons@USU, 2010. https://digitalcommons.usu.edu/etd/824.
Повний текст джерелаWang, Qian, and 王倩. "Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206750.
Повний текст джерелаpublished_or_final_version
Physiology
Doctoral
Doctor of Philosophy
Gueffier, Mélanie. "Rôle du canal TRPM4 dans l'hypertrophie cardiaque : utilisation d'un modèle d'entraînement." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT035.
Повний текст джерелаAbstract: Cardiac muscle is an organ that adapts to different hemodynamic stress by activating protein synthesis and increasing cardiomyocytes size, resulting in cardiac hypertrophy. The objective of this PhD is to study the potential role of TRPM4 channel in different types of cardiac hypertrophy. Impaired diastolic Ca2+ is responsible for the initial signal activating signaling pathways in a deleterious cardiac hypertrophy pathological type such as Calcineurin-NFAT pathway and the re-expression of fetal genes. This hypertrophy is first compensatory and preserves the myocardial pump function. This alteration can be carried out by various stimuli such as increased angiotensin II or by cardiovascular diseases such as myocardial infarction and hypertension.However, a beneficial cardiac hypertrophy is also described in the literature, especially during development stages during embryogenesis or even in response to regular moderate physical activity. It is characterized by the activation one different signaling pathway, the IGF-1 - PI3K –Akt, generated by an increase in growth factor levels that is the insulin growth factor -1. These signaling pathways have been widely described in the literature and cross-talking. TRPM4 channel is a nonselective cation channel permeable equally to Na+ and K+, impermeable to Ca2+ but activated by the intracellular Ca2+. In the immune system, it downregulates Ca2+ entry and therefore appears to be involve in many Ca2+-dependent cellular functions in different cell types. By the use of two models of cardiac hypertrophy, a physiological generated by four weeks of training in endurance and pathological after myocardial infarction induced by ligation of the left coronary artery on wild-type and knockout mice -out (KO) for TRPM4 channel, we have demonstrated a functional expression increased TRPM4 channel within the left ventricle associated with down-regulation of Ca2 + entry. TRPM4 the channel being a regulator of calcium homeostasis in cardiomyocytes functional expression after myocardial infarction as well as the drive promotes the activation of the pathway of IGF-1-PI3K-Akt and partially prevents the pathway activation of the NFAT-calcineurin and the development of pathological cardiac hypertrophy, in particular myocardial infarction model. Indeed, in the absence of expression of the channel, the Ca2 + is not regulated, the path of Calcineurin-NFAT is favored. Keywords: TRPM4, cardiac hypertrophy, training, IGF-1-PI3K-Akt, calcineurin
Mellott, Alayna N. "Divalent Metal Cation Entry and Cytotoxicity in Jurkat T Cells: Role of TRPM7 Channels." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1597319673881729.
Повний текст джерелаHampe, Sarah [Verfasser], and Ingrid [Akademischer Betreuer] Boekhoff. "Domain-specific role of the channel-kinase TRPM7 in cell signaling / Sarah Hampe ; Betreuer: Ingrid Boekhoff." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1225682487/34.
Повний текст джерелаHuynh, Kevin Weijian. "Structural Analysis of TRPV2 by Cryo-Electron Microscopy Reveals Regulatory Diversity Among the ThermoTRPV Channels." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1467996438.
Повний текст джерелаAbdulkareem, Zana Azeez. "SK potassium and TRPM7 ion channel role in CNS cell survival and breast cancer cell death decisions." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/80343/.
Повний текст джерелаCurry, Haley Nicole. "Characterization of a Conserved Transient Receptor Potential Channel Supporting Spermatogenesis in Planarian Flatworms." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1589976835122505.
Повний текст джерелаZhang, Yanhui, and 张雁惠. "Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47161644.
Повний текст джерелаpublished_or_final_version
Medicine
Doctoral
Doctor of Philosophy
Uriu, Yoshitsugu. "Biochemical and biophysical characterization of Ca2+ channel complexes in neurotransmission." 京都大学 (Kyoto University), 2010. http://hdl.handle.net/2433/126814.
Повний текст джерелаMittermeier, Lorenz [Verfasser], and Dietmar [Akademischer Betreuer] Martin. "The kinase-coupled TRPM7 channel is the central gatekeeper of intestinal mineral absorption / Lorenz Mittermeier ; Betreuer: Dietmar Martin." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1185979298/34.
Повний текст джерелаVettore, Valentina [Verfasser], and Alexander [Akademischer Betreuer] Dietrich. "TRPM7 in T-cell signaling : kinase-coupled ion channel in immune system homeostasis / Valentina Vettore ; Betreuer: Alexander Dietrich." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1196009090/34.
Повний текст джерелаLucius, Alexander [Verfasser]. "Characterization of temperature-sensitive transient receptor potential channel melastatin 8 (TRPM8) in cultivated human ocular surface cells / Alexander Lucius." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1126503886/34.
Повний текст джерелаYang, Heng. "TRPM4, a non selective cation-permeable channel regulates Foxp3+ regulatory T cells suppressive function and survival trough modulating calcium influx." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114840.
Повний текст джерелаTRPM4, a Ca2+-activated non-selective cation ion channel is an important regulator of Ca2+ signaling and cell activation in conventional T cells, but its role in Foxp3+ Tregs function remains unknown. Using a model in which Trpm4 gene was selectively invalidated in Foxp3+ Tregs population (Foxp3(YFP)Cre+Trpm4flox/flox mice) we have shown in different in vivo models of acute and chronic inflammation that TRPM4 is an important regulator of Tregs functions and survival. In a model of primary carcinogenesis induced by methylcholantrene (3-MCA) or implanted fibrosarcoma (MCA205 model), in which Tregs role has been documented, lack of TRPM4 expression and function induced significantly decreased incidence and tumor growth. We found that within chronic inflammatory and hypoxic tumor microenvironment, TRPM4 protected Tregs from ATP-induced cell death and therefore promoted tumor initiation and progression. In contrast, TRPM4 deficiency in Tregs favored IFN-g-mediated spontaneous anti-tumor immune response. Thus, through inhibiting Ca2+ influx, TRPM4 acts as a negative modulator of Tregs suppressive functions and protects Tregs from activation-induced cell death
Kaiser, Simone [Verfasser], Matthias [Gutachter] Dürst, Thomas [Gutachter] Börner, and Wolfgang [Gutachter] Kemmner. "Identification and characterization of the ion channel TRPM8 in prostate cancer / Simone Kaiser ; Gutachter: Matthias Dürst, Thomas Börner, Wolfgang Kemmner." Berlin : Humboldt-Universität zu Berlin, 2004. http://d-nb.info/1206182024/34.
Повний текст джерелаBauerle, Erin Ruane. "ASSOCIATION OF MASSETER MUSCLE CACNA2D1, CACNA1S, GABARAP, AND TRPM7 GENE EXPRESSION IN TEMPOROMANDIBULAR JOINT DISORDERS." Master's thesis, Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/392863.
Повний текст джерелаM.S.
A major physiological risk factor of temporomandibular disorders (TMD) is sensitization of peripheral and central nervous system pain processing pathways. Calcium channel, voltage-dependent, alpha-2/delta subunit-1 (CACNA2D1) has a crucial role in relaying nociceptive information in the spinal dorsal horn. Up-regulation of CACNA2D1 results in abnormal excitatory synapse formation and enhanced presynaptic excitatory neurotransmitter release. Blocking CACNA2D1 with gabapentinoid-class drugs relieves orofacial hypersensitivity. Drs. Foley, Horton, and Sciote previously reported that in a small sample group (n=12), CACNA2D1 expression was greater in males than females, but increased in women with TMD. The objectives of this study are to corroborate these data and investigate expression patterns of other ion channel and conducting system genes. Additionally, since the null polymorphism ACTN3-577XX associates with muscle fiber microdamage during eccentric contraction, we tested for possible gene associations with ACTN3-R577XX genotypes. Masseter muscle samples came from human subjects (n=23 male; 48 female) with malocclusions undergoing orthognathic surgery. This population had skeletal disharmony of the jaws and thus was prone to eccentric contraction. Three males and eighteen females were diagnosed with localized masticatory myalgia. Muscle total RNA was isolated and CACNA2D1, CACNA1S, GABARAP, and TRPM7 expression was quantified using RT-PCR. Expression of these genes were compared based on TMD status and various characteristics that may influence TMD including: sex, age, facial symmetry, sagittal dimension, vertical dimension, ACTN3-577 genotype and fiber type. CACNA2D1 expression differed significantly between sexes, overall (p<0.02), and without TMD (p=0.001). Women with (n=13) and without (n=23) TMD differed significantly (p<0.03). CACNA2D1 expression was also significantly higher (p=0.031) in subjects below age 25. Similarly, GABARAP expression was significantly higher (p=0.001) for patients younger than 25 and for patients less than or equal to age 18 (p=0.013). Otherwise, CACNA1S, TRPM7 and GABARAP differences were not significant. GABARAP expression differed, but not significantly by sex and for the ACTN3-577XX-null genotype. In a population of malocclusion patients, masseter muscle CACNA2D1 expression is significantly higher than CACNA1S, TRPM7, and GABARAP. CACNA2D1 expression is greater in males than females without TMD. However, CACNA2D1 expression increases significantly in females with TMD-associated myalgia. This may support evidence for calcium channel regulation of nociception differences seen between sexes in TMD. It was also found that expression of CACNA2D1 and GABARAP is significantly higher in younger subjects. Additionally, observations presented here suggest potential influence of ACTN3-null condition on function of GABARAP.
Temple University--Theses
Lefebvre, Thibaut. "Rôle du canal TRPM7 dans la prolifération des cellules stellaires pancréatiques humaines activées." Electronic Thesis or Diss., Amiens, 2019. http://www.theses.fr/2019AMIE0057.
Повний текст джерелаPancreatic Ductal Adenocarcinoma (PDAC) is one of the deadliest cancers with a 5 years survival rate under 5%. PDAC development and aggressivness involve pancreatic stellate cells (PSC) activation occurring during desmoplasia. PSC activation induces α-SMA expression, increases proliferative capacities of the CSP, and leads to cancer growth and metastasis. Ion channels are involved in many cellular mechanisms including cell migration, invasion and proliferation. We previously described the role of TRPM7 in PDAC cell invasion and migration (Rybarczyk et al. 2012 and 2017) but its role in PSC remains unknown. Here we show that TRPM7 is involved in magnesium homeostasis and PSC cell proliferation throughPI3K/AKT pathway activation by magnesium. TRPM7 mediated magnesium entry inducing PI3K/AKT pathway activation and leading to P53 and GSK3 inhibition, and CDK2 and PCNA upregulation inducing G1 to S transition. Our results show that TRPM7 is also involved in α-SMA expression by regulating ERK activation in a magnesium dependent manner. PSC activation also regulates TRPM7 expression. Taking together our results show TRPM7 as a potential biomarker for CSP activation and proliferation in PDAC
Straub, Isabelle [Verfasser], Rudolf [Gutachter] Rübsamen, and Michael [Gutachter] Schaefer. "Identification and application of novel and selective blockers for the heat-activated cation channel TRPM3 / Isabelle Straub ; Gutachter: Rudolf Rübsamen, Michael Schaefer." Leipzig : Universitätsbibliothek Leipzig, 2014. http://d-nb.info/123878819X/34.
Повний текст джерела銭, 年超. "成長板軟骨細胞におけるTRPM7チャネルを介する自発的Ca2+変動". Kyoto University, 2018. http://hdl.handle.net/2433/232324.
Повний текст джерелаSkandarani, Nadia. "Développement de nanocapsules lipidiques pour la délivrance de principes actifs." Thesis, Besançon, 2014. http://www.theses.fr/2014BESA2071/document.
Повний текст джерелаThe development of nanotechnology in the medical field has attracted considerable interest in recent years, including the use of nanoparticles for drug delivery. Nanoparticles offer unique opportunities for delivery of active drugs such as genes (gene therapy), anti-cancer (chemotherapy) or photosensitizers (photodynamic therapy, PDT). The major challenge, however, remains the delivery of therapeutic molecules to their site of action while keeping their integrity and their therapeutic effect.The research focus of this thesis is the use of lipid nanocapsules as a multifunctional platform for the delivery of drugs. One goal is the development of stable lipid nanocapsules, functionalized with polyethyleneimine and capable of effectively delivering a plasmid DNA and an anti-cancer (paclitaxel) as part of a combination therapy. The applications of these nanocarriers for transfection and delivery of chemotherapeutic were performed in vitro.Moreover, the ability of lipid nanocapsules to encapsulate photosensitizers for photodynamic therapy has been studied in vitro, and the results showed that the encapsulation of two molecules of PS in the nanocapsules allows a synergy photodynamic effect while protecting the PS from photo degradation.Finally, encapsulating an ion channel TRPM8 agonist (menthol) is the subject of the last chapter. The study by calcium imaging of the release of this lipophilic molecule in vitro confirmed the potential of lipid nanocapsules as nanocarriers of drugs
Fearey, Brenna C. [Verfasser]. "The role of the TRPM4 channel in hippocampal synaptic transmission and the development of genetically-encoded tools for mapping neuronal and synaptic activity : Die Rolle des TRPM4-Kanals bei der synaptischen Übertragung im Hippocampus und die Entwicklung genetisch kodierter Werkzeuge zur Kartierung neuronaler und synaptischer Aktivität / Brenna C. Fearey." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2020. http://d-nb.info/1221276395/34.
Повний текст джерелаRamos-Filho, Antonio Celso Saragossa 1985. "Participação do receptor de potencial transiente vanilóide do tipo 4 (TRPV4) e do melastatina do tipo 8 (TRPM8) nas disfunções miccionais do diabetes em camundongos." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312586.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-25T08:00:03Z (GMT). No. of bitstreams: 1 Ramos-Filho_AntonioCelsoSaragossa_D.pdf: 3024613 bytes, checksum: a03a80c65d863acd441249f461461216 (MD5) Previous issue date: 2014
Resumo: Os receptores TRPV4 e TRPM8 são expressos no urotélio e em fibras aferentes sensitivas da bexiga. Fisiologicamente, a ativação mecânica do receptor TRPV4 na parede da bexiga participa do controle miccional. Em doenças de origem inflamatória, esses receptores adquirem funcionalidade importante. As disfunções da bexiga no diabetes podem estar associadas a alterações ao nível de detrusor, inervação e urotélio. A disfunção urotelial parece ser a responsável por desencadear as alterações neurais e musculares da bexiga. Assim, o objetivo do presente estudo foi investigar os mecanismos fisiopatológicos da ativação dos receptores TRPV4 e TRPM8 no estado diabético em camundongos. Para tanto, dividimos o estudo em duas etapas, sendo que na primeira avaliamos a participação dos receptores TRPV4 e TRPM8 nos mecanismos contráteis e relaxantes do detrusor isolado de animais controles e knockout para esses canais. Em uma segunda etapa estudamos a ativação desses canais em camundongos diabéticos pela injeção intraperitoneal de estreptozotocina (180 mg/Kg) por 4 semanas. Em fragmentos do detrusor isolados de camundongos mostramos que o agonista do receptor TRPV4, GSK1016790A, causou resposta contrátil dependente da concentração. Por outro lado, quando os tecidos foram contraídos com solução despolarizante de KCl, o GSK1016790A causou relaxamento da preparação. No detrusor isolado de animais TRPV4-/- verificamos hipercontratilidade ao carbacol (agonista muscarínico) e à estimulação elétrica, assim como redução no relaxamento ao agonista ?-adrenérgico não-seletivo, isoprenalina. Estes efeitos não foram obtidos com os antagonistas dos receptores TRPV4, RN1734 e HC067047. A indução do diabetes causou nocicepção mecânica e aumento da proporção entre bexiga e peso corpóreo após 4 semanas da injeção. A avaliação miccional dos animais diabéticos mostrou aumento da capacidade, frequência urinária e das contrações involuntárias da bexiga. Observamos ainda hipercontratilidade do detrusor ao carbacol, à estimulação elétrica e ao KCl. A indução do diabetes em animais TRPV4-/- não modificou as disfunções "in vivo" e "in vitro" observadas nos animais wyld type diabéticos, mostrando que a ausência crônica dos receptores TRPV4 desencadeia alterações miccionais que são anteriores as causadas pelo diabetes. Também verificamos que os animais TRPM8-/- não apresentam alteração na resposta contrátil ao carbacol e à estimulação elétrica. Por outro lado, o mentol, mas não a icilina, reduziu significativamente as respostas contráteis nestes animais. O mentol inibiu o influxo de cálcio extracelular em cultura de células da musculatura lisa da bexiga por mecanismo inibitório direto nos canais Cav1.2. O tratamento agudo com mentol, intraperitoneal e intravesical, atenuou as disfunções miccionais observadas nos camundongos diabéticos. "In vitro" o pré-tratamento com mentol reduziu a hipercontratilidade ao carbacol no grupo diabético, sem alterar a resposta no grupo controle. Concluímos que o mentol impede a resposta contrátil da bexiga por mecanismo independente do receptor TRPM8 bloqueando o influxo de cálcio extracelular nos canais Cav1,2, podendo ser utilizado como tratamento na hiperatividade de bexiga de origem miogênica
Abstract: The TRPV4 and TRPM8 receptors are expressed in bladder urothelium and sensitive afferent fibers. Physiologically, the mechanical activation of TRPV4 receptor in the bladder wall is involved in micturition control. In inflammatory diseases, these receptors may have important roles. The bladder dysfunction in diabetes may be associated with changes at the level of detrusor, innervation and urothelium. The urothelial dysfunction triggers neural changes, modifying consequently the smooth muscle contractility. Thus, the goal of the present study was to investigate the pathophysiological mechanisms of TRPV4 and TRPM8 receptor activation in physiological and diabetic conditions in mice. For this purpose we divided the study in two phases, the first of which we evaluated the participation of TRPV4 and TRPM8 receptors in detrusor contractile and relaxing mechanisms in control and knockout animals for these channels. In the second phase we studied the activation of these channels in diabetic mice induced by intraperitoneal injection of streptozotocin (STZ; 180 mg / kg, 4 weeks). The TRPV4 agonist GSK1016790A produced concentration-dependent detrusor contractions. On the other hand, in detrusor pré-contracted with KCl (80 mM), GSK1016790A caused relaxation responses. In TRPV4-/- animals, we verified hypercontractility to carbachol (muscarinic agonist) and electrical-field stimulation, as well as a decreased relaxation to isoprenaline (non-selective ?-adrenergic agonist). These effects were not obtained with the TRPV4 antagonists, RN1734 and HC067047. Induction of diabetes with STZ caused hyperglycemia, mechanical nocicepton, and increased ratio between bladder and body weight after 4 weeks. The miccturition evaluationin diabetic animals showed increased capacity, urinary frequency, and non-voiding contractions. Hypercontractility to carbachol, electrical-field stimulation and KCl in isolated detrusor were lso observed. The induction of diabetes in TRPV4-/- animals did not change the urinary dysfunctions. Our data are consistent with the proposal that TRPV4 receptor has a physiological function in micturition control by decreasing muscarinic-induced contractions and increasing ?-adrenergic-mediated relaxations. Moreover, the bladder contractions to carbachol and EFS in TRPM8-/- did not significantly change compared to TRPM8+/+. However, menthol (300 ?M), but not icilin (1 ?M), significantly inhibited these contractile responses. The menthol (300 ?M) inhibited extracellular calcium influx in bladder smooth muscle cell culture by direct mechanism though Cav1.2 channels. In addition the acute treatment with menthol, intraperitoneal and intravesical, atenuated the micturition dysfunctions observed in diabetic mice. Also, detrusor preparations pre-treated with menthol decreased carbachol hypercontractility, without changing the responses in normoglycemic group. Menthol reduces bladder contractions by mechanisms independent of TRPM8 receptor activation, inhibiting extracellular calcium influx through Cav1.2 channel, thus been considered as treatment for bladder overactivity of myogenic origin
Doutorado
Farmacologia
Doutor em Farmacologia
Chen, Wenchun [Verfasser], and Bernhard [Gutachter] Nieswandt. "Studies on the role of calcium channels and the kinase domain of transient receptor potential melastatin-like 7 (TRPM7) in platelet function / Wenchun Chen. Gutachter: Bernhard Nieswandt." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1111783284/34.
Повний текст джерелаGambade, Audrey. "Rôle du peptide LL-37 dans le cancer du sein : son interaction avec la membrane plasmique stimule l'entrée de calcium et la migration cellulaire par l'activation des canaux ioniques TRPV2 et BKCa." Thesis, Tours, 2015. http://www.theses.fr/2015TOUR3312/document.
Повний текст джерелаThe antimicrobial peptide LL-37 is overexpressed in several types of cancer, among which breast cancer were it is associated with metastasis development. Our experiments on three mammary cancer cell lines have shown that LL-37 increases cell migration. Both its natural (L)-form and its (D)-enantiomer are equally active, excluding a specific binding to a protein receptor. On the MDA-MB-435s cell line, LL-37 attaches to plasma membrane and reduces its fluidity. Electron microscopy localized LL-37 on the surface of pseudopodia, structures implicated in cell migration, and in caveolae. LL-37 induces calcium entry via the TRPV2 channel, which is recruited to pseudopodia. Recruitment depends on activation of PI3K/AKT signaling induced by LL-37. Calcium entry via TRPV2 is potentiated by activation of the BKCa potassium channel also located in pseudopodia. TRPV2 suppression by RNA interference results in 70% reduction of cell migration induced by LL-37, attributing a crucial role of this channel to the promigratory effects of the peptide. Binding of LL-37 to cancer cell membranes and in consequence the activation of ion channels constitutes a novel research field to understand its role in tumor progression
Shamsaldeen, Yousif. "Endothelial TRPV4 dysfunction in a streptozotocin-diabetic Rat Model." Thesis, University of Hertfordshire, 2016. http://hdl.handle.net/2299/17622.
Повний текст джерелаLange, Ingo [Verfasser]. "The TRPM2 ion channel in nucleotide gated calcium signaling / vorgelegt von Ingo Lange." 2008. http://d-nb.info/989951200/34.
Повний текст джерелаEhsan, Kheradpezhouh. "The role of TRPM2 channels in oxidative stress-induced liver damage." Thesis, 2015. http://hdl.handle.net/2440/92813.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2015
Roy, Jeremy. "THE CONTRIBUTION OF K+ ION CHANNELS AND THE Ca2+-PERMEABLE TRPM8 CHANNEL TO BREAST CANCER CELL PROLIFERATION." 2010. http://hdl.handle.net/10222/13118.
Повний текст джерела