Дисертації з теми "Endothelin converting enzyme 1"
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Park, Sung-Hae 1971. "Role of endothelin-1 and endothelin converting enzyme-1 in bleomycin-induced pulmonary fibrosis in rats." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=24032.
Повний текст джерелаBaluyut, Crystal. "Characterization of human endothelin converting enzyme (ECE-1) promoter diversity in vasular endothelial cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0010/MQ40767.pdf.
Повний текст джерелаKido, Tsuneo. "Processing of proendothelin-1 at the carboxyl-terminus of big endothelin-1 is essential for proteolysis by endothelin-converting enzyme-1 in vivo." Kyoto University, 1997. http://hdl.handle.net/2433/202209.
Повний текст джерелаKaburagi, Satoshi. "The role of endothelin-converting enzyme-1 in the development of α1-adrenergic-stimulated hypertrophy in cultured neonatal rat cardiac myocytes". Kyoto University, 2001. http://hdl.handle.net/2433/150597.
Повний текст джерелаMasatsugu, Ken. "Shear stress attenuates endothelin and endothelin-converting enzyme expression through oxidative stress." Kyoto University, 2004. http://hdl.handle.net/2433/147555.
Повний текст джерелаHasegawa, Hiroshi. "Purification of a novel endothelin-converting enzyme specific for big endothelin-3." Kyoto University, 1998. http://hdl.handle.net/2433/182268.
Повний текст джерелаHarrison, Vanessa Jane. "The characterisation of endothelin-converting enzyme in endothelial cells." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307673.
Повний текст джерелаIkura, Takeshi. "cDNA cloning and expression of bovine endothelin converting enzyme." Kyoto University, 1997. http://hdl.handle.net/2433/202206.
Повний текст джерелаGovender, Ureshnie. "The characterisation of RAS converting enzyme 1 activity and regulation." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527705.
Повний текст джерелаHocharoen, Lalintip. "Catalytic Metallopeptide Promoted Inactivation of Enzyme Targets Related to Disease: Angiotensin Converting Enzyme-1 and SortaseA." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354634371.
Повний текст джерелаJaworski, Jakub. "The role of the deubiquitinating enzyme USP17 in endocytosis and the regulation of Ras converting enzyme 1 activity." Thesis, Queen's University Belfast, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.602551.
Повний текст джерелаScott, Alasdair James. "The regulation of tumor necrosis factor-alpha converting enzyme (TACE/ADAM17) during acute inflammation." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6041.
Повний текст джерелаScott, Christopher John. "Investigation of expression methodologies for the dissection of the catalytic mechanism of interleukin-1#beta#-converting enzyme." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325991.
Повний текст джерелаChisi, John Eugenes. "The regulatory role of AcSDKP and angiotensin 1-converting enzyme (ACE) inhibitors on haematopoietic stem and progenitor cell proliferation." Thesis, University of St Andrews, 1999. http://hdl.handle.net/10023/14971.
Повний текст джерелаO'Callaghan, David John Patrick. "Investigation into the role of monocyte tumour necrosis factor-alpha converting enzyme as a regulator of the inflammatory response in sepsis." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/17943.
Повний текст джерелаSamnegård, Björn. "Renal effects of C-peptide in experimental type-1 diabetes mellitus /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-502-X/.
Повний текст джерелаDean, Stephanie A. "Regulation of angiotensin converting enzyme and angiotensin II type 1 receptor by 17beta-estradiol in female rats: Implications following experimental myocardial infarction." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26883.
Повний текст джерелаSerfözö, Peter Daniel [Verfasser]. "Angiotensin-Converting Enzyme 2- and Prolyl Carboxypeptidase-Independent Conversion of Angiotensin II to Angiotensin-(1-7) in Circulation and Peripheral Tissues / Peter Daniel Serfözö." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1218076844/34.
Повний текст джерелаGlover, Zoe. "Acer, a homologue of the human angiotensin-1 converting enzyme, modulates the response of sleep, glycogen storage, lifespan, fecundity and stress resistance to diet in Drosophila melanogaster." Thesis, Lancaster University, 2017. http://eprints.lancs.ac.uk/86909/.
Повний текст джерелаWang, Yu. "THE ROLE OF THE ACE2/ANG-(1-7)/MASR AXIS IN THE DEVELOPMENT OF OBESITY-HYPERTENSION IN MALE AND FEMALE MICE." UKnowledge, 2016. http://uknowledge.uky.edu/pharmacol_etds/13.
Повний текст джерелаWang, Peiyu. "Strategy and molecular mechanism study of cold atmospheric plasma applications in oncotherapy, virucide and nanotechnology." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/214016/1/Peiyu_Wang_Thesis.pdf.
Повний текст джерелаAl, Bacha Jeanne D'Arc. "Nouvelles fonctions de l'enzyme de conversion de l'angiotensine et du récepteur de la (pro)rénine en pathologies cardiovasculaires et neurologiques." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066415.
Повний текст джерелаNew components of the renin angiotensin system (RAS) continue to be discovered and their functions studied. This thesis provides new insights on the role of angiotensin converting enzyme (ACE) in thrombosis and cardiovascular diseases (CVD) and of the (pro)renin receptor in the development of the central nervous system (CNS). First, we studied the role of ACE in CVD by analyzing the impact and the association of a mutation in ACE and in plasminogen activator inhibitor-1 (PAI-1) genes compared to other polymorphic cardiovascular genes of proinflammatory cytokines in peripheral blood mononuclear cells in hypertensive hypercholesterolemic Lebanese patients. We showed that Lebanese patients expressing a double mutation (Del/4G) of ACE and PAI-1, respectively, are at high risk of developing CVD, suggesting that combined ACE/PAI-1 mutations may be considered as a potential marker of CVD onset. In the second part, we studied the relation between the (pro)renin receptor, whose gene is called Atp6ap2, and Wnt/beta-catenin signaling pathway, in neural stem/progenitor cells (NSPC) during development. To this end, we used an in vitro model of neural stem cells (NSC) isolated from Atp6ap2-/Y mice embryos and studied their self-renewal capacity and their differentiation into neurons, astrocytes and oligodendrocytes. Our results suggest that Atp6ap2 is necessary for self-renewal of NSC independently of the Wnt/beta-catenin signaling pathway in mammals. In addition, we showed that the expression of ATP6AP2 in human mesenchymal stem cells (hMSC) isolated from adipose tissue was correlated with their degree of neuronal differentiation
Raji, Ismaila. "Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive wistar rats." Thesis, University of the Western Cape, 2011. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_5212_1367481132.
Повний текст джерелаTulbaghia violacea Harv. (Alliaceae) is a small bulbous herb which belongs to the family, Alliaceae, most commonly associated with onions and garlic. In South Africa (SA), this 
herb has been traditionally used in the treatment of various ailments, including fever, colds, asthma, paralysis, hypertension (HTN) and stomach problems. The aim of this study 
was to evaluate the effect of methanol leaf extracts (MLE) of T. violacea on the blood pressure (BP) and heart rate (HR) in anaesthetized male spontaneously hypertensive rats
 
and to find out the mechanism(s) by which it acts. The MLE of T. violacea (5 - 150 mg/kg), angiotensin I (ang I, 3.1 - 100 &mu
g/kg), captopril (10 mg/kg), angiotensin II (ang II, 3.1 - 50 
g/kg), losartan (30 mg/kg), phenylephrine (0.01 &ndash
0.16 mg/kg), prazosin (1 mg/kg), dobutamine (0.2 &ndash
10.0 &mu
g/kg), propranolol (0.1 - 12.8 mg/kg), muscarine (0.16 -10 &mu
g/kg), 
and atropine (0.02 - 20.48 mg/kg) were administered intravenously into male spontaneously hypertensive rats (SHR) weighing between 300 g and 350 g and aged less than 5 
months. The MLE of T. violacea and/or the standard drugs were infused alone, simultaneously, or separately into each animal. The BP and HR were measured via a pressure 
transducer connecting the femoral artery and the Powerlab. The vehicle (0.2 mls of a mixture of dimethylsulfoxide and normal saline), T. violacea (60 mg/kg) and captopril (10 
mg/kg) were injected intraperitoneally into some SHR for 21 days to investigate the chronic effect of these agents on plasma levels of aldosterone. The mean change, the mean 
of the individual percentage changes and the percentage difference (in mean) observed with each intervention was calculated and statistically analyzed using the Student&rsquo
s t test 
for significant difference (p <
0.05). The Microsoft Excel software was used for statistical analysis. T. violacea significantly (p <
0.05) reduced the systolic, diastolic, and mean 
arterial BP
and HR dose-dependently. In a dose-dependent manner, ang I, ang II, phenylephrine significantly (p <
0.05) increased the BP, while propranolol, muscarine and 
atropine reduced the BP. The increases in BP due to dobutamine were not dose-dependent. In a dose dependent manner, phenylephrine and propranolol reduced the HR, while dobutamine increased the HR. The effect of ang I, ang II, muscarine and atropine on HR were not dose-dependent
with both increases as well as decreases observed with ang 
I, and II and atropine, while decreases were seen with muscarine. Captopril produced 
significant (p <
0.05) reduction in BP which were not associated with any change in HR. The co-infusion of ang I with the MLE produced significant (p <
0.05) reduction in BP, which were not associated with significant changes in HR. The co-infusion of ang II with the 
MLE did not produce any significant changes in BP or HR when compared to the infusion of the standard drug alone. The co-infusion of phenylephrine with the MLE did not 
produce any significant change in BP or HR when compared to the values obtained with the infusion of the standard drug alone, in both the absence and presence of prazosin. 
The co-infusion of dobutamine with T. violacea produced siginificant (p <
0.05) increases in DBP which were associated with significant (p <
0.05) reductions in HR, when 
compared to the values obtained with the infusion of the standard drug alone. Theco-infusion of atropine with the MLE did not produce any significant change in BP or HR when 
compared to the values obtained with the infusion of atropine alone. However, the infusion of T. violacea, 20 minutes after pre-treating animals with atropine (5.12 mg/kg) lead to 
dose dependent significant (p <
0.05) increases in BP, which were associated with dose-dependent increases in HR. The chronic treatment of animals with T. violacea or 
captropril produced (a) signicant (p <
0.05) reductions in the plasma levels of aldosterone when compared to the values obtained in the vehicle-treated group, (b) produced 
signifiant (p <
0.05) reduction in BP in the captopril treated group when compared to the vehicle-treated, (c) did not produce any signficant change in BP in the T. violacea-treated 
group when compared to the vehicle-treated group and (d) did not produce any signifiant change in HR or body weight in any of the groups. The result obtained in this study 
suggests that T. violacea reduced BP and HR in the SHR. Secondly, the BP and HR reducing effect of the MLE may involve a) the inhibition of the ACE, b) the inhibition of the &beta
1 
adrenoceptors, c) the stimulation of the muscarinic receptors and d) the reduction of the levels of aldosternone in plasma. The results also 
suggest that the MLE may not act 
through the angiotensin II receptors or the &alpha
1 adrenergic receptors. 
Cobas, Roberta Arnoldi. "Polimorfismo I/D do gene da enzima conversora de angiotensina e C242T do gene do componente p22phox da NADPH oxidase em pacientes com diabetes tipo 1." Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=1694.
Повний текст джерелаThe renin-angiotensin system and the oxidative stress play an important role in the pathogenesis of the diabetic complications.In the present study 103 patients with type 1 diabetes (T1DM) aged 28.8 10.6 years and with a disease duration of 13.1 8.5 years and 158 non-diabetic controls were evaluated for the presence of the I / D polymorphism of the angiotensin converting enzyme (ACE) and the C242T polymorphism of the p22phox, an essential component for NADPH oxidase activation. The analysis was performed using polymerase chain reaction for both polymorphisms, followed by enzymatic restriction for C242T p22phox polymorphism. Genotypic distributions of both polymorphisms were in Hardy-Weinberg equilibrium. Diabetic patients underwent clinical and laboratory evaluation for the presence of risk factors associated with complications of diabetes (smoking and family history of type 2 diabetes, daily insulin dose, blood pressure, body mass index, waist hip ratio, urinary albumin excretion, glomerular filtration rate, lipid profile, glycemic control, C-reactive protein levels) and screened for the presence of diabetic nephropathy, considered as the presence of micro or macroalbuminuria, diabetic retinopathy and hypertension. There was no significant difference between the presence of ACE D or I allele and p22phox C or T allele between diabetic patients and controls. The evaluated polymorphisms were not associated with the presence of nephropathy, retinopathy or hypertension. Patients with the D allele showed higher levels of diastolic blood pressure (72.2 12.3 vs 65.4 11.6 mmHg, p = 0.047) and C-reactive protein compared with those carrying the II genotype [0.18 (0.04-0.38) vs 0.09 (0.04-0.16) mg/dl, p = 0.05], but both analysis lost statistical significance after correction for duration of diabetes. The combination of both polymorphisms was not associated with microvascular complications or hypertension. We conclude that in the studied population of type 1 diabetic patients, the frequency of ACE I / D and C242T of p22phox polymorphisms, alone or in combination, was not different in patients with or without early microvascular complications or hypertension. Also, the levels of different markers of cardiovascular risk did not differ for patients with the polymorphisms described above. However, prospective studies may determine the possible interaction between these polymorphisms and duration of diabetes in the clinical expression of chronic complications of diabetes.
Wiklund, Per-Gunnar. "Genetic aspects of stroke : association and linkage studies in a northern Swedish population." Doctoral thesis, Umeå : Public Health and Clinical Medicine, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-668.
Повний текст джерелаJackson, C. D., K. Barnes, Shervanthi Homer-Vanniasinkam, and A. J. Turner. "Expression and localization of human endothelin-converting enzyme-1 isoforms in symptomatic atherosclerotic disease and saphenous vein." 2006. http://hdl.handle.net/10454/3922.
Повний текст джерелаEndothelln-converting enzyme (ECE-1) is a critical enzyme in the production of the potent vasoconstrictor peptide endothelin (ET-1). It has previously been shown that the levels of both ET-1 and ECE-1 are raised in atherosclerosis, but the possible relevance of the isoforms of ECE-1 in these changes has not yet been investigated. The aim of this study was to examine the expression of the ECE-1a and ECE-1c isoforms in human atherosclerotic pathologies. Immunohistochemical analysis was carried out on sections from atherosclerotic and non-atherosclerotic vascular tissue using a combination of ECE-1 isoform-specific antibodies, anti-¿-actin antibodies to identify smooth muscle cells (SMC) and anti-CD68 antibodies to identify macrophages. ECE-1 isoform expression was also examined in cultured SMC and in macrophages isolated from human blood. Results indicated differences in isoform expression in atherosclerotic lesions, with distinct patterns of staining for ECE-1 a and ECE-1 c. ECE-1 c immunoreactivity was seen in macrophages, and also correlated with actin staining. ECE-1a was also localized to macrophages and SMC. Results of this study suggest that these local changes influence the expression patterns of the ECE-1 isoforms within individual cell types. Correlation of these isoform expression patterns with the stage of atherosclerosis could provide novel indicators of disease progression.
Xu, Enny-Sonia, and 許恩旎. "The Study of Cytokeratin 17 and Endothelin-Converting Enzyme-1 for Expressions and Prognoses in Head and Neck Cancer." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/kbju63.
Повний текст джерела國立陽明大學
臨床醫學研究所
106
Backgrounds: Head and neck cancer (HNC) affects over 500,000 people worldwide. Head and neck/oral squamous cell carcinoma (HN/OSCC) is the most common histology type of HNC. Cytokeratins (CKs) are mainly expressed in epithelial carcinomas and are valuable for making diagnoses and identifying metastatic status. Changes in the expression of individual CKs in certain carcinoma may be relevant to establishing a prognosis. However, the expression pattern and prognosis status of ECE-1 and the prognostic metastatic and significance of CKs in HNSCC remain vague. In addition, Endothelins (ETs) are 21-amino-acid peptides that have a variety of biologic activities and have been implicated in various pathophysiological conditions, including cancer. Endothelin-1 (ET-1) can promote progression of HNSCC and may be a novel therapeutic target. Endothelin-converting enzyme-1 (ECE-1) primarily converts Big Endothelins (ETs) into active Endothelin-1 (ET-1). However, the expression pattern and prognostication status of ECE-1 in HNSCC are enigmatic. In this study, we investigated the diverse and unique expression patterns of Cytokeratin 13 (CK13) and Cytokeratin 17 (CK17) in epithelial change and assessed the role of CK17 as a predictor for HNSCC metastasis and prognosis; and the role of ECE-1 for expression patterns in tumor differentiation and potential predictor for clinic prognosis in HNC. Methods: CK13, CK17 and ECE-1 expressions were evaluated by using immunohistochemical tissue microarray (TMA) analysis with 126 patients of HNSCC along with their non-neoplastic counterparts. The correlation of CKs and ECE-1 expression to clinicopathologic variables and prognosis was analyzed by using a serial statistical method, during 12-year follow-up. Furthermore, to clarify the characterization of CK17 expression with respect to its ability in predicting metastatic disease, an in-vitro study of cells migration/invasion assays was conducted. Results: CK13 was predominately expressed in noncancerous tissues and was lost in HNSCC. The expression of CK17 was proved that higher in G1 differentiation category than in G2 and G3 differentiation (P = 0.0045). Decreasing expression of CK17 correlated with cancerous cell migration and invasion (P<0.0001) in an in-vitro study. CK17 expression was lower in the N1 and N2 nodal metastases category compared to the N0 stage. Moreover, Kaplan-Meier survival analyses showed that a lower CK17 expression was associated with a poorer survival connotation in HNSCC patients (P < 0.05). On multivariate Cox proportional hazards models analysis, CK17 under-expression proved to be an independent prognostic factor with a hazard ratio (HR) of 1.854 (P = 0.065 < 0.1). In addition, ECE-1 may be over-expressed in HNC carcinoma cells. Higher ECE-1 level was detected more frequently in moderately to poorly differentiated tumors and showed a lower differentiation category compared to the G1 cases (P = 0.015); this finding was further confirmed by an adjusted odds ratio (OR) of 4.071 (P = 0.042). Moreover, Kaplan-Meier survival analyses showed that a higher ECE-1 expression was associated with a poorer survival in HNC patients (P < .0001). On multivariate Cox proportional hazards models analysis, ECE-1 of high-expression proved to be an independent prognostic factor with a hazard ratio (HR) of 3.985 (P < .001). Conclusion: Our findings provide the first evidence that CK17 under-expression might be a potential predictor of nodal metastasis and adverse prognosis, and over-expression ECE-1 in HNC is associated with HNC poor tumor differentiation and clinic outcome.
Benoit, Alexandre. "Étude de l'Endothelin-converting enzyme-like 1 (ECEL1), un nouveau membre de la famille de l'endopeptidase neutre-24.11 (EPN)." Thèse, 2004. http://hdl.handle.net/1866/15210.
Повний текст джерелаDabouz, Rabah. "La biosynthèse et la localisation subcellulaire de l'endothéline 1 dans les myocytes et les fibroblasts ventriculaires cardiaques adultes." Thèse, 2016. http://hdl.handle.net/1866/18645.
Повний текст джерелаType B endothelin receptors (ETB) are located in the nuclear envelope of adult ventricular cardiomyocytes (ACVMs). In both ACVMs and endothelial cells, endocytosed rhodamine endothelin colocalized with Lysotracker but was not observed at the nuclear membrane. In this study we have characterized the regulation and subcellular localization of endothelin biosynthesis in ACVMs and adult cardiac fibroblasts. In both cell types immunocytofluorescence experiments revealed endothelin-1 immunoreactivity, comprising all stages of peptide maturation, either on or near the nuclear membrane. Endothelin converting enzyme 1 (ECE1) is a metalloprotease that converts big endothelin to the biologically active 21-amino acid peptide. ECE1 immunoreactivity was associated with the T-tubules and nuclear or perinuclear membranes in ACVMs. In contrast, ECE1 immunoreactivity was observed both in the nucleus and the cytosol, but not at the plasma membrane, in passage 3 cardiac fibroblasts. Endothelin-1 mRNA was detected in both cell types. Regulation of endothelin production is primarily at the level of transcription. Application of TGFβ1 increased ET-1 mRNA in ACVMs whereas angiotensin II was effective in increasing ET-1 mRNA in fibroblasts. In AVCMs, the increase in ET-1 mRNA was associated with an increase of intracellular ET-1 peptide and nuclear calcium. These data suggest that endogenous endothelin is available and may activate nuclear ETB in ACVMs in response to extracellular stimuli.
"The angiotensin converting enzyme 2 - angiotensin (1-7) axis protects endothelial function against oxidative stress in diabetes." 2013. http://library.cuhk.edu.hk/record=b5884510.
Повний текст джерелаThesis (Ph.D.)--Chinese University of Hong Kong, 2013.
Includes bibliographical references (leaves 147-169).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
"Molecular cloning and characterization of endothelin converting enzyme-2." 2001. http://library.cuhk.edu.hk/record=b5890740.
Повний текст джерелаThesis (M.Phil.)--Chinese University of Hong Kong, 2001.
Includes bibliographical references (leaves 81-92).
Abstracts in English and Chinese.
Table of Contents --- p.1
Abbreviations --- p.4
Chapter Chapter 1 --- Introduction and Background --- p.5
Chapter 1.1 --- Endothelin system --- p.5
Chapter 1.1.1 --- Endothelins --- p.5
Chapter 1.1.2 --- Endothelin converting enzyme (ECE) isoforms --- p.12
Chapter 1.1.3 --- Endothelin receptors --- p.24
Chapter 1.2 --- Signal-transduction mechanisms in ET system --- p.27
Chapter 1.3 --- The aim of the present thesis --- p.31
Chapter Chapter 2 --- Materials and Methods --- p.32
Chapter 2.1 --- Primer Design --- p.32
Chapter 2.2 --- Total RNA Isolation --- p.33
Chapter 2.3 --- Reverse transcriptase polymerase chain reaction (RT-PCR) --- p.34
Chapter 2.3.1 --- First Strand cDNA Synthesis --- p.34
Chapter 2.3.2 --- PCR reaction --- p.34
Chapter 2.4 --- Agarose gel electrophoresis --- p.35
Chapter 2.5 --- Ligation of PCR inserts to cloning vector by TA cloning method --- p.35
Chapter 2.6 --- Competent cell preparation --- p.36
Chapter 2.7 --- Transformation and Screening --- p.37
Chapter 2.8 --- Plasmid DNA Extraction --- p.38
Chapter 2.9 --- DNA sequencing --- p.38
Chapter 2.10 --- DIG RNA Labeling --- p.38
Chapter 2.10.1 --- Plasmid Linearization --- p.38
Chapter 2.10.2 --- Transcription --- p.39
Chapter 2.10.3 --- Probe purification --- p.39
Chapter 2.11 --- In situ hybridizaion --- p.40
Chapter 2.11.1 --- Tissue preparation and slide mounting --- p.40
Chapter 2.11.2 --- Non-radioactive in situ hybridization --- p.41
Chapter 2.12 --- Whole Mount non-radioactive in situ hybridization --- p.42
Chapter 2.12.1 --- Dissection and fixation --- p.42
Chapter 2.12.2 --- Hybridization --- p.43
Chapter 2.12.3 --- Antibody incubation --- p.43
Chapter 2.12.4 --- Histochemistry --- p.44
Chapter Chapter 3 --- Results --- p.46
Chapter 3.1 --- The molecular cloning of ECE-2 from rat brain --- p.46
Chapter 3.2 --- Sequence characteristics of rat ECE-2 --- p.52
Chapter 3.3 --- Comparison of rat ECE-2 with bovine and human ECE-2 and with the rat ECE-1 --- p.53
Chapter 3.4 --- Tissue distribution of ECE-2 in rat and localization in C6 glial cells by RT-PCR --- p.60
Chapter 3.5 --- ECE-2 in rat embryos at different gestation stages by RT-PCR --- p.60
Chapter 3.6 --- ECE-2 distribution in C6 glioma cells --- p.63
Chapter 3.7 --- ECE-2 distribution in rat embryo E15.5 --- p.63
Chapter 3.8 --- ECE-2 distribution in rat brain sections --- p.63
Chapter Chapter 4 --- p.74
Discussion --- p.74
References --- p.81
吳淑釧. "Improve Morphological Changes and Reduce Vasospasm by Treatment with Selective Endothelin- converting Enzyme Inhibitor Following Experimental Subarachnoid Hemorrhage." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/57750690512237485790.
Повний текст джерела高雄醫學大學
醫學研究所
90
Endothelin-1(ET-1)is a potent vasoconstrictor that has been implicated in the pathogenesis of cerebral vasospasm after SAH. Endothelin-1(ET-1)is synthesized initially as a large prepropeptide that requires multiple steps of post-translational processing for activation. The final step of this processing involves the proteolytic cleavage of a relatively inactive precursor, big Endothelin-1 (big ET-1), by the metalloprotease endothelin-converting enzyme (ECE). Previous studies have demonstrated that endothelin-converting enzyme inhibitor (CGS 26303)could prevent and reverse arterial narrowing in a rabbit model of subarachnoid hemorrhage(SAH). However, attenuation of vasospastic response was incomplete and required relatively high dose to be effective in reversing vasospasm. Therefore, the first study was designed to examined the effects of a highly selective endothelin-converting enzyme inhibitor, CGS 35066, in the preventing SAH-induced cerebral vasospasm in rabbit model. The ultrastructural changes of mitochondria and endothelial cells of basilar arteries were examined by Transmission Electron Microscopy(TEM). The reasons why we adapt experiments with rats are comely product just produced from rabbit anti-Endothelin-1 serum and highly selective Endothelin-converting enzyme inhibitor CGS 35066 was difficult to be purified and available. Therefore,the second study planned to another use the Endothelin-converting enzyme inhibitor CGS 26303 in Sprague-Dawley Rat model. In prevention and reversion study,we examined the expression of ET-1 in the basilar arteries of experiment rats with the immunohistochemical stain. Via the use of Transmission Electron Microscopy(TEM), the ultrastructure was different between the SAH and treatment groups. This gave us an information whether to evaluate the relationship between Endothelial cells change and Endothelin-converting enzyme inhibitor under TEM? (A)New Zealand white rabbits were subjected to experimental SAH by injecting autogenous blood into the cisterna magna. Endothelin-converting enzyme inhibitor CGS 35066(10 mg/kg)or vehicle was injected intravenously twice daily for two days initially at 1 hour after SAH. Animals were divided into the following seven groups: (1)control(no SAH);(2)2 days after SAH(no treatment);(3)7 days after SAH(no treatment);(4)2 days after SAH+CGS 35066;(5)7 days after SAH+CGS 35066;(6)2 days after SAH+Vehicle;(7)7 days after SAH+Vehicle. Animals were sacrificed by perfusion fixation 7 days post-SAH. Basilar arteries were removed, sectioned and stained. The ultrastructural changes of mitochondria and endothelial cells were examined by Transmission Electron Microscopy (TEM). Our results showed that corrugation of endothelial cells and destruction of endothelial cells and mitochondria were obvious in 2 days after SAH and 2 days after SAH+vehicle animals. In 7days after SAH only animals, no more corrugation of endothelial cells was found, but endothelial cells and mitochondria were severely damaged. However, endothelin-converting enzyme inhibitor CGS 35066 could reserve the intact endothelial cells and mitochondria at 2 days and 7 days after SAH. These finding indicate that intravenous injection of highly selective endothelin-converting enzyme inhibitor can prevent endothelial cells and mitochondrial damage after SAH. Endothelin-converting enzyme inhibitor CGS 35066 can be an alternative approach in the treatment of SAH-induced vasospasm. (B) Reduce level of ET-1 can attenuate vasospastic response. Intravenous infusion of CGS 26303 at doses of 0.24, 0.8, or 2.4 mg/100g/d was initiated 1 hour after SAH in Sprague-Dawley Rat. In prevention study animals were divided into the following six groups: (1)control(no SAH);(2)SAH only(no treatment);(3)SAH+2.4 mg/100 g/d CGS 26303;(4)SAH+0.8 mg/100 g/d CGS 26303;(5)SAH+0.24 mg/100 g/d CGS 26303 ;(6)SAH+Vehicle. In reverse study animals were divided into the following six groups: (1)control(no SAH); (2) SAH only(no treatment);(3)SAH+2.4 mg/100 g/d CGS 26303;(4)SAH+0.8 mg/100 g/d CGS 26303;(5)SAH+0.24 mg/100 g/d CGS 26303 ;(6)SAH+Vehicle. The same procedure was repeated 48 hours after the first experimental SAH. One week later, all animals were killed. Basilar arteries were removed, ET-1 immunohistochemical stain was applied, embedded and sectioned, observed with T.E.M. Dose related attenuation to the positive staining was noticed when compared with SAH only.
Chen, Tai-I., and 陳太乙. "Neuroprotective effect of CGS 26303, an endothelin- converting enzyme inhibitor, on the ischemia-reperfusion spinal cord injury in rats." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/66755693595678062984.
Повний текст джерела高雄醫學大學
醫學研究所碩士班
94
Endothelin-1 (ET-1) has been implicated in many neurological diseases, including subarachnoid hemorrhage and cerebral ischemia. ET-1 is also proved to deteriorate the ischemia-reperfusion injury in many organs yet the spinal cord was not.Our previous studies demonstrated the endothelin-converting enzyme (ECE) inhibitor, CGS26303, possessed beneficial effects for the treatment of SAH and transient middle cerebral artery occlusion. In this study, we investigated the neuroprotective effect of CGS 26303 on locomotor function of rats and mRNA expression of heme-oxygenase-1 (HO-1) using semi-quantitative reverse transcription-polymerase chain reaction after 15 minutes spinal cord ischemia. The results showed rats subjected to spinal cord ischemia with pretreatment by CGS 26303 appeared a significant in preservation in the locomotor function and decreasing the paraplegia rate at Day 1 and 3 as compared with saline-treated group. Furthermore, the rats pretreated with CGS 26303 showed a significant increase in the levels of HO-1 mRNA expression at Day 3 in contrast with the rats pretreated with saline and sham operation group after spinal cord ischemia. These results demonstrated that CGS 26303 may hold the promising neuroprotection in the spinal cord ischemia-reperfusion injury and result from an adaptive mechanism involved by HO-1 overexpression.
Bauer, Christian [Verfasser]. "Der Interleukin-1β-converting-enzyme-Inhibitor [Interleukin-1-beta-converting-enzyme-Inhibitor] Pralnacasan reduziert die Dextran-Sulfat-Sodium-induzierte Kolitis und die IL-18-vermittelte Th1-Zell-Aktivierung / vorgelegt von Christian Bauer". 2006. http://d-nb.info/980224101/34.
Повний текст джерелаPei-Chun, Hsieh, and 謝佩君. "Association study between hypertension and polymorphisms of angiotensinogen, angiotensin-1 converting enzyme, and lipoprotein lipase genes in Taiwanese." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/45186786515950632452.
Повний текст джерела國立臺灣大學
農業化學研究所
89
Angiotensinogen (AGT) and angiotensin-I converting enzyme (ACE) play important roles in controlling blood pressure. Nevertheless, studies in various ethnic groups have shown contradictory results on the association between hypertension and genotype of ACE I/D, AGT M235T and T174M polymorphism. Two microsatellite markers, ATA108a05 and LPL, have been linked to young-onset hyperetension in Taiwan. Using 456 Taiwanese subjects that were randomly selected from the general population (the Nutrition and Health Survey in Taiwan, 1993-1996), we examined the association between these genetic polymorphisms and hypertension, and interaction between genetic polymorphisms and dietary factors. Hypertensive subjects had higher levels of body mass index (BMI), plasma triglyceride and uric acid. No association was found between genotypes of any single gene studied and hypertension in this population, but there was an increased risk associated with the presence of both M174 and allele4 of ATA108a05 marker. In people with II genotype, the risk of hypertension decreased with P/S ratio. However, the risk of hypertension increased with P/S ratio in people with DD+DI genotype. The risk of hypertension in people with M235 allele but not in people with T235 significant increased with BMI values. Hypertension risk increased with level of sodium intake in people with M174 allele. However, the risk of hypertension decreased with sodium intake in people with TT genotype. A significant relationship between I/D polymorphism and plasma triglyceride level was incidentally observed in men, but not in women. Further studies are required to confirm the above findings. These results suggest that hypertension is a complex disease which is modulated by gene-environment and gene-gene interactions.
Liu, George. "Studies on Angiotensin Converting Enzyme 2, Angiotensin-(1-7), and p47phox-Dependent NADPH Oxidase and their Roles in Diabetic Nephropathy." Thesis, 2012. http://hdl.handle.net/1807/34787.
Повний текст джерелаWen, Cheng-Hao, and 溫証皓. "Interplay of Angiotensin II and Angiotensin 1-7 in the Modulation of Cardiac Angiotensin-Converting Enzyme II of Human Cardiofibroblasts." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/80516546561355121015.
Повний текст джерела國立交通大學
生物科技系所
97
Components of renin–angiotensin system (RAS) are well established targets for pharmacological intervention in a variety of disorders. Many such therapies abrogate the effects of the hypertensive and mitogenic peptide, angiotensin II (Ang II), by antagonising its interaction with its receptor, or by inhibiting its formative enzyme, angiotensin-converting enzyme (ACE). At the turn of the millennium, a novel homologous enzyme, termed ACE2, was identified which increasingly shares the limelight with its better-known homologue. In common with ACE, ACE2 is a type I transmembrane metallopeptidase; however, unlike ACE, ACE2 functions as a carboxypeptidase, cleaving a single C-terminal residue from a distinct range of substrates. ACE2 is a potential therapeutic target for the control of cardiovascular disease owing to its key role in the formation of vasoprotective peptides angiotensin 1-7 (Ang 1-7) from Ang II [cleavage from angiotensin I by angiotensin-converting enzyme (ACE)]. Ang II and Ang 1-7 are both critical regulatory peptides in RAS. Ang II has been documented to play important role in the progression of cardiac remodeling. Elevated Ang II paralleled to cardiac ACE2 upregulation was reported in some pathophysiological conditions, such as myocardial infarction, heart failure and atrial fibrillation. Intracardiac overexpression of ACE2 prevents Ang II induced hypertension and cardiac fibrosis, implicating a direct in vivo cardioprotective role for ACE2, in addition to suggesting possible therapeutic utility. Further evidence for a role of ACE2 in maintaining cardiovascular homeostasis is via Ang II regulation which detected increased ACE2 and Ang 1-7 forming activity in failing human hearts. Hence, we tested the hypothesis that upregulation of ACE2 may provide cardio-protection effects to counteract the elevated Ang II. In the present study, human cardiofibroblast (HCF) cells were used to test the regulatory effects of Ang II and Ang 1-7 on the ACE2 expression at transcriptional and translational level. The results show that Ang II could upregulate ACE2 expression and this action may modulate through the activation of Ang II type I receptor (AT1R). Ang II-mediated ACE2 upregulation could be blocked by the antagonists of downstream targets of AT1R, NADPH oxidase and ERK讣MAPK cascades. To test the Ang II mediated ACE2 promoter activity, our result showed that human cardiac ACE2 promoter activity was significantly upregulation with Ang II stimulation. Additionally, Ang II-induced ACE2 promoter activity could be abolished when the HCF cells pretreated with Valsartan. Furthermore, Ang 1-7 also could up-regulate ACE2 expression in the HCF cells and this upregulation could be inhibited by Mas receptor blocker, A779. Our result shows that the Ang 1-7讣depedent ACE2 upregulation is via Mas receptor signaling pathway and even go through the NADPH oxidase and ERK-MAPK cascades. The confocal fluorescence imaging results provide further validation for Ang II讣 and Ang 1-7讣mediated ACE2 expression and an actual presentation of AT1R and ACE2 localization in HCF cells. Additionally, the image data also show the consistent results with our previous data. In conclusion, our observation implicate that Ang II-induced ACE2 may increase Ang 1-7 formation from Ang II and then the ACE2 expression is further enhanced by the Ang 1-7. According to the results, we proposed a positive feedback-like loop on the cardiac ACE2 regulation for heart to maintain a steady state of RAS. Our results may point out new targets and possibilities for developing novel therapeutic strategies in cardiovascular diseases induced by the dysfunction of RAS.
Hsu, Wei-Chieh, and 許為捷. "Angiotensin Converting Enzyme Inhibitory Activity and the 2,2-Diphenyl-1-picrylhydrazyl (DPPH) Radical-Scavenging Effect of Various Koji Mold-fermented Black Soybeans." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/03795707061477793224.
Повний текст джерела國立臺灣大學
食品科技研究所
99
In this study, black soybeans were fermented with Aspergillus oryzae BCRC 30222, A. sojae BCRC 30103 or Monascus pilosus BCRC 31526 at 30oC and 95% relative humidity for 6 days. The Angiotensin converting enzyme (ACE) inhibitory effect and 2,2-diphenyl -1-picrylhydrazyl (DPPH) radical-scavenging effect exerted by the various fermented black soybeans were then investigated. Besides, the degree of protein hydrolysis, total phenolics, flavonoids and anthocyanin contents of the fermented black soybeans were examined.Results revealed that fermentation, regardless of starters used, significantly enhanced (P<0.05) the ACE inhibitory activity and DPPH radical-scavenging effect of black soybeans and their water extracts. The ACE inhibitory activity and DPPH radical-scavenging effect of the fermented-black soybeans varied with starter organism and fermentation period. The M. pilosus BCRC 31526-fermented black soybeans possessed the highest ACE inhibitory activity and DPPH radical-scavenging effect followed by that fermented by A. oryzae BCRC 30222, and A. sojae BCRC 30103 in descending order. Regardless of starters used, fermentation increased the contents of total phenolics, flavonoids and anthocyanins as well as the degree of protein hydrolysis of black soybean. The enhanced ACE inhibitory activity and DPPH radical-scavenging effect of fermented black soybeans correlated positively with the increases in the degree of protein hydrolysis as well as the contents of total phenolics, flavonoids and anthocyanins.
Ali, Ismael Mahmoud. "Cardiovascular and sensory abnormalities in a rat model of insulin resistance : beneficial effect of an antioxidant and an angiotensin-1 converting enzyme inhibitor." Thèse, 2007. http://hdl.handle.net/1866/8204.
Повний текст джерелаHeller, Samuel. "Aldosteron syntáza u arteriální hypertenze a možný vliv polymorfismu jejího genu na hypertrofii levé komory srdeční." Doctoral thesis, 2013. http://www.nusl.cz/ntk/nusl-326710.
Повний текст джерелаCabrita, Brigite Ladeira. "Characterization and modulation of the Renin-Angiotensin System in Diabetic Retinopathy." Master's thesis, 2019. http://hdl.handle.net/10362/89766.
Повний текст джерелаShi, Yixuan. "Caractérisation du gène de l'enzyme de conversion de l'angiotensine-2 dans le rein diabétique et implication dans le développement de la néphropathie diabétique et de l'hypertension." Thèse, 2014. http://hdl.handle.net/1866/11828.
Повний текст джерелаIt is well accepted that renin-angiotensin system (RAS) activation plays an important role in the development of hypertension and diabetic nephropathy (DN). With the discovery of angiotensin-converting enzyme-2 (ACE2) and recognition of MAS as the receptor of Angiotensin 1-7 (Ang 1-7), new players in RAS, ACE2/Ang 1-7/MAS axis, have been identified to counteract the effect of ACE/Ang II/ AT1 axis. Evidence implicates the intrarenal RAS’s contribution to DN. Previous studies from our laboratory using transgenic mice overexpressing rat Angiotensinogen (Agt) in their renal proximal tubular cells (RPTCs) have demonstrated the importance of the intrarenal RAS in renal damage and the induction of hypertension. We also recently observed that renal ACE2 expression and urinary Ang 1–7 were lower in type 1 diabetic Akita mice and that treatment with RAS blockers normalized ACE2 expression and prevented hypertension development in these Akita mice. In the diabetic milieu, both glycemia and angiotensin II (Ang II) can induce reactive oxygen species (ROS) generation, which contributes to kidney injury. To explore the relationship among ROS, ACE2 and DN, we created Akita transgenic mice overexpressing catalase (Cat) in RPTCs by crossbreeding type I diabetic Akita mice with our established transgenic mice overexpressing rat Cat in RPTCs. In another study, Akita mice were treated with Ang 1-7 or combination of Ang 1-7 and its antagonist, A779, to investigate the relations between Ang 1-7 action, systolic hypertension (sHTN), oxidative stress, kidney injury, ACE2 and Mas receptor expression. Our results showed that overexpression of Cat attenuated renal oxidative stress; prevented hypertension; ameliorated glomerular filtration rate, albuminuria, kidney hypertrophy, tubulointerstitial fibrosis, and tubular apoptosis; and suppressed profibrotic and proapoptotic gene expression in RPTCs of Akita Cat-Tg mice compared with Akita mice. Furthermore, overexpression of Cat in RPTCs of Akita mice normalized renal ACE2 expression and urinary Ang 1–7 levels. On the other hand, Ang 1-7 administration prevented systemic hypertension, normalized urinary albumin/creatinine ratio and attenuated glomerular hyperfiltration without affecting blood glucose levels in Akita mice. Furthermore, Ang 1-7 treatment also attenuated oxidative stress and the expression of NADPH oxidase 4, Agt, ACE, transforming growth factor-β1 (TGF-β1) and collagen IV, and increased the expression of ACE2 and Mas receptor in Akita mouse kidneys. These effects were reversed by co-administration of A779. These data demonstrated that Cat overexpression prevents hypertension and progression of nephropathy and highlight the importance of intrarenal oxidative stress and ACE2 expression contributing to hypertension and renal injury in diabetes. Furthermore, our data suggest that Ang 1-7 plays a protective role in hypertension and RPTC injury in diabetes, predominantly through decreasing renal oxidative stress-mediated signaling and normalizing ACE2 and Mas receptor expression. Our results also indicate Ang 1-7 as a potential therapeutic agent for treatment of systemic hypertension and kidney injury in diabetes. Therefore, Ang 1-7 mediates the major protective role of ACE2 in the hypertension and DN.