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Article ; Online: miR-619-5p and cardiogenic shock in patients with ST-segment elevation myocardial infarction.

Escate, Rafael / Padró, Teresa / Suades, Rosa / Sans-Roselló, Jordi / Devaux, Yvan / Lakkisto, Päivi / Harjola, Veli-Pekka / Sionis, Alessandro / Badimon, Lina

European journal of clinical investigation

2024 , Page(s) e14186

Abstract: Background: Cardiogenic shock (CS) is a severe myocardial dysfunction secondary to various cardiac conditions including ST-segment elevation acute myocardial infarction (STEMI) and associated with a high risk of death. Little is known on epigenetic ... ...

Abstract	Background: Cardiogenic shock (CS) is a severe myocardial dysfunction secondary to various cardiac conditions including ST-segment elevation acute myocardial infarction (STEMI) and associated with a high risk of death. Little is known on epigenetic determinants in CS. Here, we investigated plasma miRNAs in relation to CS stratification in STEMI-patients. Methods: STEMI-patients (n = 49), with (CS, n = 25) and without CS (non-CS, n = 24) fulfilling inclusion criteria were included from HSCSP-cohort (Derivation-cohort). CS-miRNAs were analysed by Affymetrix-microarray and RT-PCR. Results were validated in a second cohort of CS-patients (CardShock: n = 35) with similar inclusion/exclusion criteria as the derivation cohort. In silico analysis were performed to identify potential miRNA target genes. Results: Of the 5-miRNA signature obtained from microarray analysis, miR-619-5p showed higher levels in CS than in Non-CS patients (p = .003) and discriminating power for CS by ROC (AUC: .752, p = .003). miR-619-5p directly associated with risk scores [GRACE, p = .001; CardShock, p < .001]. Furthermore, miR-619-5p showed discrimination power for death in CS. Thus, miRNA levels were significantly higher in patients with mortality outcome both in the Derivation HSCSP-cohort (p = .02; AUC: .78 ± .095) and the Validation CardShock-cohort (p = .017; AUC: .737 ± .086) By in silico analysis, miR-619-5p target genes and TNF-alpha were involved in the regulation of inflammation. miR-619-5p and TNF-alpha levels discriminated mortality outcome in CS-patients during 30-day follow-up (Validation-Cohort: ROC: .812, p = .002; HR: 9.99, p = .003). Conclusions: Up-regulation of miR-619-5p is found in the plasma of STEMI-patients with CS and mortality outcome. These findings highlight the specificity of epigenetic regulation of inflammation on the disease severity of MI.
Language	English
Publishing date	2024-02-20
Publishing country	England
Document type	Journal Article
ZDB-ID	186196-7
ISSN	1365-2362 ; 0014-2972 ; 0960-135X
ISSN (online)	1365-2362
ISSN	0014-2972 ; 0960-135X
DOI	10.1111/eci.14186
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Zs.A 677: Show issues

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Article ; Online: Deficiency of heme oxygenase 1a causes detrimental effects on cardiac function.

Wang, Hong / Siren, Juuso / Perttunen, Sanni / Immonen, Katariina / Chen, Yu-Chia / Narumanchi, Suneeta / Kosonen, Riikka / Paavola, Jere / Laine, Mika / Tikkanen, Ilkka / Lakkisto, Päivi

Journal of cellular and molecular medicine

2024 Volume 28, Issue 7, Page(s) e18243

Abstract: Humans lacking heme oxygenase 1 (HMOX1) display growth retardation, haemolytic anaemia, and vulnerability to stress; however, cardiac function remains unclear. We aimed to explore the cardiac function of zebrafish lacking hmox1a at baseline and in ... ...

Abstract	Humans lacking heme oxygenase 1 (HMOX1) display growth retardation, haemolytic anaemia, and vulnerability to stress; however, cardiac function remains unclear. We aimed to explore the cardiac function of zebrafish lacking hmox1a at baseline and in response to stress. We generated zebrafish hmox1a mutants using CRISPR/Cas9 genome editing technology. Deletion of hmox1a increases cardiac output and further induces hypertrophy in adults. Adults lacking hmox1a develop myocardial interstitial fibrosis, restrain cardiomyocyte proliferation and downregulate renal haemoglobin and cardiac antioxidative genes. Larvae lacking hmox1a fail to respond to hypoxia, whereas adults are insensitive to isoproterenol stimulation in the heart, suggesting that hmox1a is necessary for cardiac response to stress. Haplodeficiency of hmox1a stimulates non-mitochondrial respiration and cardiac cell proliferation, increases cardiac output in larvae in response to hypoxia, and deteriorates cardiac function and structure in adults upon isoproterenol treatment. Intriguingly, haplodeficiency of hmox1a upregulates cardiac hmox1a and hmox1b in response to isoproterenol. Collectively, deletion of hmox1a results in cardiac remodelling and abrogates cardiac response to hypoxia and isoproterenol. Haplodeficiency of hmox1a aggravates cardiac response to the stress, which could be associated with the upregulation of hmox1a and hmox1b. Our data suggests that HMOX1 homeostasis is essential for maintaining cardiac function and promoting cardioprotective effects.
MeSH term(s)	Animals ; Humans ; Heme Oxygenase (Decyclizing) ; Zebrafish/genetics ; Isoproterenol/pharmacology ; Heme Oxygenase-1/genetics ; Myocardium ; Cardiomyopathies ; Hypoxia ; Myocytes, Cardiac
Chemical Substances	Heme Oxygenase (Decyclizing) (EC 1.14.14.18) ; Isoproterenol (L628TT009W) ; Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2024-03-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.18243
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Zs.A 5752: Show issues

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Article: Zebrafish Heart Failure Models.

Narumanchi, Suneeta / Wang, Hong / Perttunen, Sanni / Tikkanen, Ilkka / Lakkisto, Päivi / Paavola, Jere

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 662583

Abstract: Heart failure causes significant morbidity and mortality worldwide. The understanding of heart failure pathomechanisms and options for treatment remain incomplete. Zebrafish has proven useful for modeling human heart diseases due to similarity of ... ...

Abstract	Heart failure causes significant morbidity and mortality worldwide. The understanding of heart failure pathomechanisms and options for treatment remain incomplete. Zebrafish has proven useful for modeling human heart diseases due to similarity of zebrafish and mammalian hearts, fast easily tractable development, and readily available genetic methods. Embryonic cardiac development is rapid and cardiac function is easy to observe and quantify. Reverse genetics, by using morpholinos and CRISPR-Cas9 to modulate gene function, make zebrafish a primary animal model for
Language	English
Publishing date	2021-05-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.662583
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Article ; Online: Development of circulating microRNA-based biomarkers for medical decision-making: a friendly reminder of what should NOT be done.

Lakkisto, Päivi / Dalgaard, Louise Torp / Belmonte, Thalia / Pinto-Sietsma, Sara-Joan / Devaux, Yvan / de Gonzalo-Calvo, David

Critical reviews in clinical laboratory sciences

2022 Volume 60, Issue 2, Page(s) 141–152

Abstract: Circulating cell-free microRNAs (miRNAs) represent a major reservoir for biomarker discovery. Unfortunately, their implementation in clinical practice is limited due to a profound lack of reproducibility. The great technical variability linked to major ... ...

Abstract	Circulating cell-free microRNAs (miRNAs) represent a major reservoir for biomarker discovery. Unfortunately, their implementation in clinical practice is limited due to a profound lack of reproducibility. The great technical variability linked to major pre-analytical and analytical caveats makes the interpretation of circulating cell-free miRNA data challenging and leads to inconsistent findings. Additional efforts directed to standardization are fundamental. Several well-established protocols are currently used by independent groups worldwide. Nonetheless, there are some specific aspects in specimen collection and processing, sample handling, miRNA quantification, and data analysis that should be considered to ensure reproducibility of results. Here, we have addressed this challenge using an alternative approach. We have highlighted and discussed common pitfalls that negatively impact the robustness of circulating miRNA quantification and their application for clinical decision-making. Furthermore, we provide a checklist usable by investigators to facilitate and ensure the control of the whole miRNA quantification and analytical process. We expect that these recommendations improve the reproducibility of findings, and ultimately, facilitate the incorporation of circulating miRNA profiles into clinical practice as the next generation of disease biomarkers.
MeSH term(s)	Humans ; Circulating MicroRNA ; Reproducibility of Results ; Biomarkers ; MicroRNAs/genetics ; Clinical Decision-Making
Chemical Substances	Circulating MicroRNA ; Biomarkers ; MicroRNAs
Language	English
Publishing date	2022-11-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	280641-1
ISSN	1549-781X ; 1040-8363 ; 0590-8191
ISSN (online)	1549-781X
ISSN	1040-8363 ; 0590-8191
DOI	10.1080/10408363.2022.2128030
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Zs.A 771: Show issues

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Article ; Online: Moderate hyperuricaemia ameliorated kidney damage in a low-renin model of experimental renal insufficiency.

Kurra, Venla / Eräranta, Arttu / Paavonen, Timo / Honkanen, Teemu / Myllymäki, Juhani / Riutta, Asko / Tikkanen, Ilkka / Lakkisto, Päivi / Mustonen, Jukka / Pörsti, Ilkka

Basic & clinical pharmacology & toxicology

2022 Volume 132, Issue 1, Page(s) 21–32

Abstract: Uric acid has promoted renal fibrosis and inflammation in experimental studies, but some studies have shown nephroprotective effects due to alleviated oxidative stress. We studied the influence of experimental hyperuricaemia in surgically 5/6 ... ...

Abstract	Uric acid has promoted renal fibrosis and inflammation in experimental studies, but some studies have shown nephroprotective effects due to alleviated oxidative stress. We studied the influence of experimental hyperuricaemia in surgically 5/6 nephrectomized rats. Three weeks after subtotal nephrectomy or sham operation, the rats were allocated to control diet or 2.0% oxonic acid (uricase inhibitor) diet for 9 weeks. Then blood, urine and tissue samples were taken, and renal morphology and oxidative stress were examined. Inflammation and fibrosis were evaluated using immunohistochemistry and real-time PCR (RT-PCR). Remnant kidney rats ingesting normal or oxonic acid diet presented with ~60% reduction of creatinine clearance and suppressed plasma renin activity. Oxonic acid diet increased plasma uric acid levels by >80 μmol/L. In remnant kidney rats, moderate hyperuricaemia decreased glomerulosclerosis, tubulointerstitial damage and kidney mast cell count, without influencing the fibrosis marker collagen I messenger RNA (mRNA) content. In both sham-operated and 5/6 nephrectomized rats, the mast cell product 11-epi-prostaglandin-F
MeSH term(s)	Animals ; Rats ; Fibrosis ; Hyperuricemia/pathology ; Inflammation/pathology ; Kidney ; Kidney Diseases ; Nephrectomy ; Oxonic Acid/pharmacology ; Renal Insufficiency/pathology ; Renin/genetics ; Uric Acid
Chemical Substances	Oxonic Acid (5VT6420TIG) ; Renin (EC 3.4.23.15) ; Uric Acid (268B43MJ25)
Language	English
Publishing date	2022-10-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2134679-3
ISSN	1742-7843 ; 1742-7835
ISSN (online)	1742-7843
ISSN	1742-7835
DOI	10.1111/bcpt.13806
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Article ; Online: Heme oxygenase-1 repeat polymorphism in septic acute kidney injury.

Vilander, Laura M / Vaara, Suvi T / Donner, Kati M / Lakkisto, Päivi / Kaunisto, Mari A / Pettilä, Ville

PloS one

2019 Volume 14, Issue 5, Page(s) e0217291

Abstract: Acute kidney injury (AKI) is a syndrome that frequently affects the critically ill. Recently, an increased number of dinucleotide repeats in the HMOX1 gene were reported to associate with development of AKI in cardiac surgery. We aimed to test the ... ...

Abstract	Acute kidney injury (AKI) is a syndrome that frequently affects the critically ill. Recently, an increased number of dinucleotide repeats in the HMOX1 gene were reported to associate with development of AKI in cardiac surgery. We aimed to test the replicability of this finding in a Finnish cohort of critically ill septic patients. This multicenter study was part of the national FINNAKI study. We genotyped 300 patients with severe AKI (KDIGO 2 or 3) and 353 controls without AKI (KDIGO 0) for the guanine-thymine (GTn) repeat in the promoter region of the HMOX1 gene. The allele calling was based on the number of repeats, the cut off being 27 repeats in the S-L (short to long) classification, and 27 and 34 repeats for the S-M-L2 (short to medium to very long) classification. The plasma concentrations of heme oxygenase-1 (HO-1) enzyme were measured on admission. The allele distribution in our patients was similar to that published previously, with peaks at 23 and 30 repeats. The S-allele increases AKI risk. An adjusted OR was 1.30 for each S-allele in an additive genetic model (95% CI 1.01-1.66; p = 0.041). Alleles with a repeat number greater than 34 were significantly associated with lower HO-1 concentration (p<0.001). In septic patients, we report an association between a short repeat in HMOX1 and AKI risk.
MeSH term(s)	Acute Kidney Injury/enzymology ; Acute Kidney Injury/epidemiology ; Acute Kidney Injury/genetics ; Aged ; Alleles ; Cohort Studies ; Comorbidity ; Critical Illness ; Female ; Finland/epidemiology ; Genetic Predisposition to Disease ; Genotype ; Heme Oxygenase-1/blood ; Heme Oxygenase-1/genetics ; Humans ; Male ; Middle Aged ; Minisatellite Repeats ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Prospective Studies ; Risk Factors ; Sepsis/enzymology ; Sepsis/epidemiology ; Sepsis/genetics
Chemical Substances	HMOX1 protein, human (EC 1.14.14.18) ; Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2019-05-23
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Observational Study ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0217291
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Article: Alterations of Cardiac Protein Kinases in Cyclic Nucleotide-Dependent Signaling Pathways in Human Ischemic Heart Failure.

Wang, Chunguang / Taskinen, Juuso H / Segersvärd, Heli / Immonen, Katariina / Kosonen, Riikka / Tolva, Johanna M / Mäyränpää, Mikko I / Kovanen, Petri T / Olkkonen, Vesa M / Sinisalo, Juha / Laine, Mika / Tikkanen, Ilkka / Lakkisto, Päivi

Frontiers in cardiovascular medicine

2022 Volume 9, Page(s) 919355

Abstract: Objectives: Impaired protein kinase signaling is a hallmark of ischemic heart disease (IHD). Inadequate understanding of the pathological mechanisms limits the development of therapeutic approaches. We aimed to identify the key cardiac kinases and ... ...

Abstract	Objectives: Impaired protein kinase signaling is a hallmark of ischemic heart disease (IHD). Inadequate understanding of the pathological mechanisms limits the development of therapeutic approaches. We aimed to identify the key cardiac kinases and signaling pathways in patients with IHD with an effort to discover potential therapeutic strategies. Methods: Cardiac kinase activity in IHD left ventricle (LV) and the related signaling pathways were investigated by kinomics, transcriptomics, proteomics, and integrated multi-omics approach. Results: Protein kinase A (PKA) and protein kinase G (PKG) ranked on top in the activity shift among the cardiac kinases. In the IHD LVs, PKA activity decreased markedly compared with that of controls (62% reduction, Conclusion: The deficiency in cAMP/PKA signaling pathway is strongly implicated in the pathogenesis of IHD. Natriuretic peptide CNP could be a potential therapeutic target for the modulation of cGMP/PKG signaling.
Language	English
Publishing date	2022-06-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.919355
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Article ; Online: Tankyrase Inhibition Attenuates Cardiac Dilatation and Dysfunction in Ischemic Heart Failure.

Wang, Hong / Segersvärd, Heli / Siren, Juuso / Perttunen, Sanni / Immonen, Katariina / Kosonen, Riikka / Chen, Yu-Chia / Tolva, Johanna / Laivuori, Mirjami / Mäyränpää, Mikko I / Kovanen, Petri T / Sinisalo, Juha / Laine, Mika / Tikkanen, Ilkka / Lakkisto, Päivi

International journal of molecular sciences

2022 Volume 23, Issue 17

Abstract: Hyperactive poly(ADP-ribose) polymerases (PARP) promote ischemic heart failure (IHF) after myocardial infarction (MI). However, the role of tankyrases (TNKSs), members of the PARP family, in pathogenesis of IHF remains unknown. We investigated the ... ...

Abstract	Hyperactive poly(ADP-ribose) polymerases (PARP) promote ischemic heart failure (IHF) after myocardial infarction (MI). However, the role of tankyrases (TNKSs), members of the PARP family, in pathogenesis of IHF remains unknown. We investigated the expression and activation of TNKSs in myocardium of IHF patients and MI rats. We explored the cardioprotective effect of TNKS inhibition in an isoproterenol-induced zebrafish HF model. In IHF patients, we observed elevated TNKS2 and DICER and concomitant upregulation of miR-34a-5p and miR-21-5p in non-infarcted myocardium. In a rat MI model, we found augmented TNKS2 and DICER in the border and infarct areas at the early stage of post-MI. We also observed consistently increased TNKS1 in the border and infarct areas and destabilized AXIN in the infarct area from 4 weeks onward, which in turn triggered Wnt/β-catenin signaling. In an isoproterenol-induced HF zebrafish model, inhibition of TNKS activity with XAV939, a TNKSs-specific inhibitor, protected against ventricular dilatation and cardiac dysfunction and abrogated overactivation of Wnt/β-catenin signaling and dysregulation of miR-34a-5p induced by isoproterenol. Our study unravels a potential role of TNKSs in the pathogenesis of IHF by regulating Wnt/β-catenin signaling and possibly modulating miRNAs and highlights the pharmacotherapeutic potential of TNKS inhibition for prevention of IHF.
MeSH term(s)	Animals ; Dilatation ; Heart Failure/drug therapy ; Isoproterenol/pharmacology ; MicroRNAs/genetics ; Rats ; Tankyrases/antagonists & inhibitors ; Tankyrases/metabolism ; Wnt Signaling Pathway ; Zebrafish/metabolism ; beta Catenin/metabolism
Chemical Substances	MIRN21 microRNA, zebrafish ; MicroRNAs ; beta Catenin ; mirn21 microRNA, rat ; Tankyrases (EC 2.4.2.30) ; Isoproterenol (L628TT009W)
Language	English
Publishing date	2022-09-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231710059
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Article: Consensus guidelines for the validation of qRT-PCR assays in clinical research by the CardioRNA consortium.

de Gonzalo-Calvo, David / Marchese, Monica / Hellemans, Jan / Betsou, Fay / Skov Frisk, Nanna Lond / Dalgaard, Louise Torp / Lakkisto, Päivi / Foy, Carole / Scherer, Andreas / Garcia Bermejo, María Laura / Devaux, Yvan

Molecular therapy. Methods & clinical development

2022 Volume 24, Page(s) 171–180

Abstract: Despite promising findings, quantitative PCR (qPCR)-based tests for RNA quantification have experienced serious limitations in their clinical application. The noticeable lack of technical standardization remains a huge obstacle in the translation of qPCR- ...

Abstract	Despite promising findings, quantitative PCR (qPCR)-based tests for RNA quantification have experienced serious limitations in their clinical application. The noticeable lack of technical standardization remains a huge obstacle in the translation of qPCR-based tests. The incorporation of qPCR-based tests into the clinic will benefit from guidelines for clinical research assay validation. This will ultimately impact the clinical management of the patient, including diagnosis, prognosis, prediction, monitoring of the therapeutic response, and evaluation of toxicity. However, clear assay validation protocols for biomarker investigation in clinical trials using molecular assays are currently lacking
Language	English
Publishing date	2022-01-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2872938-9
ISSN	2329-0501 ; 2329-0501
ISSN (online)	2329-0501
ISSN	2329-0501
DOI	10.1016/j.omtm.2021.12.007
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Zs.A 7107: Show issues

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Article ; Online: Unfavorable Reduction in the Ratio of Endothelin B to A Receptors in Experimental 5/6 Nephrectomy and Adenine Models of Chronic Renal Insufficiency.

Törmänen, Suvi / Lakkisto, Päivi / Eräranta, Arttu / Kööbi, Peeter / Tikkanen, Ilkka / Niemelä, Onni / Mustonen, Jukka / Pörsti, Ilkka

International journal of molecular sciences

2020 Volume 21, Issue 3

Abstract: Chronic renal insufficiency (CRI) is characterized by increased endothelin 1 (ET-1) synthesis. We studied rat kidney endothelin receptor A (ETA) and receptor B (ETB) expressions after 12 and 27 weeks of 5/6 nephrectomy, and after 12 weeks of 0.3% adenine ...

Abstract	Chronic renal insufficiency (CRI) is characterized by increased endothelin 1 (ET-1) synthesis. We studied rat kidney endothelin receptor A (ETA) and receptor B (ETB) expressions after 12 and 27 weeks of 5/6 nephrectomy, and after 12 weeks of 0.3% adenine diet, representing proteinuric and interstitial inflammation models of CRI, respectively. Uric acid and calcium-phosphate metabolism were modulated after 5/6 nephrectomy, while ETA blocker and calcimimetic were given with adenine. Endothelin receptor mRNA levels were measured using RT-qPCR and protein levels using autoradiography (5/6 nephrectomy) or ELISA (adenine model). Both 12 and 27 weeks after 5/6 nephrectomy, kidney cortex ETA protein was increased by ~60% without changes in ETB protein, and the ETB:ETA ratio was reduced. However, the ETB:ETA mRNA ratio did not change. In the adenine model, kidney ETA protein was reduced by ~70%, while ETB protein was suppressed by ~95%, and the ETB:ETA ratio was reduced by ~85%, both at the protein and mRNA levels. The additional interventions did not influence the observed reductions in the ETB:ETA ratio. To conclude, unfavorable reduction in the ETB:ETA protein ratio was observed in two different models of CRI. Therefore, ETA blockade may be beneficial in a range of diseases that cause impaired kidney function.
MeSH term(s)	Adenine/adverse effects ; Animals ; Calcium/metabolism ; Disease Models, Animal ; Gene Expression Regulation/drug effects ; Kidney Cortex/metabolism ; Male ; Nephrectomy/adverse effects ; Phosphates/metabolism ; Rats ; Receptor, Endothelin A/genetics ; Receptor, Endothelin A/metabolism ; Receptor, Endothelin B/genetics ; Receptor, Endothelin B/metabolism ; Renal Insufficiency, Chronic/chemically induced ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism ; Uric Acid/metabolism
Chemical Substances	Phosphates ; Receptor, Endothelin A ; Receptor, Endothelin B ; ednrb protein, rat ; Uric Acid (268B43MJ25) ; Adenine (JAC85A2161) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-01-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21030936
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