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Sökning: WFRF:(Chernogubova Ekaterina) > H19 Induces Abdomin...

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FältnamnIndikatorerMetadata
00006299naa a2200637 4500
001oai:DiVA.org:uu-368446
003SwePub
008181207s2018 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:139376313
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3684462 URI
0247 a https://doi.org/10.1161/CIRCULATIONAHA.117.0321842 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1393763132 URI
040 a (SwePub)uud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Li, Daniel Y.u Tech Univ Munich, Dept Vasc & Endovasc Surg, Klinikum Rechts Isar, Munich, Germany4 aut
2451 0a H19 Induces Abdominal Aortic Aneurysm Development and Progression
264 1b LIPPINCOTT WILLIAMS & WILKINS,c 2018
338 a print2 rdacarrier
520 a Background: Long noncoding RNAs have emerged as critical molecular regulators in various biological processes and diseases. Here we sought to identify and functionally characterize long noncoding RNAs as potential mediators in abdominal aortic aneurysm development. Methods: We profiled RNA transcript expression in 2 murine abdominal aortic aneurysm models, Angiotensin II (ANGII) infusion in apolipoprotein E-deficient (ApoE(-/-)) mice (n=8) and porcine pancreatic elastase instillation in C57BL/6 wild-type mice (n=12). The long noncoding RNA H19 was identified as 1 of the most highly upregulated transcripts in both mouse aneurysm models compared with sham-operated controls. This was confirmed by quantitative reverse transcription-polymerase chain reaction and in situ hybridization. Results: Experimental knock-down of H19, utilizing site-specific antisense oligonucleotides (LNA-GapmeRs) in vivo, significantly limited aneurysm growth in both models. Upregulated H19 correlated with smooth muscle cell (SMC) content and SMC apoptosis in progressing aneurysms. Importantly, a similar pattern could be observed in human abdominal aortic aneurysm tissue samples, and in a novel preclinical LDLR-/- (low-density lipoprotein receptor) Yucatan mini-pig aneurysm model. In vitro knock-down of H19 markedly decreased apoptotic rates of cultured human aortic SMCs, whereas overexpression of H19 had the opposite effect. Notably, H19-dependent apoptosis mechanisms in SMCs appeared to be independent of miR-675, which is embedded in the first exon of the H19 gene. A customized transcription factor array identified hypoxia-inducible factor 1 as the main downstream effector. Increased SMC apoptosis was associated with cytoplasmic interaction between H19 and hypoxia-inducible factor 1 and sequential p53 stabilization. Additionally, H19 induced transcription of hypoxia-inducible factor 1 via recruiting the transcription factor specificity protein 1 to the promoter region. Conclusions: The long noncoding RNA H19 is a novel regulator of SMC survival in abdominal aortic aneurysm development and progression. Inhibition of H19 expression might serve as a novel molecular therapeutic target for aortic aneurysm disease.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kardiologi0 (SwePub)302062 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cardiac and Cardiovascular Systems0 (SwePub)302062 hsv//eng
653 a abdominal aortic aneurysm
653 a long noncoding RNA
653 a molecular medicine
653 a smooth muscle cells
653 a translations
7001 a Busch, Albertu Tech Univ Munich, Dept Vasc & Endovasc Surg, Klinikum Rechts Isar, Munich, Germany4 aut
7001 a Jin, Hongu Karolinska Institutet4 aut
7001 a Chernogubova, Ekaterinau Karolinska Institutet4 aut
7001 a Pelisek, Jaroslavu Tech Univ Munich, Dept Vasc & Endovasc Surg, Klinikum Rechts Isar, Munich, Germany4 aut
7001 a Karlsson, Joakimu Univ Gothenburg, Sahlgrenska Acad, Inst Biomed, Gothenburg, Sweden4 aut
7001 a Sennblad, Bengtu Uppsala universitet,Molekylär evolution,Science for Life Laboratory, SciLifeLab4 aut0 (Swepub:uu)bengtsb
7001 a Liu, Shengliangu Tech Univ Munich, Dept Vasc & Endovasc Surg, Klinikum Rechts Isar, Munich, Germany4 aut
7001 a Lao, Shen4 aut
7001 a Hofmann, Patricku Univ Hosp Frankfurt, Inst Cardiovasc Regenerat, Frankfurt, Germany;German Ctr Cardiovasc Res DZHK, Partner Site Rhein Main, Frankfurt, Germany4 aut
7001 a Baecklund, Alexandrau Karolinska Institutet4 aut
7001 a Eken, Suzanne M.u Karolinska Institutet4 aut
7001 a Roy, Joyu Karolinska Institutet4 aut
7001 a Eriksson, Peru Karolinska Institutet4 aut
7001 a Dacken, Brianu Exemplar Genet, Sioux Ctr, IA USA4 aut
7001 a Ramanujam, Deepaku Tech Univ Munich, Inst Pharmacol & Toxicol, Munich, Germany;German Ctr Cardiovasc Res DZHK, Partner Site Munich, Munich, Germany4 aut
7001 a Dueck, Anneu Tech Univ Munich, Inst Pharmacol & Toxicol, Munich, Germany;German Ctr Cardiovasc Res DZHK, Partner Site Munich, Munich, Germany4 aut
7001 a Engelhardt, Stefanu Tech Univ Munich, Inst Pharmacol & Toxicol, Munich, Germany;German Ctr Cardiovasc Res DZHK, Partner Site Munich, Munich, Germany4 aut
7001 a Boon, Reinier A.u Univ Hosp Frankfurt, Inst Cardiovasc Regenerat, Frankfurt, Germany;German Ctr Cardiovasc Res DZHK, Partner Site Rhein Main, Frankfurt, Germany4 aut
7001 a Eckstein, Hans-Henningu Tech Univ Munich, Dept Vasc & Endovasc Surg, Klinikum Rechts Isar, Munich, Germany4 aut
7001 a Spin, Joshua M.u Stanford Univ, Div Cardiovasc Med, Stanford, CA 94305 USA4 aut
7001 a Tsao, Philip S.u Stanford Univ, Div Cardiovasc Med, Stanford, CA 94305 USA4 aut
7001 a Maegdefessel, Larsu Karolinska Institutet4 aut
7102 a Karolinska Institutetb Tech Univ Munich, Dept Vasc & Endovasc Surg, Klinikum Rechts Isar, Munich, Germany4 org
7730 t Circulationd : LIPPINCOTT WILLIAMS & WILKINSg 138:15, s. 1551-1568q 138:15<1551-1568x 0009-7322x 1524-4539
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-368446
8564 8u https://doi.org/10.1161/CIRCULATIONAHA.117.032184
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:139376313

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