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Altered PPARγ coact...
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Gabrielson, MarikeKarolinska Institutet,Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm
(author)
Altered PPARγ coactivator-1 alpha expression in abdominal aortic aneurysm : Possible effects on mitochondrial biogenesis
- Article/chapterEnglish2016
Publisher, publication year, extent ...
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2016-06-25
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S. Karger,2016
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Numbers
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LIBRIS-ID:oai:DiVA.org:hj-31210
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https://urn.kb.se/resolve?urn=urn:nbn:se:hj:diva-31210URI
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https://doi.org/10.1159/000446653DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-132699URI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:134465660URI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Introduction: Abdominal aortic aneurysm (AAA) is a complex and deadly vascular disorder. The pathogenesis of AAA includes destruction and phenotypic alterations of the vascular smooth muscle cells (VSMCs) and aortic tissues. PPARγ coactivator-1 alpha (PGC1α) regulates VSMC migration and matrix formation and is a major inducer of mitochondrial biogenesis and function, including oxidative metabolism. Methods: Protein and gene expression of PGC1α and markers for mitochondria biogenesis and cell type-specificity were analysed in AAA aortas from humans and mice and compared against control aortas. Results: Gene expression of PPARGC1A was decreased in human AAA and angiotensin (Ang) II-induced AAA in mice when compared to control vessels. However, high expression of PGC1α was detected in regions of neovascularisation in the adventitia layer. In contrast, the intima/media layer of AAA vessel exhibited defective mitochondrial biogenesis as indicated by low expression of PPARGC1A, VDAC, ATP synthase and citrate synthase. Conclusion: Our results suggest that mitochondrial biogenesis is impaired in AAA in synthetic SMCs in the media, with the exception of newly formed supporting vessels in the adventitia where the mitochondrial markers seem to be intact. To our knowledge, this is the first study investigating PGC1α and mitochondria biogenesis in AAA.
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Vorkapic, EminaLinköpings universitet,Avdelningen för läkemedelsforskning,Medicinska fakulteten,Department of Medical and Health Sciences, Linköping University(Swepub:liu)emivo27
(author)
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Folkesson, MaggieLinköpings universitet,Medicinska fakulteten,Avdelningen för läkemedelsforskning,Avdelningen för kardiovaskulär medicin,Department of Medical and Health Sciences, Linköping University(Swepub:liu)magfo82
(author)
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Welander, MartinLinköpings universitet,Avdelningen för kardiovaskulär medicin,Medicinska fakulteten,Region Östergötland, Thorax-kärlkliniken i Östergötland,Department of Medical and Health Sciences, Linköping University(Swepub:liu)marwe12
(author)
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Matussek, AndreasKarolinska Institutet,Department of Laboratory Services, County Hospital Ryhov
(author)
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Dimberg, JanJönköping University,HHJ, Avdelningen för naturvetenskap och biomedicin,HHJ. Biomedicinsk plattform,University of Coll Health Science, Sweden(Swepub:hj)DiJa
(author)
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Länne, TosteLinköpings universitet,Avdelningen för kardiovaskulär medicin,Medicinska fakulteten,Centrum för medicinsk bildvetenskap och visualisering, CMIV,Region Östergötland, Thorax-kärlkliniken i Östergötland,Department of Medical and Health Sciences, Linköping University(Swepub:liu)tosla34
(author)
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Skogberg, JosefinDivision of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm,Karolinska Institute, Sweden
(author)
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Wågsäter, DickLinköpings universitet,Avdelningen för läkemedelsforskning,Medicinska fakulteten,Department of Medical and Health Sciences, Linköping University(Swepub:liu)dicwa60
(author)
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Karolinska InstitutetDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm
(creator_code:org_t)
Related titles
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In:Journal of Vascular Research: S. Karger53:1-2, s. 17-261018-11721423-0135
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