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Sökning: id:"swepub:oai:DiVA.org:uu-348111" > Vascular dysfunctio...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004450naa a2200445 4500
001oai:DiVA.org:uu-348111
003SwePub
008180411s2018 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3481112 URI
0247 a https://doi.org/10.1038/s41598-018-21087-52 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Cat, Aurelie Nguyen Dinhu Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.4 aut
2451 0a Vascular dysfunction in obese diabetic db/db mice involves the interplay between aldosterone/mineralocorticoid receptor and Rho kinase signaling
264 c 2018-02-13
264 1b NATURE PUBLISHING GROUP,c 2018
338 a electronic2 rdacarrier
520 a Activation of aldosterone/mineralocorticoid receptors (MR) has been implicated in vascular dysfunction of diabetes. Underlying mechanisms are elusive. Therefore, we investigated the role of Rho kinase (ROCK) in aldosterone/MR signaling and vascular dysfunction in a model of diabetes. Diabetic obese mice (db/db) and control counterparts (db/+) were treated with MR antagonist (MRA, potassium canrenoate, 30 mg/kg/day, 4 weeks) or ROCK inhibitor, fasudil (30 mg/kg/day, 3 weeks). Plasma aldosterone was increased in db/db versus db/+. This was associated with enhanced vascular MR signaling. Norepinephrine (NE)-induced contraction was increased in arteries from db/db mice. These responses were attenuated in mice treated with canrenoate or fasudil. Db/db mice displayed hypertrophic remodeling and increased arterial stiffness, improved by MR blockade. Vascular calcium sensitivity was similar between depolarized arteries from db/+ and db/db. Vascular hypercontractility in db/db mice was associated with increased myosin light chain phosphorylation and reduced expression of PKG-1 alpha. Vascular RhoA/ROCK signaling and expression of pro-inflammatory and pro-fibrotic markers were exaggerated in db/db mice, effects that were attenuated by MRA. Fasudil, but not MRA, improved vascular insulin sensitivity in db/db mice, evidenced by normalization of Irs1 phosphorylation. Our data identify novel pathways involving MR-RhoA/ROCK-PKG-1 that underlie vascular dysfunction and injury in diabetic mice.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
7001 a Callera, Glaucia E.u Univ Ottawa, Ottawa Hosp, Res Inst, Kidney Res Ctr, Ottawa, ON, Canada.4 aut
7001 a Friederich, Malou,d 1983-u Uppsala universitet,Institutionen för medicinsk cellbiologi,Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland4 aut0 (Swepub:uu)malfr648
7001 a Sanchez, Anau Univ Complutense, Fac Farm, Dept Fisiol, Madrid, Spain.4 aut
7001 a Dulak-Lis, Maria Gabrielau Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.4 aut
7001 a Tsiropoulou, Sofiau Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.4 aut
7001 a Montezano, Augusto C.u Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.4 aut
7001 a He, Yingu Univ Ottawa, Ottawa Hosp, Res Inst, Kidney Res Ctr, Ottawa, ON, Canada.4 aut
7001 a Briones, Ana M.u Univ Autonoma Madrid, CIBER Enfermedades Cardiovasc, Sch Med, Dept Pharmacol, Madrid, Spain.4 aut
7001 a Jaisser, Fredericu Ctr Rech Cordeliers, INSERM Team 1 1138, Paris, France.4 aut
7001 a Touyz, Rhian M.u Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.;Univ Ottawa, Ottawa Hosp, Res Inst, Kidney Res Ctr, Ottawa, ON, Canada.4 aut
7102 a Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.b Univ Ottawa, Ottawa Hosp, Res Inst, Kidney Res Ctr, Ottawa, ON, Canada.4 org
7730 t Scientific Reportsd : NATURE PUBLISHING GROUPg 8q 8x 2045-2322
8564 u https://doi.org/10.1038/s41598-018-21087-5y Fulltext
8564 u https://uu.diva-portal.org/smash/get/diva2:1196780/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u https://www.nature.com/articles/s41598-018-21087-5.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-348111
8564 8u https://doi.org/10.1038/s41598-018-21087-5

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