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  • Wang, Renjun (author)

Sympathoexcitation in Rats With Chronic Heart Failure Depends on Homeobox D10 and MicroRNA-7b Inhibiting GABBR1 Translation in Paraventricular Nucleus

  • Article/chapterEnglish2016

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  • 2016
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:uu-272536
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-272536URI
  • https://doi.org/10.1161/CIRCHEARTFAILURE.115.002261DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • BACKGROUND: Chronic heart failure (CHF) increases sympathoexcitation through angiotensin II (ANG II) receptors (AT1R) in the paraventricular nucleus (PVN). Recent publications indicate both γ-aminobutyric acid B-type receptor 1 (GABBR1) and microRNA-7b (miR-7b) are expressed in the PVN. We hypothesized that ANG II regulates sympathoexcitation through homeobox D10 (HoxD10), which regulates miR-7b in other tissues.METHODS AND RESULTS: Ligation of the left anterior descendent coronary artery in rats caused CHF and sympathoexcitation. PVN expression of AT1R, HoxD10, and miR-7b was increased, whereas GABBR1 was lower in CHF. Infusion of miR-7b in the PVN caused sympathoexcitation in control animals and enhanced the changes in CHF. Antisense miR-7b infused in PVN normalized GABBR1 expression while attenuating CHF symptoms, including sympathoexcitation. A luciferase reporter assay detected miR-7b binding to the 3' untranslated region of GABBR1 that was absent after targeted mutagenesis. ANG II induced HoxD10 and miR-7b in NG108 cells, effects blocked by AT1R blocker losartan and by HoxD10 silencing. miR-7b transfection into NG108 cells decreased GABBR1 expression, which was inhibited by miR-7b antisense. In vivo PVN knockdown of AT1R attenuated the symptoms of CHF, whereas HoxD10 overexpression exaggerated them. Finally, in vivo PVN ANG II infusion caused dose-dependent sympathoexcitation that was abrogated by miR-7b antisense and exaggerated by GABBR1 silencing.CONCLUSIONS: There is an ANG II/AT1R/HoxD10/miR-7b/GABBR1 pathway in the PVN that contributes to sympathoexcitation and deterioration of cardiac function in CHF.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Huang, Qian (author)
  • Zhou, Rui (author)
  • Dong, Zengxiang (author)
  • Qi, Yunfeng (author)
  • Li, Hua (author)
  • Wei, Xiaowei (author)
  • Wu, Hui (author)
  • Wang, Huiping (author)
  • Wilcox, Christopher S (author)
  • Hultström, Michael,1978-Uppsala universitet,Integrativ Fysiologi,Anestesiologi och intensivvård(Swepub:uu)mihul498 (author)
  • Zhou, Xiaofu (author)
  • Lai, En Yin (author)
  • Uppsala universitetIntegrativ Fysiologi (creator_code:org_t)

Related titles

  • In:Circulation Heart Failure9:11941-32891941-3297

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