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Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy.

Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy. Research Abstract Details 

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  • Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy. Abstract Text:

    hiroshi ideuraHiroshi Ideura,keiju hiromuraKeiju Hiromura,noriyuki hiramatsuNoriyuki Hiramatsu,tetsuya shigeharaTetsuya Shigehara,shigeru takeuchiShigeru Takeuchi,mai tomiokaMai Tomioka,toru sakairiToru Sakairi,shin yamashitaShin Yamashita,akito maeshimaAkito Maeshima,yoriaki kanekoYoriaki Kaneko,takashi kuroiwaTakashi Kuroiwa,jeffrey b koppJeffrey B Kopp,yoshihisa nojimaYoshihisa Nojima,

    Conditional transgenic mice that express one of the human immunodeficiency virus (HIV)-1 accessory genes, vpr, selectively in podocytes using a podocin promoter and a tetracycline-inducible system develop renal injuries similar to those of patients with HIV-associated nephropathy (HIVAN). We have shown that a heminephrectomy accelerates podocyte injury, which is alleviated by angiotensin II (ANG II) type 1 receptor blocker (ARB). The current study further explores the role of ANG II in the genesis of HIVAN in this murine model. With ANG II infusion, heavy proteinuria was observed at 1 wk after the initiation of doxycycline administration to induce vpr expression in podocytes. Severe morphological and phenotypical changes in the podocytes were observed at 2 wk, together with extensive glomerulosclerosis. Norepinephrine infusion, instead of ANG II, increased the systemic blood pressure to the same level as that achieved using ANG II. However, albuminuria and glomerular injury were modest in norepinephrine-infused mice. Treatment with an ARB, olmesartan, almost completely inhibited glomerular injury. In contrast, lowering the blood pressure with a vasodilator, hydralazine, partially decreased albuminuria but did not produce any histological changes. ANG II infusion alone without doxycycline resulted in a lower level of albuminuria and minimal histological changes. These data demonstrate that excessive ANG II accelerates vpr-induced podocyte injury in a mouse model of HIVAN.

    Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy. Publishing Authors By Initials

    h ideuraH Ideura,k hiromuraK Hiromura,n hiramatsuN Hiramatsu,t shigeharaT Shigehara,s takeuchiS Takeuchi,m tomiokaM Tomioka,t sakairiT Sakairi,s yamashitaS Yamashita,a maeshimaA Maeshima,y kanekoY Kaneko,t kuroiwaT Kuroiwa,jb koppJB Kopp,y nojimaY Nojima,

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    Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Renal physiology

    VOLUME: 293

    Page Numbers: F1214-21

    Journal Abbreviation: Am. J. Physiol. Renal Physiol.

    ISSN: 0363-6127

    DAY: 25

    MONTH: 07

    YEAR: 2007

    Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy. Information

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    LANGUAGE: eng

    NlmUniqueID: 100901990

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    Grant and Affiliation Information for Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy.

    AFFILIATION: Department of Medicine and Clinical Science, Gunma University Graduste School of Medicine, Maebashi, Gunma, Japan.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Am J Physiol Renal Physiol

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