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Research ArticleOriginal Research

Angiotensin II Receptor Antagonism Reduces Transforming Growth Factor Beta and Smad Signaling in Thoracic Aortic Aneurysm

Maria Nataatmadja, Jennifer West, Sulistiana Prabowo and Malcolm West
Ochsner Journal March 2013, 13 (1) 42-48;
Maria Nataatmadja
*Department of Medicine, The University of Queensland, Prince Charles Hospital, Brisbane, Australia
MDSc, PhD
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  • For correspondence: m.nataatmadja{at}uq.edu.au
Jennifer West
*Department of Medicine, The University of Queensland, Prince Charles Hospital, Brisbane, Australia
RN
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Sulistiana Prabowo
†Department of Biochemistry, Hang Tuah University, Surabaya, Indonesia
MD, PhD
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Malcolm West
*Department of Medicine, The University of Queensland, Prince Charles Hospital, Brisbane, Australia
MD, PhD, FRACP
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Article Figures & Data

Figures

  • Figure 1.
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    Figure 1.

    Increased accumulation of Smad3 (A-C) and transforming growth factor beta (TGF-β) (D-F) observed in the area of pathological remodeling/focal degeneration in the aortic wall of Marfan syndrome (MFS) (B, E) and bicuspid aortic valve (BAV) (C, F) aneurysms. Positive expression of Smad3 and TGF-β is identified as areas of dark brown color (arrows). The control aortic wall (A, D) showed weak to negligible expression (hematoxylin;magnification 250×).

  • Figure 2.
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    Figure 2.

    Increased expression (identified as dark brown color) of angiotensin II type 1 (AT1R) and type 2 receptors (AT2R) was observed in vascular smooth muscle cells of Marfan syndrome (MFS) (B, E) and bicuspid aortic valve (BAV) (C, F) aortic media compared to control aortic media (A, D) (hematoxylin;magnification 250×).

  • Figure 3.
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    Figure 3.

    Smad3 expression is identified as dark brown areas of color in cultured aortic vascular smooth muscle cells (VSMCs). Nuclear accumulation is shown in Marfan syndrome (MFS) and bicuspid aortic valve (BAV) VSMCs (open arrows; B, C). Lack of Smad3 nuclear expression in the control (A) is indicated with arrows. Losartan treatment of MFS and BAV VSMCs reduced nuclear accumulation of nuclear Smad3 (E, F) (hematoxylin;magnification 250×).

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    Figure 4.

    Transforming growth factor beta (TGF-β) expression (brown color) in cultured aortic vascular smooth muscle cells (VSMCs). Increased expression of TGF-β is shown in VSMCs from Marfan syndrome (MFS) and bicuspid aortic valve (BAV) samples where vesicular localization is also increased (B, C). Losartan treatment resulted in decreased expression and diffuse localization of intracellular TGF-β (E, F) similar to control VSMCs (A, D) (hematoxylin;magnification 500×).

  • Figure 5.
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    Figure 5.

    Angiotensin II type 1 receptor (AT1R) expression (brown color) in cultured aortic vascular smooth muscle cells (VSMCs). Increased expression of AT1R in cultured Marfan syndrome (MFS) and bicuspid aortic valve (BAV) VSMCs (B, C) was found. Losartan treatment reduced AT1R in cultured MFS and BAV VSMCs (E, F) to the same level as losartan-treated control VSMCs (D) (hematoxylin;magnification 500×).

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Mar 2013
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Angiotensin II Receptor Antagonism Reduces Transforming Growth Factor Beta and Smad Signaling in Thoracic Aortic Aneurysm
Maria Nataatmadja, Jennifer West, Sulistiana Prabowo, Malcolm West
Ochsner Journal Mar 2013, 13 (1) 42-48;

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Angiotensin II Receptor Antagonism Reduces Transforming Growth Factor Beta and Smad Signaling in Thoracic Aortic Aneurysm
Maria Nataatmadja, Jennifer West, Sulistiana Prabowo, Malcolm West
Ochsner Journal Mar 2013, 13 (1) 42-48;
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Cited By...

  • Vascular Smooth Muscle Cell Phenotypic Changes in Patients With Marfan Syndrome
  • Aneurysm Development in Patients With a Bicuspid Aortic Valve Is Not Associated With Transforming Growth Factor-{beta} Activation
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Keywords

  • Aneurysm
  • aorta
  • immunohistochemistry
  • Smad3 protein
  • transforming growth factor beta
  • vascular smooth muscle

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