Role of Angiopoietin-1 in Experimental and Human Pulmonary Arterial Hypertension

Kugathasan, Lakshmi; Dutly, André; Zhao, Yidan; Deng, Yupu; Robb, Malcolm; Keshavjee, Shaf; Stewart, Duncan J.

doi:10.1378/chest.128.6_suppl.633s

Cited by 33 publications

(31 citation statements)

References 39 publications

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“…Furthermore, although Thistlethwaite and colleagues report an increase in Tie2 phosphorylation with no change in total Tie2 protein levels in extracts of lungs of rats with pulmonary hypertension after Ang1-gene transfer (94) or of patients with idiopathic PAH and PAH associated with other diseases (22), Eddahibi and colleagues (19) report a fourfold increase in total Tie2 levels in lungs of patients with idiopathic PAH with parallel increase in phosphorylated Tie2. In contrast Stewart and colleagues (45) report no change in phosphorylated Tie2 in lungs of patients with idiopathtic PAH or PAH associated with other diseases. Finally, although Thistlethwaite and colleagues (22) report increased Ang1 in lungs of patients with PAH, Stewart and colleagues (45) and Eddahibi and colleagues (19) failed to observe any changes in Ang1 or Ang2.…”

Section: Discordant Reports Concerning the Ang1/tie2 Pathway In Pahmentioning

confidence: 83%

“…In contrast Stewart and colleagues (45) report no change in phosphorylated Tie2 in lungs of patients with idiopathtic PAH or PAH associated with other diseases. Finally, although Thistlethwaite and colleagues (22) report increased Ang1 in lungs of patients with PAH, Stewart and colleagues (45) and Eddahibi and colleagues (19) failed to observe any changes in Ang1 or Ang2.…”

Section: Discordant Reports Concerning the Ang1/tie2 Pathway In Pahmentioning

confidence: 83%

“…Stewart and colleagues (45,107) have pointed to a loss of the Tie2 receptor for the growth factor angiopoietin-1 (Ang1) from endothelial cell elements in pulmonary arteries after MCT or hypoxia in rats and the ability of cell-based gene-transferred Ang1 to ameliorate PAH due to MCT or hypoxia. This cellbased Ang1-gene transfer by itself did not produce PAH (107).…”

Section: Discordant Reports Concerning the Ang1/tie2 Pathway In Pahmentioning

confidence: 99%

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Pulmonary arterial hypertension: a disease of tethers, SNAREs and SNAPs?

Sehgal

Mukhopadhyay²

2007

American Journal of Physiology-Heart and Circulatory Physiology

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Histological and electron microscopic studies over the past four decades have highlighted “plump,” “enlarged” endothelial, smooth muscle, and fibroblastic cellular elements with increased endoplasmic reticulum, Golgi stacks, and vacuolation in pulmonary arterial lesions in human and in experimental (hypoxia and monocrotaline) pulmonary arterial hypertension. However, the contribution of disrupted intracellular membrane trafficking in the pathobiology of this disease has received insufficient attention. Recent studies suggest a pathogenetic role of the disruption of intracellular trafficking of vasorelevant proteins and cell-surface receptors in the development of this disease. The purpose of this essay is to highlight the molecular regulation of vesicular trafficking by membrane tethers, SNAREs and SNAPs, and to suggest how their dysfunction, directly and/or indirectly, might contribute to development of pulmonary arterial hypertension in experimental models and in humans, including that due to mutations in bone morphogenetic receptor type 2.

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Section: Discordant Reports Concerning the Ang1/tie2 Pathway In Pahmentioning

confidence: 83%

Section: Discordant Reports Concerning the Ang1/tie2 Pathway In Pahmentioning

confidence: 83%

Section: Discordant Reports Concerning the Ang1/tie2 Pathway In Pahmentioning

confidence: 99%

See 1 more Smart Citation

Pulmonary arterial hypertension: a disease of tethers, SNAREs and SNAPs?

Sehgal

Mukhopadhyay²

2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…the endothelial progenitor cells (EPCs)] and gene [eg. DNA of aderenomedullin (AM), a potent vasodilator peptide] therapy, has been used in experimental animal models or clinical cases with pulmonary vascular disease from ALI/ARDS or primary pulmonary hypertension (Campbell et al, 1999;Zhao et al, 2003;Kugathasan et al, 2005;Nagaya et al, 2003a). Campbell et al(1999; used rat smooth muscle cells (SMC) in ex vivo transfection of DNA of nitric oxide synthase (NOS) or endothelial growth factor to the syngeneic recipient.…”

Section: Cell Therapies For Ali/ardsmentioning

confidence: 99%

“…Zhao et al(2003) applied the rat model with SMC transfection of angiopoietin-1 (Ang-1), which can protect animals from pulmonary arterial hypertension. Cell-based gene therapy with the Ang-1 (Kugathasan et al, 2005) or AM (Nagaya et al, 2003a) cDNA vector has been successfully applied in human pulmonary arterial hypertension.…”

Section: Cell Therapies For Ali/ardsmentioning

confidence: 99%

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS): the mechanism, present strategies and future perspectives of therapies

Luh

Chiang²

2007

J. Zhejiang Univ. - Sci. B

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Acute lung injury/acute respiratory distress syndrome (ALI/ARDS), which manifests as non-cardiogenic pulmonary edema, respiratory distress and hypoxemia, could be resulted from various processes that directly or indirectly injure the lung. Extensive investigations in experimental models and humans with ALI/ARDS have revealed many molecular mechanisms that offer therapeutic opportunities for cell or gene therapy. Herein the present strategies and future perspectives of the treatment for ALI/ARDS, include the ventilatory, pharmacological, as well as cell therapies.

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Pulmonary Vascular Disease Related to Hemodynamic Stress in the Pulmonary Circulation

Chan

Loscalzo

2010

Comprehensive Physiology

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Hemodynamic stress in the pulmonary vessel is directly linked to the development of vascular remodeling and dysfunction, ultimately leading to pulmonary hypertension. Recently, some advances have been made in our molecular understanding of the exogenous upstream stimuli that initiate hemodynamic pertubations as well as the downstream vasoactive effectors that control these responses. However, much still remains unknown regarding how these complex signaling pathways connect in order to result in these characteristic pathophysiological changes. This chapter will describe our current understanding of and needed areas of research into the clinical, physiological, and molecular changes associated with pressure/volume overload in the pulmonary circulation. © 2011 American Physiological Society. Compr Physiol 1:123‐139, 2011.

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Role of Angiopoietin-1 in Experimental and Human Pulmonary Arterial Hypertension

Cited by 33 publications

References 39 publications

Pulmonary arterial hypertension: a disease of tethers, SNAREs and SNAPs?

Pulmonary arterial hypertension: a disease of tethers, SNAREs and SNAPs?

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS): the mechanism, present strategies and future perspectives of therapies

Pulmonary Vascular Disease Related to Hemodynamic Stress in the Pulmonary Circulation

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