Expression of Vasoactive Intestinal Peptide and Related Receptors in Overcirculation-Induced Pulmonary Hypertension in Piglets

Vuckovic, Aline; Rondelet, Benoît; Brion, Jean Pierre; Naeije, Robert

doi:10.1203/pdr.0b013e3181b33804

Cited by 10 publications

(2 citation statements)

References 26 publications

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“…Furthermore, both the right ventricular hypertrophy and the vascular remodeling can be significantly decreased after VIP treatment of the mice 52 . In piglets with high ouput-induced PAH (achieved by a shunt from the left subclavian artery to the PA trunk), circulating VIP is significantly decreased together with an up-regulation of VPAC1 53 , further supporting a role for VIP in the remodeling process.…”

Section: Growth Factors In Pah: Tyrosine Kinase Signalling As a Pomentioning

confidence: 89%

Immune and inflammatory mechanisms in pulmonary arterial hypertension

Chami¹,

Hassoun²

2012

Progress in Cardiovascular Diseases

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Altered immunity and inflammation are increasingly recognized features of pulmonary arterial hypertension (PAH). This is suggested by infiltration of various inflammatory cells (e.g., macrophages, T and B lymphocytes), increased cytokine and growth factor (e.g., VEGF and PDGF) expression in remodeled pulmonary vessels, and the presence of circulating chemokines and cytokines. In certain diseases associated with PAH, increased expression of growth and transcriptional (e.g., Nuclear Factor of Activated T cells or NFAT) factors, and viral protein components (e.g., HIV-1 Nef), appear to contribute directly to recruitment of inflammatory cells in remodeled vessels, and may potentially serve as specific therapeutic targets. This section provides an overview of inflammatory pathways highlighting their potential role in pulmonary vascular remodeling in PAH and the possibility of future targeted therapy.

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Section: Growth Factors In Pah: Tyrosine Kinase Signalling As a Pomentioning

confidence: 89%

Immune and inflammatory mechanisms in pulmonary arterial hypertension

Chami¹,

Hassoun²

2012

Progress in Cardiovascular Diseases

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show abstract

“…In addition, piglets with increased left to right shunt and PH exhibit low levels of VIP and increased expression of one of the VIP receptors, VPAC1. Interestingly, VIP does not affect precapillary PH, although bronchial constriction is ameliorated [193,194].…”

Section: Vasoactive Intestinal Peptide (Vip)mentioning

confidence: 90%

Pulmonary Hypertension: Current Therapy and Future Prospects

Mathew¹

2011

CHAMC

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Pulmonary hypertension (PH) is a sequel of a variety of cardiovascular and systemic diseases. Heterozygous mutation of BMPRII, a member of the TGFβ superfamily is the commonest genetic defect so far identified in PH. Recent advances have contributed a great deal to the understanding of the disease; however, the actual mechanism/s is not yet clear. Endothelial damage is the key underlying feature of PH. The main effects are loss of vascular relaxation response, increased cell proliferation and impaired apoptosis, matrix deposition, obstruction in the small pulmonary arteries, right ventricular hypertrophy; and eventually leading to right heart failure and death. The diagnosis of PH is often made late because of the insidious onset of symptoms, therefore the treatment poses a daunting challenge. Furthermore, depending on the underlying pathology, not all patients respond equally to same therapeutic agents. Current therapy includes a group of drugs mainly involved in improving vascular relaxation (cAMP and cGMP mechanisms) and endothelin receptor blockers alone or in combination. Newer drugs such as guanylate cyclase activators, PDGF blocker, RhoA/Rho kinase blockers have shown encouraging results in animal studies and in a few clinical cases of PH. Other drugs and signaling pathways such as nitrites, PPARγ, ACE2, ghrelin etc. are under investigation. Studies with gene therapy are being actively pursued. This review summarizes the available therapy and the future prospects.

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Inflammatory Mechanisms in the Pathogenesis of Pulmonary Arterial Hypertension

Chami

Hassoun

2011

Comprehensive Physiology

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Inflammation is a prominent feature of human and experimental pulmonary hypertension (PH) as suggested by infiltration of various inflammatory cells and increased expression of certain cytokines in remodeled pulmonary vessels. Macrophages, T and B lymphocytes, and dendritic cells are found in the vascular lesions of idiopathic pulmonary arterial hypertension (PAH) as well as in PAH associated with connective tissue diseases or infectious etiologies such as HIV. In addition, PAH is often characterized by the presence of circulating chemokines and cytokines, increased expression of growth (such as VEGF and PDGF) and transcriptional (e.g., nuclear factor of activated T cells or NFAT) factors, and viral protein components (e.g., HIV-1 Nef), which directly contribute to further recruitment of inflammatory cells and the pulmonary vascular remodeling process. These inflammatory pathways may thus serve as potential specific therapeutic targets. This article provides an overview of inflammatory pathways involving chemokines and cytokines as well as growth factors, highlighting their potential role in pulmonary vascular remodeling and the possibility of future targeted therapy.

show abstract

Expression of Vasoactive Intestinal Peptide and Related Receptors in Overcirculation-Induced Pulmonary Hypertension in Piglets

Cited by 10 publications

References 26 publications

Immune and inflammatory mechanisms in pulmonary arterial hypertension

Immune and inflammatory mechanisms in pulmonary arterial hypertension

Pulmonary Hypertension: Current Therapy and Future Prospects

Inflammatory Mechanisms in the Pathogenesis of Pulmonary Arterial Hypertension

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