Leukotriene D4 facilitates airway smooth muscle cell proliferation via modulation of the IGF axis

Cohen, Pinchas; Noveral, James P.; Bhala, Ajay; Nunn, Steven E.; Herrick, David; Grunstein, Michael

doi:10.1152/ajplung.1995.269.2.l151

Cited by 60 publications

(46 citation statements)

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“…2, A and B, and 3, A, B, and F), we could speculate that the inhibitory effects of aerobic training on the arterial collagen and elastic fiber deposition and smooth muscle thickness could have been mediated by aerobic training, decreased vascular inflammatory cell recruitment, and IL-4 and IL-5 expression. We also add that, one time that IGF-I is an important mediator of synthesis of collagen, elastic fibers, and also of smooth muscle proliferation (9,10,62), these inhibitory effects of aerobic training also could have been mediated by a inhibited expression of IGF-I by inflammatory cells in the lung perivascular compartment in sensitized animals submitted to aerobic training of low and moderate intensities (Fig. 3F).…”

Section: Discussionmentioning

confidence: 93%

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

Vieira¹,

Andrade²,

Duarte³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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In addition, some studies demonstrated that aerobic training decreases chronic allergic inflammation in the airways; however, its effects on the pulmonary vessels and parenchyma have not been previously evaluated. Our objective was to test the hypothesis that aerobic conditioning reduces inflammation and remodeling in pulmonary vessels and parenchyma in a model of chronic allergic lung inflammation. Balb/c mice were sensitized at days 0, 14, 28, and 42 and challenged with ovalbumin (OVA) from day 21 to day 50. Aerobic training started on day 21 and continued until day 50. Pulmonary vessel and parenchyma inflammation and remodeling were evaluated by quantitative analysis of eosinophils and mononuclear cells and by collagen and elastin contents and smooth muscle thickness. Immunohistochemistry was performed to quantify the density of positive cells to interleukin (IL)-2, IL-4, IL-5, interferon-␥, IL-10, monocyte chemotatic protein (MCP)-1, nuclear factor (NF)-B p65, and insulin-like growth factor (IGF)-I. OVA exposure induced pulmonary blood vessels and parenchyma inflammation as well as increased expression of IL-4, IL-5, MCP-1, NF-B p65, and IGF-I by inflammatory cells were reduced by aerobic conditioning. OVA exposure also induced an increase in smooth muscle thickness and elastic and collagen contents in pulmonary vessels, which were reduced by aerobic conditioning. Aerobic conditioning increased the expression of IL-10 in sensitized mice. We conclude that aerobic conditioning decreases pulmonary vascular and parenchymal inflammation and remodeling in this experimental model of chronic allergic lung inflammation in mice.

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Section: Discussionmentioning

confidence: 93%

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

Vieira¹,

Andrade²,

Duarte³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Cohen and colleagues investigated the mechanism of proliferation of bronchial smooth muscle cells in their series of papers and speculated that insulin-like growth factor-I (IGF-I) may induce smooth muscle cell proliferation through activation of a latent form of IGF-I by leukotrienes and MMP (Noveral et al 1994;Cohen et al 1995;Rajah et al 1996).…”

Section: Hypertrophy and Hyperplasia Of Airway Smooth Muscle Cellsmentioning

confidence: 99%

Airway Remodeling in Asthma and its Influence on Clinical Pathophysiology

Yamauchi

2006

Tohoku J. Exp. Med.

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“…What makes IGFBP-5 potentiate IGF actions? Recent studies indicate that unlike IGFBP-4, IGFBP-5 is not only present in the extracellular fluid but is also localized on the cell surface by its association with glycosaminoglycans (GAG) and proteoglycans (Jones et al 1993, Arai et al 1994, Cohen et al 1995, Andress 1996. This has been attributed to the presence of the heparin-binding motifs in IGFBP-5.…”

Section: Ligand-dependent Actions Of Igfbpsmentioning

confidence: 99%

Specifying the cellular responses to IGF signals: roles of IGF-binding proteins

Duan

2002

Journal of Endocrinology

129

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Regulation of peptide growth factor/hormone activities by secreted hormone-binding proteins has emerged as a common theme in cell-cell signaling. Among the beststudied examples are members of the IGF-binding protein (IGFBP) gene family. These secreted proteins bind the IGF ligands with equal or even greater affinities than do the IGF receptors, and therefore are placed in a critical regulatory position between IGFs and their cell surface receptors. The circulating IGF/IGFBP complexes prolong the half-lives of IGFs and buffer the potential hypoglycemic effects of IGFs. Locally expressed IGFBPs provide a means of localizing IGFs in specific cells and can alter the IGF biological activity. While some members of the IGFBP gene family have been consistently shown to inhibit IGF actions by preventing them from gaining access to the IGF receptors, others potentiate IGF actions by facilitating the ligand-receptor interaction. Furthermore, recent studies indicate that some IGFBPs can regulate several cellular processes through ligandindependent mechanisms. This review will focus on the roles of IGFBPs in vascular smooth muscle cells. A conceptual model of the molecular mechanisms by which IGFBPs act to determine the specific physiological outcomes of IGF stimulation is proposed and discussed.

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Leukotriene D4 facilitates airway smooth muscle cell proliferation via modulation of the IGF axis

Cited by 60 publications

References 0 publications

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

Airway Remodeling in Asthma and its Influence on Clinical Pathophysiology

Specifying the cellular responses to IGF signals: roles of IGF-binding proteins

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