Targeting Insulin-Like Growth Factor-I and Insulin-Like Growth Factor–Binding Protein-3 Signaling Pathways. A Novel Therapeutic Approach for Asthma

Lee, Hyun; Kim, So Ri; Oh, Youngman; Cho, Seong Ho; Schleimer, Robert P.; Lee, Yong Chul

doi:10.1165/rcmb.2013-0397tr

Cited by 60 publications

(57 citation statements)

References 140 publications

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“…Since Igf1 and Igfbp3 levels have been involved in controlling colonic epithelial stem cell function [80], upregulation of their expression in the lungs of our Igf1r mutants could alter BASC function during airway epithelial regeneration. Additionally, Igfbp3 overexpression could be the consequence of a protective molecular mechanism in response to lung damage or pathological conditions, as demonstrated respectively in mice and patients [21, 81–84]. Expression of Insr in the rodent lung was verified some time ago, at both fetal and adult stages [85, 86], and alterations in insulin signaling, including diabetes and metabolic syndrome have been associated with an increased risk in lung diseases (reviewed in [87]).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Igf1r in Bronchiolar Epithelial Regeneration: Role during Repair Kinetics after Selective Club Cell Ablation

López¹,

Piñeiro‐Hermida²,

Pais³

et al. 2016

PLoS ONE

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Regeneration of lung epithelium is vital for maintaining airway function and integrity. An imbalance between epithelial damage and repair is at the basis of numerous chronic lung diseases such as asthma, COPD, pulmonary fibrosis and lung cancer. IGF (Insulin-like Growth Factors) signaling has been associated with most of these respiratory pathologies, although their mechanisms of action in this tissue remain poorly understood. Expression profiles analyses of IGF system genes performed in mouse lung support their functional implication in pulmonary ontogeny. Immuno-localization revealed high expression levels of Igf1r (Insulin-like Growth Factor 1 Receptor) in lung epithelial cells, alveolar macrophages and smooth muscle. To further understand the role of Igf1r in pulmonary homeostasis, two distinct lung epithelial-specific Igf1r mutant mice were generated and studied. The lack of Igf1r disturbed airway epithelial differentiation in adult mice, and revealed enhanced proliferation and altered morphology in distal airway club cells. During recovery after naphthalene-induced club cell injury, the kinetics of terminal bronchiolar epithelium regeneration was hindered in Igf1r mutants, revealing increased proliferation and delayed differentiation of club and ciliated cells. Amid airway restoration, lungs of Igf1r deficient mice showed increased levels of Igf1, Insr, Igfbp3 and epithelial precursor markers, reduced amounts of Scgb1a1 protein, and alterations in IGF signaling mediators. These results support the role of Igf1r in controlling the kinetics of cell proliferation and differentiation during pulmonary airway epithelial regeneration after injury.

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Section: Discussionmentioning

confidence: 99%

Involvement of Igf1r in Bronchiolar Epithelial Regeneration: Role during Repair Kinetics after Selective Club Cell Ablation

López¹,

Piñeiro‐Hermida²,

Pais³

et al. 2016

PLoS ONE

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“…Reduced tPA and elevated M2 macrophages containing XIIIA result from increased expression of interleukin 13 (IL-13) in polyp tissue. Deposition of fibrin resulting from strong type 2 inflammation may be of benefit in immobilization and destruction of parasite worms (30, 31). …”

Section: Tissue Remodeling and Polyp Formation In Crsmentioning

confidence: 99%

Immunopathogenesis of Chronic Rhinosinusitis and Nasal Polyposis

Schleimer

2017

Annu. Rev. Pathol. Mech. Dis.

Self Cite

411

419

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Chronic rhinosinusitis (CRS) is a troublesome, chronic inflammatory disease that affects over 10% of the adult population, causing decreased quality of life, lost productivity, and lost time at work and leading to more than a million surgical interventions annually worldwide. The nose, paranasal sinuses, and associated lymphoid tissues play important roles in homeostasis and immunity, and CRS significantly impairs these normal functions. Pathogenic mechanisms of CRS have recently become the focus of intense investigations worldwide, and significant progress has been made. The two main forms of CRS that have been long recognized, with and without nasal polyps, are each now known to be heterogeneous, based on underlying mechanism, geographical location, and race. Loss of the immune barrier, including increased permeability of mucosal epithelium and reduced production of important antimicrobial substances and responses, is a common feature of many forms of CRS. One form of CRS with polyps found worldwide is driven by the cytokines IL-5 and IL-13 coming from Th2 cells, type 2 innate lymphoid cells, and probably mast cells. Type 2 cytokines activate inflammatory cells that are implicated in the pathogenic mechanism, including mast cells, basophils, and eosinophils. New classes of biological drugs that block the production or action of these cytokines are making important inroads toward new treatment paradigms in polypoid CRS.

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“…These large volumes of compelling data suggest a pro-tumorigenic role of inflammation in CRC. Additionally, the influence of IGF1R signal on inflammation has been observed in some chronic inflammation diseases and cancers, such as osteoarthritis, asthma, neurodegenerative disease, neonatial immune response and prostate cancer [33][34][35][36][37]. Nonetheless, it still needs more researches to demonstrate the mechanism of this pro-inflammation effect.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of type I insulin-like growth factor receptor inhibits human colorectal cancer cell growth and downstream PI3K/Akt, WNT/β-catenin signal pathways

Zhang

Wang

Song

et al. 2015

Biomedicine & Pharmacotherapy

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Targeting Insulin-Like Growth Factor-I and Insulin-Like Growth Factor–Binding Protein-3 Signaling Pathways. A Novel Therapeutic Approach for Asthma

Abstract: Insulin-like growth factor (IGF

Cited by 60 publications

References 140 publications

Involvement of Igf1r in Bronchiolar Epithelial Regeneration: Role during Repair Kinetics after Selective Club Cell Ablation

Involvement of Igf1r in Bronchiolar Epithelial Regeneration: Role during Repair Kinetics after Selective Club Cell Ablation

Immunopathogenesis of Chronic Rhinosinusitis and Nasal Polyposis

Knockdown of type I insulin-like growth factor receptor inhibits human colorectal cancer cell growth and downstream PI3K/Akt, WNT/β-catenin signal pathways

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