Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation: I. Effects on lung remodeling and pathology

Baarsma, Hoeke A.; Bos, Sophie; Visser, Kim H.; Smit, Marieke; Schols, A.M.W.J.; Langen, Ramon; Kerstjens, Huib A. M.; Gosens, Reinoud

doi:10.1186/1465-9921-14-113

Cited by 20 publications

(13 citation statements)

References 42 publications

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“…GSK-3 inhibitors have been evaluated in animal models of asthma, showing inhibition of tissue eosinophilia and airway mucus expression by the GSK-3 inhibitor TDZD-8 [79]. In addition, SB216763 inhibits TGF-b induced myofibroblast differentiation [80], IL-1b induced proinflammatory cytokine production by airway smooth muscle [81] and lipopolysaccharide induced airway fibrosis in guinea pigs [82]. As GSK-3 inhibition would be expected to stabilize b-catenin, these inhibitory effects of GSK-3 inhibition are likely not explained as such but are more likely the result of phosphorylation of other GSK-3 substrates.…”

Section: Gsk-3 Inhibitorsmentioning

confidence: 98%

β-catenin as a regulator and therapeutic target for asthmatic airway remodeling

Kumawat

Koopmans

Gosens

2014

Expert Opinion on Therapeutic Targets

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The aberrant activation of β-catenin signaling by both WNT-dependent and -independent mechanisms in asthmatic airways plays a key role in remodeling the airways, including cell proliferation, differentiation, tissue repair and extracellular matrix production. These findings are interesting from both a mechanistic and therapeutic perspective, as several drug classes have now been described that target β-catenin signaling directly.

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Section: Gsk-3 Inhibitorsmentioning

confidence: 98%

β-catenin as a regulator and therapeutic target for asthmatic airway remodeling

Kumawat

Koopmans

Gosens

2014

Expert Opinion on Therapeutic Targets

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“…A single LPS exposure induces pulmonary inflammation in many animals, characterized by neutrophil and macrophage influx [200][201][202][203][204][205]. Chronic exposure to LPS induces structural changes to the murine and guinea pig lung, which persist after LPS exposure has ceased, mediated primarily by increases in TNF-α, IFN-γ, and IL-18 [203,[206][207][208][209][210]. The advantages of using LPS-induced inflammation and fibrosis models over other models such as CS include the relatively short time frame to achieve pathological features of COPD [211].…”

Section: Lipopolysaccharide Exposurementioning

confidence: 99%

Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance

Tanner

Single

2019

J Innate Immun

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Chronic obstructive pulmonary disease (COPD) affects the lives of an ever-growing number of people worldwide. The lack of understanding surrounding the pathophysiology of the disease and its progression has led to COPD becoming the third leading cause of death worldwide. COPD is incurable, with current treatments only addressing associated symptoms and sometimes slowing its progression, thus highlighting the need to develop novel treatments. However, this has been limited by the lack of experimental standardization within the respiratory disease research area. A lack of coherent animal models that accurately represent all aspects of COPD clinical presentation makes the translation of promising in vitro data to human clinical trials exceptionally challenging. Here, we review current knowledge within the COPD research field, with a focus on current COPD animal models. Moreover, we include a set of advantages and disadvantages for the selection of pre-clinical models for the identification of novel COPD treatments.

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“…In these studies, guinea pigs were given intranasal instillation of LPS twice weekly, for 12 consecutive weeks [69, 77, 82], (Table 1). …”

Section: Introductionmentioning

confidence: 99%

Experimental animal models for COPD: a methodological review

Ghorani¹,

Boskabady²,

Khazdair³

et al. 2017

Tob. Induced Dis.

170

111

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IntroductionChronic obstructive pulmonary disease (COPD) is a progressive disorder that makes the breathing difficult and is characterized by pathological conditions ranging from chronic inflammation to tissue proteolysis. With regard to ethical issues related to the studies on patients with COPD, the use of animal models of COPD is inevitable. Animal models improve our knowledge about the basic mechanisms underlying COPD physiology, pathophysiology and treatment. Although these models are only able to mimic some of the features of the disease, they are valuable for further investigation of mechanisms involved in human COPD.MethodsWe searched the literature available in Google Scholar, PubMed and ScienceDirect databases for English articles published until November 2015. For this purpose, we used 5 keywords for COPD, 3 for animal models, 4 for exposure methods, 3 for pathophysiological changes and 3 for biomarkers. One hundred and fifty-one studies were considered eligible for inclusion in this review.ResultsAccording to the reviewed articles, animal models of COPD are mainly induced in mice, guinea pigs and rats. In most of the studies, this model was induced by exposure to cigarette smoke (CS), intra-tracheal lipopolysaccharide (LPS) and intranasal elastase. There were variations in time course and dose of inducers used in different studies. The main measured parameters were lung pathological data and lung inflammation (both inflammatory cells and inflammatory mediators) in most of the studies and tracheal responsiveness (TR) in only few studies.ConclusionThe present review provides various methods used for induction of animal models of COPD, different animals used (mainly mice, guinea pigs and rats) and measured parameters. The information provided in this review is valuable for choosing appropriate animal, method of induction and selecting parameters to be measured in studies concerning COPD.

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Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation: I. Effects on lung remodeling and pathology

Cited by 20 publications

References 42 publications

β-catenin as a regulator and therapeutic target for asthmatic airway remodeling

β-catenin as a regulator and therapeutic target for asthmatic airway remodeling

Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance

Experimental animal models for COPD: a methodological review

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