Vasoactive Intestinal Peptide Knockout (VIP KO) mouse model of sulfite-sensitive asthma: up-regulation of novel lung carbonyl reductase

Szema, Anthony M.; Hamidi, Sayyed A.; Koller, Antonius; Martin, Dwight W.

doi:10.1186/1471-2172-12-66

Cited by 16 publications

(10 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PAC1 expression level was unaffected by VIP loss. Deletion of the VIP gene in C57Bl/6 mice has been associated with modification of gene expression (18,39,41). However, this is the first report of VPAC receptor overexpression in VIP-KO mice.…”

Section: Correction Of Lung and Intestinal Pathology In C57bl/6mentioning

confidence: 65%

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

Alcolado

Conrad

Poroca

et al. 2014

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

Vasoactive intestinal peptide (VIP), a neuropeptide, controls multiple functions in exocrine tissues, including inflammation, and relaxation of airway and vascular smooth muscles, and regulates CFTR-dependent secretion, which contributes to mucus hydration and local innate defense of the lung. We had previously reported that VIP stimulates the VPAC1 receptor, PKCϵ signaling cascade, and increases CFTR stability and function at the apical membrane of airway epithelial cells by reducing its internalization rate. Moreover, prolonged VIP stimulation corrects the molecular defects associated with F508del, the most common CFTR mutation responsible for the genetic disease cystic fibrosis. In the present study, we have examined the impact of the absence of VIP on CFTR maturation, cellular localization, and function in vivo using VIP knockout mice. We have conducted pathological assessments and detected signs of lung and intestinal disease. Immunodetection methods have shown that the absence of VIP results in CFTR intracellular retention despite normal expression and maturation levels. A subsequent loss of CFTR-dependent chloride current was measured in functional assays with Ussing chamber analysis of the small intestine ex vivo, creating a cystic fibrosis-like condition. Interestingly, intraperitoneal administration of VIP corrected tissue abnormalities, close to the wild-type phenotype, as well as associated defects in the vital CFTR protein. The results show in vivo a primary role for VIP chronic exposure in CFTR membrane stability and function and confirm in vitro data.

show abstract

Section: Correction Of Lung and Intestinal Pathology In C57bl/6mentioning

confidence: 65%

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

Alcolado

Conrad

Poroca

et al. 2014

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

show abstract

“…141 Furthermore, VIP suppresses tumor necrosis factor-alpha and interleukin-10 and promotes T-regulatory cells, which may indicate an anti-inflammatory role for VIP. 142 However, the exact role of VIP in PH has not been elucidated, and it should also be kept in mind that this model differs from human PH with regard to hemodynamic severity and histology. 140 The VIP knockout model has greatly added to our general understanding of PH but also supports the concept of exogenous VIP therapy as therapeutic strategy in PH.…”

Section: Vasoactive Intestinal Peptide Knockout Modelmentioning

confidence: 99%

A Comprehensive Review: The Evolution of Animal Models in Pulmonary Hypertension Research; Are We there Yet?

et al. 2013

View full text Add to dashboard Cite

Pulmonary hypertension (PH) is a disorder that develops as a result of remodeling of the pulmonary vasculature and is characterized by narrowing/obliteration of small pulmonary arteries, leading to increased mean pulmonary artery pressure and pulmonary vascular resistance. Subsequently, PH increases the right ventricular afterload, which leads to right ventricular hypertrophy and eventually right ventricular failure. The pathophysiology of PH is not fully elucidated, and current treatments have only a modest impact on patient survival and quality of life. Thus, there is an urgent need for improved treatments or a cure. The use of animal models has contributed extensively to the current understanding of PH pathophysiology and the investigation of experimental treatments. However, PH in current animal models may not fully represent current clinical observations. For example, PH in animal models appears to be curable with many therapeutic interventions, and the severity of PH in animal models is also believed to correlate poorly with that observed in humans. In this review, we discuss a variety of animal models in PH research, some of their contributions to the field, their shortcomings, and how these have been addressed. We highlight the fact that the constant development and evolution of animal models will help us to more closely model the severity and heterogeneity of PH observed in humans.

show abstract

“…Further, the significance of VIP was analyzed in VIP gene deficient (−/−) mouse model of sulfite-sensitive asthma in which VIP modulate the oxidant/antioxidant balance in asthma. The wild-type mice with VIP gene have functional lung carbonyl reductase without any symptoms of asthma, whereas VIP−/− mice have abnormal carbonyl reductase and have spontaneous asthma suggesting that deficiency of VIP gene may cause a predisposition to asthma development [104]. The decreased VIP concentration in the bronchoalveolar lavage fluid in rat model is negatively correlated with c-fos protein expression and more prone to asthma attacks [105].…”

Section: Significance Of Vip In the Allergic Diseasesmentioning

confidence: 99%

Neuroendocrine cells derived chemokine vasoactive intestinal polypeptide (VIP) in allergic diseases

Verma

Manohar

Venkateshaiah

et al. 2017

Cytokine & Growth Factor Reviews

View full text Add to dashboard Cite

Worldwide increase incidences of allergic diseases have heightened the interest of clinicians and researchers to understand the role of neuroendocrine cells in the recruitment and activation of inflammatory cells. Several pieces of evidence revealed the association of neuropeptides in the pathogenesis of allergic diseases. Importantly, one such peptide that is secreted by neuronal cells and immune cells exerts a wide spectrum of immunological functions as cytokine/chemokine is termed as Vasoactive Intestinal Peptide (VIP). VIP mediates immunological function through interaction with specific receptors namely VPAC-1, VPAC-2, CRTH2 and PAC1 that are expressed on several immune cells such as eosinophils, mast cells, neutrophils, and lymphocytes; therefore, provide the basis for the action of VIP on the immune system. Additionally, VIP mediated action varies according to target organ depending upon the presence of specific VIP associated receptor, involved immune cells and the microenvironment of the organ. Herein, we present an integrative review of the current understanding on the role of VIP and associated receptors in allergic diseases, the presence of VIP receptors on various immune cells with particular emphasis on the role of VIP in the pathogenesis of allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis. Being crucial signal molecule of the neuroendocrine-immune network, the development of stable VIP analogue and/or antagonist may provide the future therapeutic drug alternative for the better treatment of these allergic diseases. Taken together, our current review summarizes the current understandings of VIP biology and further explore the significance of neuroendocrine cells derived VIP in the recruitment of inflammatory cells in allergic diseases that may be helpful to the investigators for planning the experiments and accordingly predicting new therapeutic strategies for combating allergic diseases. Summarized graphical abstract will help the readers to understand the significance of VIP in allergic diseases.

show abstract

Vasoactive Intestinal Peptide Knockout (VIP KO) mouse model of sulfite-sensitive asthma: up-regulation of novel lung carbonyl reductase

Cited by 16 publications

References 17 publications

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

A Comprehensive Review: The Evolution of Animal Models in Pulmonary Hypertension Research; Are We there Yet?

Neuroendocrine cells derived chemokine vasoactive intestinal polypeptide (VIP) in allergic diseases

Contact Info

Product

Resources

About