Mechanisms involved in VPAC receptors activation and regulation: lessons from pharmacological and mutagenesis studies

Langer, Ingrid

doi:10.3389/fendo.2012.00129

Cited by 32 publications

(38 citation statements)

References 74 publications

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“…For the VAPC1 receptor, however, the link between the phosphorylation level and its internalization is not direct and has not yet been completely clarified (13). Also, VPAC receptors form hetero-oligomers and interact with accessory proteins capable of modifying their activity, membrane expression, and recycling mechanism (24). Possible changes in VPAC interaction with accessory proteins in diseased epithelia could explain the overexpression observed in VIP-KO tissues.…”

Section: Discussionmentioning

confidence: 99%

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

Alcolado

Conrad

Poroca

et al. 2014

American Journal of Physiology-Cell Physiology

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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.

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Section: Discussionmentioning

confidence: 99%

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

Alcolado

Conrad

Poroca

et al. 2014

American Journal of Physiology-Cell Physiology

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“…The VPAC receptors (VPAC-1 & VPAC-2) are widely distributed in the body suggesting the crucial role in the diverse immunological processes [27]. These VPAC receptors belong to the subfamily of G protein-coupled receptor family (GPCR) known as class B GPCR.…”

Section: General Characteristics Of Vasoactive Intestinal Peptide mentioning

confidence: 99%

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

Verma

Manohar

Venkateshaiah

et al. 2017

Cytokine & Growth Factor Reviews

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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.

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“…VIP and pituitary adenylate cyclase polypeptide (PACAP) belong to a superfamily, together with other structurally related hormones (such as glucagon, glucagon-like peptide, and secretin) and share some receptors, termed PACAP type I and II receptors [87,127]. PACAP type I receptors show mainly affinity for PACAP, whereas PACAP type II receptors are sensitive to both PACAP and VIP.…”

Section: Vasoactive Intestinal Polypeptidementioning

confidence: 99%

“…They are known as VIP receptors, and are subdivided in VPAC1 and VPAC2. Both receptors are expressed in MC [87,127,224]. VPAC1 is mainly distributed in CNS (cortex and hippocampus), liver, lung, intestine and T lymphocytes.…”

Section: Vasoactive Intestinal Polypeptidementioning

confidence: 99%

Peripheral and Central Mechanisms in Irritable Bowel Syndrome : in search of links

Bednarska

2019

Linköping University Medical Dissertations

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Irritable bowel syndrome (IBS) is a chronic visceral pain disorder with female predominance, characterized by recurrent abdominal pain and disturbed bowel habits in the absence of an identifiable organic cause. This prevalent and debilitating disease, which accounts for a substantial economic and individual burden, lacks exact diagnostic tools and effective treatment, since its pathophysiology remains uncertain. The bidirectional and multilayered brain-gut axis is a well-established disease model, however, the interactions between central and peripheral mechanisms along the brain-gut axis remain incompletely understood. One of the welldescribed triggering factors, yet accounting for only a fraction of IBS prevalence, is bacterial gastroenteritis that affects mucosal barrier function. Altered gut microbiota composition as well as disturbed intestinal mucosal barrier function and its neuroimmune regulation have been reported in IBS, however, the impact of live bacteria, neither commensal nor pathogenic, on intestinal barrier has not been studied yet. Furthermore, abnormal central processing of visceral sensations and psychological factors such as maladaptive coping have previously been suggested as centrally-mediated pathophysiological mechanisms of importance in IBS. Brain imaging studies have demonstrated an imbalance in descending pain modulatory networks and alterations in brain regions associated with interoceptive awareness and pain processing and modulation, particularly in anterior insula (aINS), although biochemical changes putatively underlying these central alterations remain poorly understood. Most importantly, however, possible associations between these documented changes on central and peripheral levels, which may as complex interactions contribute to disease onset and chronification of symptoms, are widely unknown. VMpo ventromedial thalamic nucleus posterior portion VPAC vasoactive intestinal polypeptide receptor VSI Visceral Sensitivity Index Recurrent abdominal pain or discomfort** at least 3 days per month in the last 3 months associated with 2 or more of the following: 1. Improvement with defecation 2. Onset associated with a change in frequency of stool 3. Onset associated with a change in form (appearance) of stool *Criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis. **Discomfort means an uncomfortable sensation not described as pain. In pathophysiology research and clinical trials, a pain/discomfort frequency of at least 2 days a week during screening evaluation for subject eligibility.

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Mechanisms involved in VPAC receptors activation and regulation: lessons from pharmacological and mutagenesis studies

Cited by 32 publications

References 74 publications

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice

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

Peripheral and Central Mechanisms in Irritable Bowel Syndrome : in search of links

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