VIP

Vasoactive intestinal peptide.

Vasoactive intestinal peptide secreting tumour: An overview.

Vasoactive intestinal peptide (VIP) secreting tumour (VIPoma) is a rare functional neuroendocrine tumour that typically arises from pancreatic islet cells. These present as sporadic, solitary pancreatic neoplasias with an estimated incidence of one in ten million individuals per year. Only around 5% of VIPomas are associated with multiple endocrine neoplasia type I syndrome. Excessive VIP secretion produces a clinical syndrome characterized by refractory watery diarrhoea, hypokalemia and metabolic acidosis. These coupled with elevated plasma levels of VIP are diagnostic. The majority of VIPomas are malignant and have already metastasized at the time of diagnosis (60%). Metastases occur most frequently in the liver, or regional lymph nodes, lungs, kidneys and bones. Some reports of skin metastases have been documented. Complete surgical resection continues to be the only potentially curative treatment. However, when the neoplasia cannot be excised completely, surgical debulking may provide palliative benefit. Other palliative options have included recently the peptide receptor radionuclide therapy which has shown to be effective and well-tolerated. This article will review all aspects of pancreatic VIPomas highlighting aspects such as clinical presentation, diagnosis and management.

Vasoactive Intestinal Peptide-Secreting Tumors: A Review.

Vasoactive intestinal peptide-secreting tumors (VIPomas) are a group of rare neuroendocrine tumors, which cause a typical syndrome of watery diarrhea. Most of these tumors are found in the pancreas and are usually detected at a later stage. Although curative resection is not possible in most of these tumors, both symptom and tumor control can be achieved by a multidimensional approach, to enable a long survival of most patients. There are no clear-cut guidelines for the management of VIPomas because of the rarity of this neoplasm and lack of prospective data. In this review, we discuss the available evidence on the clinical features and management of these rare tumors.

Vasoactive intestinal peptide exerts therapeutic action by regulating PTEN in a model of Sjögren's disease.

Sjögren's disease (SjD) is a chronic autoimmune disease characterized by the loss of the secretory function of the exocrine glands. At present, drugs that can both correct the immune imbalance and improve exocrine gland function are needed. Meanwhile, vasoactive intestinal peptide (VIP) has been reported as a candidate with anti-inflammatory and immunoregulatory properties for treating autoimmune diseases. Nonobese diabetic (NOD) mice and the primary splenic lymphocyte cells (SPLCs) were used to construct the SS model. The therapeutic effects of VIP for SjD by evaluating water consumption, histopathology, T cell subsets, and related cytokines. RT-qPCR and Western blot analysis were used to identify the expression of the PTEN/PI3K/AKT pathway. We found that VIP therapy in NOD mice could increase the expression of PTEN and VIP/VPAC1 receptor, as well as decrease the PI3K/AKT pathway. In vitro, the results showed that the PTEN knockdown decreased the Treg/Th17 ratio and enhanced the phosphorylated PI3K/AKT pathway, which were reversed with VIP treatment. VIP exerts potential therapeutic action in SjD by upregulating PTEN through the PI3K/AKT pathway and Treg/Th17 cell balance.

The role of vasoactive intestinal peptide in pulmonary diseases.

Vasoactive intestinal peptide (VIP) is an abundant neurotransmitter in the lungs and other organs. Its discovery dates back to 1970. And VIP gains attention again due to the potential application in COVID-19 after a research wave in the 1980s and 1990s. The diverse biological impacts of VIP extend beyond its usage in COVID-19 treatment, encompassing its involvement in various pulmonary and systemic disorders. This review centers on the function of VIP in various lung diseases, such as pulmonary arterial hypertension, chronic obstructive pulmonary disease, asthma, cystic fibrosis, acute lung injury/acute respiratory distress syndrome, pulmonary fibrosis, and lung tumors. This review also outlines two main limitations of VIP as a potential medication and gathers information on extended-release formulations and VIP analogues.

Role of vasoactive intestinal peptide in osteoarthritis.

Vasoactive intestinal peptide (VIP) plays important roles in many biological functions, such as, stimulation of contractility in the heart, vasodilation, promoting neuroendocrine-immune communication, lowering arterial blood pressure, and anti-inflammatory and immune-modulatory activity. Osteoarthritis (OA) is a chronic and degenerative bone disease, which is one of the most common causes of disability and most common in both sexes as people become older. Interestingly VIP can prevent chronic cartilage damage and joint remodeling. This review article provides update information on the association of VIP and OA and its treatment. Evidences suggest that VIP is down-regulated in synovial fluid of OA, and VIP down-regulation leads to increase in the production of pro-inflammatory cytokines that might contribute to the pathogenesis of OA; however contradictory reports also exist suggesting that accumulation of VIP in joints can also contribute OA. A number of studies indicated that up-regulation of VIP can counteract the action of pro-inflammatory stimuli and alleviate the pain in OA. More clinical investigations are necessary to determine the biology of VIP and its therapeutic potential in OA that might represent the future standards of care for OA.

A Role for Vasoactive Intestinal Peptide Interneurons in Neurodevelopmental Disorders.

GABAergic inhibitory interneurons of the cerebral cortex expressing vasoactive intestinal peptide (VIP-INs) are rapidly emerging as important regulators of network dynamics and normal circuit development. Several recent studies have also identified VIP-IN dysfunction in models of genetically determined neurodevelopmental disorders (NDDs). In this article, we review the known circuit functions of VIP-INs and how they may relate to accumulating evidence implicating VIP-INs in the mechanisms of prominent NDDs. We highlight recurring VIP-IN-mediated circuit motifs that are shared across cerebral cortical areas and how VIP-IN activity can shape sensory input, development, and behavior. Ultimately, we extract a set of themes that inform our understanding of how VIP-INs influence pathogenesis of NDDs. Using publicly available single-cell RNA sequencing data from the Allen Institute, we also identify several underexplored disease-associated genes that are highly expressed in VIP-INs. We survey these genes and their shared related disease phenotypes that may broadly implicate VIP-INs in autism spectrum disorder and intellectual disability rather than epileptic encephalopathy. Finally, we conclude with a discussion of the relevance of cell type-specific investigations and therapeutics in the age of genomic diagnosis and targeted therapeutics.

Vasoactive intestinal peptide in the heart.

Therapeutic potential of vasoactive intestinal peptide and its receptor VPAC2 in type 2 diabetes.

Owing to the increasing prevalence of type 2 diabetes, the development of novel hypoglycemic drugs has become a research hotspot, with the ultimate goal of developing therapeutic drugs that stimulate glucose-induced insulin secretion without inducing hypoglycemia. Vasoactive intestinal peptide (VIP), a 28-amino-acid peptide, can stimulate glucose-dependent insulin secretion, particularly by binding to VPAC2 receptors. VIP also promotes islet β-cell proliferation through the forkhead box M1 pathway, but the specific molecular mechanism remains to be studied. The clinical application of VIP is limited because of its short half-life and wide distribution in the human body. Based on the binding properties of VIP and VPAC2 receptors, VPAC2-selective agonists have been developed to serve as novel hypoglycemic drugs. This review summarizes the physiological significance of VIP in glucose homeostasis and the potential therapeutic value of VPAC2-selective agonists in type 2 diabetes.

Immunomodulatory vasoactive intestinal peptide amphiphile micelles.

Two different vasoactive intestinal peptide (VIP) amphiphiles have been formulated which readily form micelles of varying shapes. Interestingly, VIP micelle structure has been found to directly correlate to anti-inflammatory behavior providing evidence that these biomaterials can serve as a promising new therapeutic modality.

Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system.

Vasoactive intestinal peptide (VIP), a gut peptide hormone originally reported as a vasodilator in 1970, has multiple physiological and pathological effects on development, growth, and the control of neuronal, epithelial, and endocrine cell functions that in turn regulate ion secretion, nutrient absorption, gut motility, glycemic control, carcinogenesis, immune responses, and circadian rhythms. Genetic ablation of this peptide and its receptors in mice also provides new insights into the contribution of VIP towards physiological signaling and the pathogenesis of related diseases. Here, we discuss the impact of VIP on gastrointestinal function and diseases based on recent findings, also providing insight into its possible therapeutic application to diabetes, autoimmune diseases and cancer.

Nanoparticle-Driven Tendon Repair: Role of Vasoactive Intestinal Peptide in Immune Modulation and Stem Cell Enhancement.

Tendon repair remains challenging owing to the limited capacity for endogenous repair. Vasoactive intestinal peptide (VIP) promotes bone tissue regeneration; however, its role in tendon repair remains unclear. In the present study, we demonstrated that VIP stimulated M2 polarization of macrophages and facilitated tendon regeneration by regulating immune homeostasis and maintaining the function of tendon stem/progenitor cells (TSPCs). Additionally, we established GelMa-loaded VIP@PLGA@ZIF-8 (VPZ) nanoparticles (VPZG) to enable the sustained and localized release of VIP at the site of patellar tendon injury in SD rats. The results of the in vitro experiments demonstrated that VPZG regulated the homeostasis of macrophage polarization by downregulating the NF-κB axis. VPZG also promoted efferocytosis and suppressed the release of proinflammatory factors. Additionally, VPZG enhanced the tenogenic differentiation of TSPCs when cocultured with macrophages. In vivo, we implanted VPZG at the site of patellar tendon injury, where it released VIP sustainably and slowly to promote tendon regeneration. This effect was achieved through the downregulation of the expression levels of various inflammatory factors, as well as the regulation of local immune homeostasis. In conclusion, our results demonstrated that VPZG facilitated tendon injury repair by regulating immune homeostasis and enhancing TSPC function. These findings suggest that VPZG is a promising avenue for the clinical improvement of tendon injury treatment.

Editorial: vasoactive intestinal peptide (vip): historic perspective and future potential.

Numerous studies, since the late 1970s, have highlighted the role of vasoactive intestinal peptide (VIP) in the immune system of mammals. Importantly, these studies have show that VIP has an inhibitory effect on the production and action of many different inflammatory mediators and many studies have now shown the therapeutic potential of VIP in animal models of human disease. This review will briefly discuss the effects of VIP on immune cell function and discuss the therapeutic potential for VIP in inflammatory diseases of humans. The review will also introduce some areas of research which are discussed by contributing authors within this special edition of EMIDDT.

Vasoactive intestinal peptide (VIP).

Vasoactive intestinal peptide, a promising agent for myopia?

To investigate the role of vasoactive intestinal peptide (VIP) in form-deprivation myopia (FDM). FDM was created in three groups of eight chicks by placing a translucent diffuser on their right eyes. Intravitreal injections of saline and VIP were applied once a day into the occluded eyes of groups 2 and 3, respectively. Retinoscopy and axial length (AL) measurements were performed on the first and 8th days of diffuser wear. The retina mRNA levels of the VIP receptors and the ZENK protein in right eyes of the three groups and left eyes of the first group on day 8 were determined using real time polymerase chain reaction (PCR). The median final refraction (D) in right eyes were -13.75 (-16.00, -12.00), -11.50 (-12.50, -7.50), and -1.50 (-4.75, -0.75) in groups 1, 2, and 3, respectively (P<0.001). The median AL (mm) in right eyes were 10.65 (10.00, 11.10), 9.90 (9.70, 10.00), and 9.20 (9.15, 9.25) in groups 1, 2, and 3, respectively (P<0.001). The median delta-delta cycle threshold (CT) values for the VIP2 receptors were 1.07 (0.82, 1.43), 1.22 (0.98, 1.65), 0.29 (0.22, 0.45) in right eyes of groups 1, 2, and 3, and 1.18 (0.90, 1.37) in left eyes of group 1, respectively (P=0.001). The median delta-delta CT values for the ZENK protein were 1.07 (0.63, 5.03), 3.55 (2.20, 5.55), undetectable in right eyes of groups 1, 2, and 3 and 1.89 (0.21, 4.73) in left eyes of group 1, respectively (P=0.001). VIP has potential inhibitory effects in the development of FDM.

Vasoactive intestinal peptide in the lung.

Stapled Vasoactive Intestinal Peptide (VIP) Derivatives Improve VPAC2 Agonism and Glucose-Dependent Insulin Secretion.

Agonists of vasoactive intestinal peptide receptor 2 (VPAC2) stimulate glucose-dependent insulin secretion, making them attractive candidates for the treatment of hyperglycaemia and type-II diabetes. Vasoactive intestinal peptide (VIP) is an endogenous peptide hormone that potently agonizes VPAC2. However, VIP has a short serum half-life and poor pharmacokinetics in vivo and is susceptible to proteolytic degradation, making its development as a therapeutic agent challenging. Here, we investigated two peptide cyclization strategies, lactamisation and olefin-metathesis stapling, and their effects on VPAC2 agonism, peptide secondary structure, protease stability, and cell membrane permeability. VIP analogues showing significantly enhanced VPAC2 agonist potency, glucose-dependent insulin secretion activity, and increased helical content were discovered; however, neither cyclization strategy appeared to effect proteolytic stability or cell permeability of the resulting peptides.

Vasoactive intestinal peptide. Messenger in a neuroimmune axis.

Myopia pathogenesis and vasoactive intestinal peptide: Molecular mechanisms, experimental models, and clinical implications.

Myopia is the most common refractive error worldwide and is projected to affect half of the global population by 2050, with high myopia significantly increasing the risk of vision-threatening complications. While multiple genetic, environmental and lifestyle factors contribute to myopia onset and progression, recent findings suggest a role for vasoactive intestinal peptide (VIP) and its receptor VIPR2 in ocular growth regulation. This review summarizes current knowledge about myopia pathogenesis and the diverse factors involved, focusing on the molecular, genetic, pharmacological, and clinical findings regarding VIP/VIPR2 signaling in the eye. Evidence from animal models reveals a complex interaction between VIP and myopia, with VIP agonists/antagonists either protecting from or promoting myopia depending on model and dosage, VIPR2 knockout mice developing spontaneous myopia, and VIP interacting with circadian rhythms and atropine signaling. Genetic association studies have identified both risk and protective VIPR2 haplotypes, with environmental light exposure modulating their effects. Mechanistic studies suggest that VIP regulates choroidal and scleral remodeling, acting in concert with dopaminergic, cholinergic, and retinoic acid pathways. We propose that VIP/VIPR2 is a key modulator of emmetropization and a promising therapeutic target for myopia, though species-specific effects and context-dependency remain to be resolved.

Immunobiology of vasoactive intestinal peptide (VIP).

Vasoactive intestinal peptide: a neuropeptide with pleiotropic immune functions.

Vasoactive intestinal peptide (VIP), a 28-amino acid neuropeptide/neurotransmitter, is widely distributed in both the central and peripheral nervous system. VIP is released by both neurons and immune cells. Various cell types, including immune cells, express VIP receptors. VIP has pleiotropic effects as a neurotransmitter, immune regulator, vasodilator and secretagogue. This review is focused on VIP production and effects on immune cells, VIP receptor signaling as related to immune functions, and the involvement of VIP in inflammatory and autoimmune disorders. The review addresses present clinical use of VIP and future therapeutic directions.

Vasoactive intestinal peptide and anterior pituitary function.

Vasoactive intestinal peptide (VIP) is a highly basic 28 amino-acid peptide which was first isolated from porcine small intestine (Said & Mutt, 1970). It is related to several other peptides including PHI (peptide with N-terminal histidine and C-terminal isoleucine amide), secretin, glucagon, and has some sequences similar to those of growth hormone releasing hormone (Fig. 1). The amino-acid sequence of human VIP is identical with that of the porcine form (Itoh et al., 1983). It has been shown that human VIP is cosynthesized with PHM (peptide with N-terminal histidine and C-terminal methionine amide, the human analogue of PHI) from the same large precursor protein (Itoh et al., 1983).

Vasoactive Intestinal Peptide Changes the Frequency and Force of Myocardial Contraction in Rats.

We studied the effect of non-selective agonist of VIP receptors of vasoactive intestinal polypeptide in different concentrations on the frequency, force, and duration of isometric contraction of myocardial strips of the right atrium under conditions of spontaneous activity, as well as the force and duration of contractions of the right ventricle in rats. It was found that the agonist produced a positive inotropic and chronotropic effect that depended on its concentration. The maximum effect was observed at vasoactive intestinal peptide concentration of 10-11 M.

The neuropeptide vasoactive intestinal peptide: direct effects on immune cells and involvement in inflammatory and autoimmune diseases.

Neuropeptides represent an important category of endogenous contributors to the establishment and maintenance of immune deviation in the immune-privileged organs such as the CNS and in the control of acute inflammation in the peripheral immune organs. Vasoactive intestinal peptide (VIP) is a major immunoregulatory neuropeptide widely distributed in the central and peripheral nervous system. In addition to neurones, VIP is synthesized by immune cells which also express VIP receptors. Here, we review the current information on VIP production and VIP-receptor-mediated effects in the immune system, the role of endogenous and exogenous VIP in inflammatory and autoimmune disorders and the present and future VIP therapeutic approaches.

Vasoactive intestinal peptide producing pheochromocytoma and intracardiac thrombosis.

A case of pheochromocytoma producing vasoactive intestinal peptide (VIP) and left ventricular thrombus in the absence of cardiomyopathy or wall motion abnormalities on echocardiogram is presented along with a review of the relevant literature. A 30-year-old female of Afghani descent with past medical history of panic attacks presented with fever, cough, sore throat, vomiting, and was found to have an 11&#x2009;cm adrenal mass consistent with primary adrenocortical adenoma versus carcinoma. Her tumor elicited catechols and vasoactive intestinal peptide. Her hospitalization was complicated by left ventricular thrombosis leading to an embolic injury to her right kidney, respiratory failure, need for transient dialysis and urinary tract infections. She developed a profuse secretory diarrhea and decision was made to treat with empiric octreotide infusion and imodium with improvement in symptoms. She underwent coil and particle embolization followed by resection. Followup PET gallium scan showed no evidence of residual disease or metastasis. VIP producing pheochromocytoma associated with intracardiac thrombosis is rare. Outcomes depend on prompt diagnosis of the pheochromocytoma and multidisciplinary approach to management.

Vasoactive Intestinal Peptide-Secreting Pancreatic Neuroendocrine Tumor: A Case Report.

A 36-year-old female with chronic watery diarrhea and persistent hypokalemia for more than eight months duration&#xa0;eventually being diagnosed as vasoactive intestinal peptide&#xa0;tumor (VIPoma) clinically and histologically is presented here. The patient achieved complete recovery after starting octreotide, a somatostatin analog. She underwent a distal pancreatectomy along with the removal of the tumor at Teaching Hospital Jaffna for the permanent cure.

Vasoactive intestinal peptide decreases inflammation and tight junction disruption in experimental necrotizing enterocolitis.

Excessive inflammatory cell infiltration and accumulation in the intestinal mucosa are pathological features of necrotizing enterocolitis (NEC) leading to intestinal barrier disruption. Vasoactive intestinal peptide (VIP) is a potent anti-inflammatory agent that regulates intestinal epithelial barrier homeostasis. We previously demonstrated that VIP-ergic neuron expression is decreased in experimental NEC ileum, and this may be associated with inflammation and barrier compromise. We hypothesize that exogenous VIP administration has a beneficial effect in NEC. NEC was induced in C57BL/6 mice by gavage feeding, hypoxia, and lipopolysaccharide administration between postnatal day (P) 5 and 9. There were four studied groups: Control (n&#x202f;=&#x202f;6): Breast feeding without stress factors; Control&#x202f;+&#x202f;VIP (n&#x202f;=&#x202f;5): Breast feeding + intraperitoneal VIP injection once a day from P5 to P9; NEC (n&#x202f;=&#x202f;9): mice exposed to NEC induction; NEC&#x202f;+&#x202f;VIP (n&#x202f;=&#x202f;9): NEC induction + intraperitoneal VIP injection. Terminal ileum was harvested on P9. NEC severity, intestinal inflammation, (IL-6 and TNF&#x3b1;), and Tight junctions (Claudin-3) were evaluated. NEC severity and intestinal inflammation were significantly decreased in NEC&#x202f;+&#x202f;VIP compared to NEC. Tight junction expression was significantly increased in NEC&#x202f;+&#x202f;VIP compared to NEC. VIP administration has a beneficial therapeutic effect in NEC by reducing inflammation and tight junction disruption.

Vasoactive intestinal peptide and other peptides as neuromodulators of colonic motility in the guinea pig.

Vasoactive intestinal peptide as a coronary vasodilator.

Pheochromocytoma producing vasoactive intestinal peptide.

The syndrome of watery diarrhea associated with hypokalemia and achlorhydria was originally described in 1958. Subsequently, this syndrome was shown to be caused by a neuroendocrine tumor secreting vasoactive intestinal peptide (VIP), and such tumors are almost always pancreatic in origin. We describe the case of a 78-year-old woman with gradual onset of hypokalemia, watery diarrhea, and weight loss. After a left adrenal mass was discovered, the patient chose medical therapy over surgical intervention. Initially her condition responded, then gradually became refractory to medical therapy. She had elevated levels of VIP, pancreatic polypeptide, dopamine, and vanillylmandelic acid. Subsequently, the patient underwent surgical excision of the mass that was found to be a VIP-producing pheochromocytoma. After surgery her diarrhea subsided, and her electrolytes and affected neuroendocrine hormone levels normalized.

Vasoactive intestinal peptide is upregulated in women with endometriosis and chronic pelvic pain.

Chronic pelvic pain (CPP) causes compromised the quality of life in women with endometriosis and is often attributed to local inflammation and ingrowth of nerve fibers. In this pilot study, we aimed to investigate whether the inflammation-related vasoactive intestinal peptide (VIP) and interleukin (IL)-6 were increased in affected patients. Endometrial and endometriotic tissue biopsy specimens, and serum and peritoneal fluid (PF) samples, were obtained from 85 endometriosis patients and 53 controls. VIP and IL-6 analysis and measurement of microvessel density in tissue were performed using immunohistochemistry, Western blotting, RT-qPCR, and ELISA. Compared with controls, VIP transcript and protein levels were increased in endometrium from endometriosis patients and further elevated in patients with CPP. In addition, microvessel density, a measurement of angiogenic activity, was increased in the endometrium and in endometriosis lesions in the same subset of patients. Serum and PF levels of VIP and IL-6 were higher in women with endometriosis and CPP compared with endometriosis patients who reported no chronic pain. Vasoactive intestinal peptide is upregulated in endometriosis patients reporting chronic pain. Increased microvessel density in tissue and peritoneal fluid concentrations of IL-6 indicate an elevated inflammation in the pelvic microenvironment of these patients.

Vasoactive intestinal peptide increases apoptosis of hepatocellular carcinoma by inhibiting the cAMP/Bcl-xL pathway.

Vasoactive intestinal peptide (VIP) is a modulator of inflammatory responses. VIP receptors are expressed in several tumor types, such as colorectal carcinoma. The study described herein was conducted to confirm the presence of VIP and its receptors (VPAC1 and VPAC2) in surgically resected hepatocellular carcinoma (HCC) tissues and in the HCC cell line Huh7. The mechanism responsible for apoptosis of HCC cells was then examined because VIP treatment (10-10 &#xa0;M) significantly suppressed proliferation of Huh7 cells. In examining apoptosis-related proteins, we found caspase-3 to be significantly increased and Bcl-xL and cyclic AMP (cAMP) response element-binding protein (CREB) to be significantly decreased in Huh7 cells cultured with VIP. Furthermore, the CREB level and phosphorylation were reduced. These effects were reversed by the addition of VIP receptor antagonist or cAMP antagonist Rp-cAMPS. Pretreatment with cAMP analogue blocked the increased apoptosis, suggesting that VIP induces apoptosis via a PKA-independent signaling mechanism. Our data indicate that VIP prevents the progression of HCC by apoptosis through the cAMP/Bcl-xL pathway.

The Role of Vasoactive Intestinal Peptide in Glucagon-like Peptide-2-Mediated Intestinal Lipid Handling.

The gut hormone glucagon-like peptide-2 (GLP-2) plays important roles in regulating lipid handling and promoting anti-inflammatory functions in the intestine. During the postprandial state, it increases lipid absorption. During post-absorptive state, it mobilizes pre-formed chylomicrons. GLP-2 acts through vasoactive intestinal peptide (VIP) in reducing inflammation in rat ileum. However, this pathway has not yet been tested for GLP-2's effects on intestinal lipid handling. Here, in mesenteric lymph duct cannulated rats, we examined whether VIP signaling mediates GLP-2's effects on postprandial lipid absorption and post-absorptive lipid mobilization in the intestine. We administered a VIP receptor antagonist and analyzed lipid output in response to intraperitoneal GLP-2 or PBS during postprandial and post-absorptive states. VIP receptor antagonism reduced GLP-2 mediated lipid output in the post-absorptive state but had no effect during the postprandial state. These results show that GLP-2 functions differently during postprandial and post-absorptive states and VIP aids in GLP-2-mediated lipid output during the post-absorptive state.

Vasoactive Intestinal Peptide in Checkpoint Inhibitor-Induced Pneumonitis.

Carcinoid heart findings in vasoactive intestinal peptide-secreting tumour.

Tricuspid valve disease in carcinoid heart syndrome is usually diagnosed via screening echocardiography in patients with known carcinoid syndrome. Vasoactive intestinal peptide tumour (VIPoma) is a rare tumour with an incidence of 0.05%-2%&#x2009;that typically presents with symptoms related to the release of vasoactive intestinal peptide: flushing, diarrhoea and electrolyte abnormalities like hypokalaemia and hypochlorhydria. Historically, the cardiac valves are unaffected. We present a case where a finding of tricuspid regurgitation and stenosis on echocardiography prompted an expedited workup for malignancy ultimately leading to a diagnosis of VIPoma.

Re: antitumoral effects of vasoactive intestinal peptide in human renal cell carcinoma xenografts in athymic nude mice.

Vasoactive intestinal peptide. Link between electrical activity and glia-mediated neurotrophism.

Vasoactive intestinal peptide has neurotrophic and neuroprotective properties that influence the survival of activity-dependent neurons in the central nervous system. Investigations of the mechanism of this neurotrophic peptide indicated that these actions are contingent on interactions with astroglia. The complex mixture of neurotrophic mediators released from astroglia include cytokines, a protease inhibitor, and activity-dependent neurotrophic factor, a protein with apparent structural similarities to hsp60. Investigations of ADNF resulted in the discovery of active peptides of extraordinary potency and broad neuroprotective properties. These studies indicate that a nine-amino acid core peptide of ADNF had significantly greater neuroprotective properties in comparison to the parent growth factor and these advantages identify ADNF-9 as an attractive lead compound for drug development.

Suprachiasmatic Nucleus Vasoactive Intestinal Peptide Neurons Mediate Light-induced Transient Forgetting.

Our research reveals the critical role of the suprachiasmatic nucleus (SCN) vasoactive intestinal peptide (VIP) neurons in mediating light-induced transient forgetting. Acute exposure to bright light selectively impairs trace fear memory by activating VIP neurons in the SCN, as demonstrated by increased c-Fos expression and Ca2+ recording. This effect can be replicated and reversed through optogenetic and chemogenetic manipulations of SCN VIP neurons. Furthermore, we identify the SCN&#x2009;&#x2192;&#x2009;PVT (paraventricular nucleus of the thalamus) VIP neuronal circuitry as essential in this process. These findings establish a novel role for SCN VIP neurons in modulating memory accessibility in response to environmental light cues, extending their known function beyond circadian regulation and revealing a mechanism for transient forgetting.

Synthesis of vasoactive intestinal peptide and related peptides.

Vasoactive intestinal peptide-oma causing refractory diarrhea in a young woman.

Vasoactive intestinal peptide (VIP)-secreting neuroendocrine tumors are an exceptionally rare cause of chronic diarrhea. We describe a 36-year-old woman presenting with a 2-year history of severe diarrhea and electrolyte derangements ultimately diagnosed with VIPoma.