Special Issue "Vasoactive Intestinal Peptide (VIP) and Related Signaling Molecules in Health and Disease"

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 1753

Special Issue Editor

Prof. Dr. Glenn P. Dorsam
E-Mail Website
Guest Editor
Department of Microbiological Sciences, North Dakota State University, Fargo, ND 58102-5060, USA
Interests: vasoactive intestinal peptide (VIP); G protein-coupled receptors (GPCR); microbiota; metabolism; gluconeogenesis; intestinal homeostasis; fatty acid metabolism; glucose metabolism; obesity; type 2 diabetes (T2D); immune function

Special Issue Information

Dear Colleagues,

Vasoactive intestinal peptide (VIP) is a 28-amino acid neuropeptide with a broad expression profile, regulating diurnal feeding behavior, metabolism, and immunity. VIP is delivered by the peripheral nervous system to numerous organs, including the mucosa-associated lymphoid tissues of the pulmonary and gastrointestinal tract. VIP signals with a high affinity (Kd = 1 nM) through at least two endogenous G protein-coupled receptors (GPCR), called vasoactive intestinal peptide/pituitary adenylyl cyclase activating polypeptide (VPAC) 1 and VPAC2. A third low affinity receptor (Kd = 1 μM), termed PAC1, also binds VIP. VIP is part of a larger family of biologically active peptides that includes pituitary adenylate cyclase activating polypeptide (PACAP), which shares a 68% amino acid identity with VIP and binds all three receptors (PAC1, VPAC1, and VPAC2) with a high affinity (≈1 nM Kd).

I invite my colleagues in this field to contribute to this Special Issue on VIP/PACAP and its related peptides in health and disease by providing research articles or relevant topic reviews. This Special Issue will act as an important depository for novel and review research summaries in the VIP/PACAP family of signaling peptides in health and disease.

Prof. Dr. Glenn P. Dorsam
Guest Editor

Manuscript Submission Information

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Keywords

  • vasoactive intestinal peptide (VIP)
  • G protein-coupled receptors (GPCR)
  • pituitary adenylate cyclase activating polypeptide (PACAP)
  • secretin (SCT)
  • peptide histidine methionine (PHM)
  • PACAP-related peptide (PRP)
  • glucagon (GCG)
  • metabolism
  • immunity

Published Papers (2 papers)

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Research

Article
Endogenous VIP VPAC1 Receptor Activation Modulates Hippocampal Theta Burst Induced LTP: Transduction Pathways and GABAergic Mechanisms
Biology 2022, 11(5), 627; https://doi.org/10.3390/biology11050627 - 20 Apr 2022
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Abstract
Vasoactive intestinal peptide (VIP), acting on both VPAC1 and VPAC2 receptors, is a key modulator of hippocampal synaptic transmission, pyramidal cell excitability and long-term depression (LTD), exerting its effects partly through modulation GABAergic disinhibitory circuits. Yet, the role of endogenous VIP [...] Read more.
Vasoactive intestinal peptide (VIP), acting on both VPAC1 and VPAC2 receptors, is a key modulator of hippocampal synaptic transmission, pyramidal cell excitability and long-term depression (LTD), exerting its effects partly through modulation GABAergic disinhibitory circuits. Yet, the role of endogenous VIP and its receptors in modulation of hippocampal LTP and the involvement of disinhibition in this modulation have scarcely been investigated. We studied the modulation of CA1 LTP induced by TBS via endogenous VIP release in hippocampal slices from young-adult Wistar rats using selective VPAC1 and VPAC2 receptor antagonists, evaluating its consequence for the phosphorylation of CamKII, GluA1 AMPA receptor subunits and Kv4.2 potassium channels in total hippocampal membranes obtained from TBS stimulated slices. Endogenous VIP, acting on VPAC1 (but not VPAC2) receptors, inhibited CA1 hippocampal LTP induced by TBS in young adult Wistar rats and this effect was dependent on GABAergic transmission and relied on the integrity of NMDA and CaMKII-dependent LTP expression mechanisms but not on PKA and PKC activity. Furthermore, it regulated the autophosphorylation of CaMKII and the expression and Ser438 phosphorylation of Kv4.2 potassium channels responsible for the A-current while inhibiting phosphorylation of Kv4.2 on Thr607. Altogether, this suggests that endogenous VIP controls the expression of hippocampal CA1 LTP by regulating disinhibition through activation of VPAC1 receptors in interneurons. This may impact the autophosphorylation of CaMKII during LTP, as well as the expression and phosphorylation of Kv4.2 K+ channels at hippocampal pyramidal cell dendrites. Full article
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Article
The VIP/VPAC1R Pathway Regulates Energy and Glucose Homeostasis by Modulating GLP-1, Glucagon, Leptin and PYY Levels in Mice
Biology 2022, 11(3), 431; https://doi.org/10.3390/biology11030431 - 11 Mar 2022
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Abstract
Vasoactive Intestinal Peptide binds with high affinity to VPAC1R and VPAC2R, thus regulating key physiologic functions. Previously, we documented in VIP−/− mice a leaner body phenotype and altered metabolic hormones. Past reports described in VPAC2−/− mice impaired circadian rhythm, reduced food [...] Read more.
Vasoactive Intestinal Peptide binds with high affinity to VPAC1R and VPAC2R, thus regulating key physiologic functions. Previously, we documented in VIP−/− mice a leaner body phenotype and altered metabolic hormones. Past reports described in VPAC2−/− mice impaired circadian rhythm, reduced food intake, and altered metabolism. To better define the effects of VPAC1R on body phenotype, energy/glucose homeostasis, and metabolism, we conducted a 12-week study in a VPAC1R null model. Our results reveal that VPAC1−/− mice experienced significant metabolic alterations during the dark cycle with greater numbers of feeding bouts (p = 0.009), lower Total Energy Expenditure (p = 0.025), VO2 (p = 0.029), and VCO2 (p = 0.016); as well as during the light cycle with lower Total Energy Expenditure (p = 0.04), VO2 (p = 0.044), and VCO2 (p = 0.029). Furthermore, VPAC1−/− mice had significantly higher levels of GLP-1 and PYY during fasting, and higher levels of GLP-1, glucagon leptin and PYY during postprandial conditions. In addition, VPAC1−/− mice had lower levels of glucose at 60′ and 120′, as assessed by insulin tolerance test. In conclusion, this study supports a key role for VPAC1R in the regulation of body glucose/energy homeostasis and metabolism. Full article
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