Biology:Vasoactive intestinal peptide

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Short description: Hormone that affects blood pressure / heart rate


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

Vasoactive intestinal peptide, also known as vasoactive intestinal polypeptide or VIP, is a peptide hormone that is vasoactive in the intestine. VIP is a peptide of 28 amino acid residues that belongs to a glucagon/secretin superfamily, the ligand of class II G protein–coupled receptors.[1] VIP is produced in many tissues of vertebrates including the gut, pancreas, cortex, and suprachiasmatic nuclei of the hypothalamus in the brain.[2][3][4] VIP stimulates contractility in the heart, causes vasodilation, increases glycogenolysis, lowers arterial blood pressure and relaxes the smooth muscle of trachea, stomach and gallbladder. In humans, the vasoactive intestinal peptide is encoded by the VIP gene.[5]

VIP has a half-life (t½) in the blood of about two minutes.[6]

Function

In the digestive system

In the digestive system, VIP seems to induce smooth muscle relaxation (lower esophageal sphincter, stomach, gallbladder), stimulate secretion of water into pancreatic juice and bile, and cause inhibition of gastric acid secretion and absorption from the intestinal lumen.[7] Its role in the intestine is to greatly stimulate secretion of water and electrolytes,[8] as well as relaxation of enteric smooth muscle, dilating peripheral blood vessels, stimulating pancreatic bicarbonate secretion, and inhibiting gastrin-stimulated gastric acid secretion. These effects work together to increase motility.[9] It also has the function of stimulating pepsinogen secretion by chief cells.[10] VIP seems to be an important neuropeptide during inflammatory bowel diseases since the communication between mast cells and VIP in colitis, as in Crohn's disease, is upregulated.[11]

In the heart

It is also found in the heart and has significant effects on the cardiovascular system. It causes coronary vasodilation[7] as well as having a positive inotropic and chronotropic effect. Research is being performed to see if it may have a beneficial role in the treatment of heart failure. VIP provokes vaginal lubrication, doubling the total volume of lubrication produced.[12][13]

In the brain

VIP is also found in the brain and some autonomic nerves:

One region includes a specific area of the suprachiasmatic nuclei (SCN), the location of the 'master circadian pacemaker'.[14] See SCN and circadian rhythm below. VIP in the pituitary helps to regulate prolactin secretion; it stimulates prolactin release in the domestic turkey.[15] Additionally, the growth-hormone-releasing hormone (GH-RH) is a member of the VIP family and stimulates growth hormone secretion in the anterior pituitary gland.[16][17]

VIP is also expressed in a subtype of inhibitory interneuron in various regions of the brain.

Mechanisms

VIP binds to both VPAC1 and VPAC2 receptors. When VIP binds to VPAC2 receptors, a G-alpha-mediated signaling cascade is triggered. In a number of systems, VIP binding activates adenyl cyclase activity leading to increases in cAMP and PKA. The PKA then activates other intracellular signaling pathways like the phosphorylation of CREB and other transcriptional factors. The mPer1 promoter has CRE domains and thus provides the mechanism for VIP to regulate the molecular clock itself. Then it will activate gene expression pathways such as Per1 and Per2 in circadian rhythm.[18]

In addition, GABA levels are connected to VIP in that they are co-released. Sparse GABAergic connections are thought to decrease synchronized firing.[18] While GABA controls the amplitude of SCN neuronal rhythms, it is not critical for maintaining synchrony. However, if GABA release is dynamic, it may mask or amplify synchronizing effects of VIP inappropriately.[18]

Circadian time is likely to affect the synapses rather than the organization of VIP circuits.[18]

SCN and circadian rhythm

Suprachiasmatic nucleus is shown in green.

The SCN coordinates daily timekeeping in the body and VIP plays a key role in communication between individual brain cells within this region. At a cellular level, the SCN expresses different electrical activity in circadian time. Higher activity is observed during the day, while during night there is lower activity. This rhythm is thought to be important feature of SCN to synchronize with each other and control rhythmicity in other regions.[14]

VIP acts as a major synchronizing agent among SCN neurons and plays a role in synchronizing the SCN with light cues. The high concentration of VIP and VIP receptor containing neurons are primarily found in the ventrolateral aspect of the SCN, which is also located above the optic chiasm. The neurons in this area receive retinal information from the retinohypothalamic tract and then relay the environmental information to the SCN.[18] Further, VIP is also involved in synchronizing the timing of SCN function with the environmental light-dark cycle. Combined, these roles in the SCN make VIP a crucial component of the mammalian circadian timekeeping machinery.[18]

After finding evidence of VIP in the SCN, researchers began contemplating its role within the SCN and how it could affect circadian rhythm. The VIP also plays a pivotal role in modulating oscillations. Previous pharmacological research has established that VIP is needed for normal light-induced synchronization of the circadian systems. Application of VIP also phase shifts the circadian rhythm of vasopressin release and neural activity. The ability of the population to remain synchronized as well as the ability of single cells to generate oscillations is composed in VIP or VIP receptor deficient mice. While not highly studied, there is evidence that levels of VIP and its receptor may vary depending on each circadian oscillation.[18]

The leading hypothesis of VIP function points to the neurons using VIP to communicate with specific postsynaptic targets to regulate circadian rhythm.[18] The depolarization of the VIP-expressing neurons by light appears to cause the release of VIP and co-transmitters (including GABA) that can in turn, alter the properties of the next set of neurons with the activation of VPAC2. Another hypothesis supports VIP sending a paracrine signal from a distance rather than the adjacent postsynaptic neuron.[18]

Signaling pathway

In SCN, there is an abundant amount of VPAC2. The presence of VPAC2 in ventrolateral side suggests that VIP signals can actually signal back to regulate VIP secreting cells. SCN has neural multiple pathways to control and modulate endocrine activity.[14][19]

VIP and vasopressin are both important for neurons to relay information to different targets and affect neuroendocrine function. They transmit information through such relay nuclei as the SPZ (subparaventricular zone), DMH (dorsomedial hypothalamic nucleus), MPOA (medial preoptic area) and PVN (paraventricular nucleus of hypothalamus).[14]

Social behavior

Ventromedial hypothalamus (VM), optic chiasm (OC), anterior pituitary (AP), and posterior pituitary (PP) are shown here.

VIP neurons located in the hypothalamus, specifically the dorsal anterior hypothalamus and ventromedial hypothalamus, have an effect on social behaviors in many species of vertebrates. Studies suggest that VIP cascades can be activated in the brain in response to a social situation that stimulates the areas of the brain that are known to regulate behavior. This social circuit includes many areas of the hypothalamus along with the amygdala and the ventral tegmental area. The production and release of the neuropeptide VIP is centralized in the hypothalamic and extrahypothalamic regions of the brain and from there it is able to modulate the release of prolactin secretion.[20] Once secreted from the pituitary gland, prolactin can increase many behaviors such as parental care and aggression. In certain species of birds with a knockout VIP gene there was an observable decrease in overall aggression over nesting territory.[21]

Pathology

VIP is overproduced in VIPoma.[8]

In addition to VIPoma, VIP has a role in osteoarthritis (OA). While there is existing conflict in whether down-regulation or up-regulation of VIP contributes to OA, VIP has been shown to prevent cartilage damage in animals.[22]

See also

References

  1. ↑ "Structural difference of vasoactive intestinal peptide in two distinct membrane-mimicking environments". Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1814 (5): 724–30. May 2011. doi:10.1016/j.bbapap.2011.03.009. PMID 21439408. 
  2. ↑ "PACAP and VIP signaling in chondrogenesis and osteogenesis". Peptides 66: 51–7. April 2015. doi:10.1016/j.peptides.2015.02.001. PMID 25701761. https://dea.lib.unideb.hu/dea/bitstream/handle/2437/208376/1_s2.0_S0196978115000406_main.pdf?sequence=5&isAllowed=y. 
  3. ↑ "Vasoactive intestinal peptide: a neuropeptide with pleiotropic immune functions". Amino Acids 45 (1): 25–39. July 2013. doi:10.1007/s00726-011-1184-8. PMID 22139413. 
  4. ↑ "VIP and PACAP". Cellular Peptide Hormone Synthesis and Secretory Pathways. Results and Problems in Cell Differentiation. 50. 2010-01-01. pp. 221–34. doi:10.1007/400_2009_24. ISBN 978-3-642-11834-0. 
  5. ↑ "Cis-regulatory elements controlling basal and inducible VIP gene transcription". Annals of the New York Academy of Sciences 865 (1): 10–26. December 1998. doi:10.1111/j.1749-6632.1998.tb11158.x. PMID 9927992. Bibcode: 1998NYASA.865...10H. 
  6. ↑ "Vasoactive intestinal peptide: cardiovascular effects". Cardiovascular Research 49 (1): 27–37. January 2001. doi:10.1016/s0008-6363(00)00229-7. PMID 11121793. 
  7. ↑ 7.0 7.1 Bowen R (1999-01-24). "Vasoactive Intestinal Peptide". Pathophysiology of the Endocrine System: Gastrointestinal Hormones. Colorado State University. http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/gi/vip.html. 
  8. ↑ 8.0 8.1 "Vasoactive intestinal polypeptide". General Practice Notebook. http://www.gpnotebook.co.uk/simplepage.cfm?ID=1892679719. 
  9. ↑ "Plate 6.111 Vasoactive Intestinal Polypeptide (VIP)". Atlas of Microscopic Anatomy: Section 6 - Nervous Tissue. www.anatomyatlases.org. http://www.anatomyatlases.org/MicroscopicAnatomy/Section06/Plate06111.shtml. 
  10. ↑ "Regulation of pepsinogen release from canine chief cells in primary monolayer culture". The American Journal of Physiology 245 (5 Pt 1): G641–6. November 1983. doi:10.1152/ajpgi.1983.245.5.G641. PMID 6195927. 
  11. ↑ "Upregulation of intestinal mucosal mast cells expressing VPAC1 in close proximity to vasoactive intestinal polypeptide in inflammatory bowel disease and murine colitis". Neurogastroenterology and Motility 31 (3): e13503. March 2019. doi:10.1111/nmo.13503. PMID 30407703. 
  12. ↑ "VIP, vagina, clitoral and periurethral glans--an update on human female genital arousal". Experimental and Clinical Endocrinology 98 (2): 61–9. 1991-01-01. doi:10.1055/s-0029-1211102. PMID 1778234. 
  13. ↑ "Helospectin and pituitary adenylate cyclase activating polypeptide in the human vagina". Regulatory Peptides 55 (3): 277–86. February 1995. doi:10.1016/0167-0115(94)00116-f. PMID 7761627. 
  14. ↑ 14.0 14.1 14.2 14.3 "Properties of VIP+ synapses in the suprachiasmatic nucleus highlight their role in circadian rhythm". Journal of Neurophysiology 115 (6): 2701–4. June 2016. doi:10.1152/jn.00393.2015. PMID 26581865. 
  15. ↑ "The relative importance of vasoactive intestinal peptide and peptide histidine isoleucine as physiological regulators of prolactin in the domestic turkey". General and Comparative Endocrinology 142 (3): 267–73. July 2005. doi:10.1016/j.ygcen.2004.12.024. PMID 15935152. 
  16. ↑ "Growth hormone-releasing hormone: not only a neurohormone". Trends in Endocrinology and Metabolism 22 (8): 311–7. August 2011. doi:10.1016/j.tem.2011.03.006. PMID 21530304. 
  17. ↑ "Neuroendocrine Regulation of Growth Hormone Secretion". Comprehensive Physiology. 6. March 2016. 687–735. doi:10.1002/cphy.c150002. ISBN 9780470650714. 
  18. ↑ 18.0 18.1 18.2 18.3 18.4 18.5 18.6 18.7 18.8 "Vasoactive intestinal peptide and the mammalian circadian system". General and Comparative Endocrinology 152 (2–3): 165–75. 2007. doi:10.1016/j.ygcen.2007.04.018. PMID 17572414. 
  19. ↑ "Neuropeptides shaping the central nervous system development: Spatiotemporal actions of VIP and PACAP through complementary signaling pathways". Journal of Neuroscience Research 94 (12): 1472–1487. December 2016. doi:10.1002/jnr.23915. PMID 27717098. 
  20. ↑ "New perspectives on vasoactive intestinal polypeptide as a widespread modulator of social behavior". Current Opinion in Behavioral Sciences 6: 139–147. December 2015. doi:10.1016/j.cobeha.2015.11.003. PMID 26858968. 
  21. ↑ "The Role of VIP in Social Behavior: Neural Hotspots for the Modulation of Affiliation, Aggression, and Parental Care". Integrative and Comparative Biology 56 (6): 1238–1249. December 2016. doi:10.1093/icb/icw122. PMID 27940615. 
  22. ↑ "Role of vasoactive intestinal peptide in osteoarthritis". Journal of Biomedical Science 23 (1): 63. August 2016. doi:10.1186/s12929-016-0280-1. PMID 27553659. 

Further reading

External links



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