Vasoactive intestinal peptide

Source: Wikipedia, the free encyclopedia.
VIP
Available structures
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_003381
NM_194435

NM_011702
NM_001313969

RefSeq (protein)

NP_003372
NP_919416

Location (UCSC)Chr 6: 152.75 – 152.76 MbChr 10: 5.59 – 5.6 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Vasoactive intestinal peptide, also known as vasoactive intestinal polypeptide or VIP, is a

G protein–coupled receptors.[5]
VIP is produced in many tissues of
trachea, stomach and gallbladder. In humans, the vasoactive intestinal peptide is encoded by the VIP gene.[9]

VIP has a half-life (t½) in the blood of about two minutes.[10]

Function

In the digestive system

In the

pepsinogen secretion by chief cells.[14] 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.[15]

In the heart

It is also found in the heart and has significant effects on the

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.[16][17]

In the brain

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

One region includes a specific area of the

growth-hormone-releasing hormone (GH-RH) is a member of the VIP family and stimulates growth hormone secretion in the anterior pituitary gland.[20][21]

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

Mechanisms

VIP binds to both

Per1 and Per2 in circadian rhythm.[22]

In addition,

GABA levels are connected to VIP in that they are co-released. Sparse GABAergic connections are thought to decrease synchronized firing.[22] 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.[22]

Circadian time is likely to affect the synapses rather than the organization of VIP circuits.[22]

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.[18]

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

circadian timekeeping machinery.[22]

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.[22]

The leading hypothesis of VIP function points to the neurons using VIP to communicate with specific postsynaptic targets to regulate

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.[22]

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.[18][23]

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).[18]

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.[24] 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.[25]

Pathology

VIP is overproduced in VIPoma.[12]

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.[26]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000146469Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000019772Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. PMID 21439408
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  11. ^ a b Bowen R (1999-01-24). "Vasoactive Intestinal Peptide". Pathophysiology of the Endocrine System: Gastrointestinal Hormones. Colorado State University. Archived from the original on 2012-02-04. Retrieved 2009-02-06.
  12. ^ a b "Vasoactive intestinal polypeptide". General Practice Notebook. Retrieved 2009-02-06.
  13. ^ Bergman RA, Afifi AK, Heidger PM. "Plate 6.111 Vasoactive Intestinal Polypeptide (VIP)". Atlas of Microscopic Anatomy: Section 6 - Nervous Tissue. www.anatomyatlases.org. Retrieved 2009-02-06.
  14. PMID 6195927
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  21. PMID 27065166. {{cite book}}: |journal= ignored (help
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Further reading

External links