Prokineticin-1 evokes secretory and contractile activity in rat small intestine

Wade, PR; Palmer, Jeffrey M.; Mabus, John R.; Saunders, PR; Prouty, Stephen M.; Chevalier, Kristen; Gareau, Mélanie G.; McKenney, Sandra; Hornby, Pamela J.

doi:10.1111/j.1365-2982.2009.01426.x

Cited by 12 publications

(21 citation statements)

References 37 publications

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“…The IL6-type cytokines (IL6, LIF and OSM) also remained unchanged. This is in contrast to studies which report PROK1 regulation of the prostaglandin E 2 receptor EP4 in intestinal epithelial cells (9) and LIF activation in endometrial epithelial cell (16) and may suggest distinct function for PROK1 in germ cells.…”

Section: Discussioncontrasting

confidence: 85%

“…The PROK ligands share 85% homology and signal interchangeably via two G-coupled protein receptors, PROK receptor 1 and 2 (PROKR1 and PROKR2) to activate the MAP kinase and STAT signaling pathways (6,7). PROK ligands promote proliferation, differentiation and survival in both endothelial and immune cells, and have well defined functions in the vascular and gastrointestinal (GI) systems (8,9).…”

mentioning

confidence: 99%

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Prokineticin Ligands and Receptors Are Expressed in the Human Fetal Ovary and Regulate Germ Cell Expression ofCOX2

Eddie¹,

Childs²,

Kinnell³

et al. 2015

The Journal of Clinical Endocrinology & Metabolism

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Section: Discussioncontrasting

confidence: 85%

mentioning

confidence: 99%

Prokineticin Ligands and Receptors Are Expressed in the Human Fetal Ovary and Regulate Germ Cell Expression ofCOX2

Eddie¹,

Childs²,

Kinnell³

et al. 2015

The Journal of Clinical Endocrinology & Metabolism

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“…In addition, PROK1 is a potent stimulator of smooth muscle contractions in the gut (Li et al . 2001, Wade et al . 2010).…”

Section: Discussionmentioning

confidence: 99%

Prokineticin 1 induces a pro-inflammatory response in murine fetal membranes but does not induce preterm delivery

Lannagan¹,

Wilson²,

Denison³

et al. 2013

Reproduction

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The mechanisms that regulate the induction of term or preterm delivery (PTD) are not fully understood. Infection is known to play a role in the induction of pro-inflammatory cascades in uteroplacental tissues associated with preterm pathological parturition. Similar but not identical cascades are evident in term labour. In the current study, we used a mouse model to evaluate the role of prokineticins in term and preterm parturition. Prokineticins are multi-functioning secreted proteins that signal through G-protein-coupled receptors to induce gene expression, including genes important in inflammatory responses. Expression of prokineticins (Prok1 and Prok2) was quantified in murine uteroplacental tissues by QPCR in the days preceding labour (days 16–19). Prok1 mRNA expression increased significantly on D18 in fetal membranes (compared with D16) but not in uterus or placenta. Intrauterine injection of PROK1 on D17 induced fetal membrane mRNA expression of the pro-inflammatory mediators Il6, Il1b, Tnf, Cxcl2 and Cxcl5, which are not normally up-regulated until D19 of pregnancy. However, intrauterine injection of PROK1 did not result in PTD. As expected, injection of lipopolysaccharide (LPS) induced PTD, but this was not associated with changes in expression of Prok1 or its receptor (Prokr1) in fetal membranes. These results suggest that although Prok1 exhibits dynamic mRNA regulation in fetal membranes preceding labour and induces a pro-inflammatory response when injected into the uterus on D17, it is insufficient to induce PTD. Additionally, prokineticin up-regulation appears not to be part of the LPS-induced inflammatory response in mouse fetal membranes.

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“…In this study, we have extended this to show that PROK2‐mediated activation of PKR1 on enteric neurons may be an important regulator of ion transport within the GI tract. The physiologic significance of PROK2‐induced changes in I sc needs to be confirmed; however, as PROK1 induces ileal fluid secretion, 19,39 the raised PROK2 levels in colitis might stimulate secretion. Although PROK2‐mediated I sc involves the enteric nerve system because effects were blocked by inhibitors of neuronal activity (ω‐conotoxin GVIA or TTX) and not affected by capsaicin pretreatment, the inhibition of ileal I sc was not complete, suggesting that there may be a non‐neuronal component to prokineticin‐mediated ion transport.…”

Section: Discussionmentioning

confidence: 99%

Increased prokineticin 2 expression in gut inflammation: role in visceral pain and intestinal ion transport

Watson

Lilley

Panesar

et al. 2011

Neurogastroenterology Motil

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Elevated Prok2 levels, as a consequence of gastrointestinal tract inflammation, induce visceral pain via prokineticin receptors. This observation, together with the finding that PROK2 can modulate intestinal ion transport, raises the possibility that inhibitors of PROK2 signaling may have clinical utility in gastrointestinal disorders, such as irritable bowel syndrome and inflammatory bowel disease.

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Prokineticin-1 evokes secretory and contractile activity in rat small intestine

Abstract: These results demonstrate that PROK1 has oral prokinetic and secretogogue activity and that it acts on the intestinal mucosa via PK-R1 and prostaglandin receptors to mediate these effects.

Cited by 12 publications

References 37 publications

Prokineticin Ligands and Receptors Are Expressed in the Human Fetal Ovary and Regulate Germ Cell Expression ofCOX2

Prokineticin Ligands and Receptors Are Expressed in the Human Fetal Ovary and Regulate Germ Cell Expression ofCOX2

Prokineticin 1 induces a pro-inflammatory response in murine fetal membranes but does not induce preterm delivery

Increased prokineticin 2 expression in gut inflammation: role in visceral pain and intestinal ion transport

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