TRPV1, Gut Inflammation and Pain

"Where there's smoke there's fire" or in this study, where there's inflammation there is pain: Robert P. Watson, Elliot Lilley, Moh Panesar, Gurdip Bhalay, Steven Langridge, Shin-Shay Tian, Conor McClenaghan, Anna Ropenga, Fanning Zeng, Mark S. Nash. Increased prokineticin 2 expression in gut inflammation: role in visceral pain and intestinal ion transport. Neurogastroenterology & Motility. Volume 24, Issue 1, pages 65–e12, January 2012....Formalin-fixed, wax-embedded tissues with no overt signs of pathology were purchased from Asterand (Detroit, MI, USA); informed consent had been sought and received from all donors. All tissues were used in accordance with the Human Tissue Act 2004 (UK)...guinea pig anti-TRPV1 antibody (GP14100 – Neuromics, Edina, MN, USA)...

Images: expression of prokineticin receptors in human and rat tissues. (A) Immunohistochemical analysis of PKR1 expression in the myenteric and submucosal ganglia of human stomach, ileum, and colon. Pkr1 (B) and Pkr2(C) expression in a range of human tissues determined using qRT-PCR. (D, E) Immunohistochemical of PKR1 distribution in rat DRG showing an absence of expression in large diameter, NF200 positive neurons (D), but co-expression with TRPV1 in presumptive nociceptive sensory neurons (E). (F) Distribution of Pkr2 mRNA by in situ hybridization in rat DRG. The IHC/ISH images shown are representative of the data obtained from n = 3 donors/animals.



Key Results Prok2 gene expression was up-regulated in biopsy samples from ulcerative colitis patients, and similar elevations were observed in rodent models of inflammatory colitis. Prokineticin receptor 1 (PKR1) was localized to the enteric neurons and extrinsic sensory neurons, whereas Pkr2 expression was restricted to sensory ganglia. In rats, PROK2-increased intracellular calcium levels in cultured enteric and dorsal root ganglia neurons, which was blocked by Compound 3. Moreover, PROK2 acting at prokineticin receptors stimulated intrinsic neuronally mediated ion transport in rat ileal mucosa. In vivo, Compound 3 reversed intracolonic mustard oil-induced referred allodynia and TNBS-induced visceral hypersensitivity, but not non-inflammatory, stress-induced visceral pain.

Check out our Pain and Inflammation Research Antibodies.

GFAP and Mouse Myenteric Plexus

Our Neuronal-Glial Markers are important tools for our customers investigating expression in the CNS and PNS. I have posted images showing staining of mouse retinal astrocytes and in the ventral horn, funiculus of adult rat spinal cord and mouse medulloblastoma stem cells using our GFAP antibodies.

I wanted to share an excellent image generated by Dr. Kate Ellacott's lab at Vanderbilt University.

GFAP (Chicken-Cat#: CH22102) staining in of enteric glia in the myenteric plexus of the mouse gastrointestinal tract. Staining was performed in methanol/acetone fixed frozen sections using 1:1000 dilution of the antibody followed by 1:500 anti-chicken Alexa 594.

Related Reagents:

• GFAP (Chicken-Cat#: CH23011)
• GFAP (Mouse-Cat#; MO15052)
• GFAP (Rabbit-Cat#:RA19063)
• Neuronal-Glial Markers -Astrocytes, Glia, Microglia, Olidogodendrocytes, Progenitors and Schwann Cell.

Vitamin A Deficiency and Hirschsprung Disease

Dr. Robert Heuckeroth and his team and Washington University recently published more results on the link between maternal Vitamin A Deficiency and Hirschsprung Disease. It underscores the importance of maternal vitamin A nutrition for preventing the diease penetrance and expressitivity:
Ming Fu, Yoshiharu Sato, Ariel Lyons-Warren, Bin Zhang, Maureen A. Kane, Joseph L. Napoli and Robert O. Heuckeroth. Vitamin A facilitates enteric nervous system precursor migration by reducing Pten accumulation. Development 137, 631-640 (2010) doi:10.1242/dev.040550.
SUMMARY

Hirschsprung disease is a serious disorder of enteric nervous system (ENS) development caused by the failure of ENS precursor migration into the distal bowel. We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinolbinding-protein-deficient (Rbp4–/–) mice. Ret heterozygosity increases the incidence and severity of distal bowel aganglionosis induced by vitamin A deficiency in Rbp4–/– animals. Furthermore, RA reduces phosphatase and tensin homolog (Pten) accumulation in migrating cells, whereas Pten overexpression slows ENS precursor migration. Collectively, these data support the hypothesis that vitamin A deficiency is a non-genetic risk factor that increases Hirschsprung disease penetrance and expressivity, suggesting that some cases of Hirschsprung disease might be preventable by optimizing maternal nutrition.

By the way, the lab has been an ongoing consumer of our Ret Antibody and referenced use of this antibody in the publication.

Image: E12.5 mouse mid-gut slices were cultured to allow crest-derived cells to migrate onto the dish in response to GDNF. Cultures were maintained for 16 hours without added retinoic acid.

Related Reagents:

Ret (C-Terminus Fused)
Ret-Fluorescein Labeled
Ret-Allophycocyanin Labeled
Ret-Phycoerythrin Labeled
Neurotrophins and Growth Factor Antibodies
Neurotrophins-Neuron/Glial Marker
Recombinant Proteins
Neuron/Glial Markers
Stem Cell Research Reagents

Vitamin A and Hirschsprung Disease

Dr Robert O. Heuckeroth and his team at Washington University have been a long time user of Neuromics' Neurotrophins and Growth Factor and Neuropeptide and Neuropeptide Receptor Antibodies.

This has resulted in our monitoring his work on Enteric Nervous System (ENS) Development andHirschsprung Disease. We are pleased to present the most recent article referencing use of our Ret Antibody. In this study, he and his team find a link between Vitamin A and the disease. This suggests that some cases of Hirschsprung disease might be preventable by optimizing maternal nutrition.

Ming Fu, Yoshiharu Sato, Ariel Lyons-Warren, Bin Zhang, Maureen A. Kane, Joseph L. Napoli, and Robert O. Heuckeroth Vitamin A facilitates enteric nervous system precursor migration by reducing Pten accumulation. Development, Feb 2010; 137: 631 - 640.

Featured Reagent:

• Ret

Related Reagents:

• Ret Biotinylated
• Ret (C-Terminus Fused)
• Ret-Fluorescein Labeled
• Ret-Allophycocyanin Labeled
• Ret-Phycoerythrin Labeled
• Neurotrophins and Growth Factor Antibodies
• Neurotrophins-Neuron/Glial Marker Recombinant Proteins
• Neuron/Glial Markers
• Stem Cell Research Reagents

New Mouse Monoclonal GFAP Antibody

Check it out!

GFAP Antibody

Excelent marker for human astrocyte intermediate filaments in the central nervous system. It has also been detected in the glial cells of the enteric nervous system and some Schwann cells in the peripheral nervous systems.

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