INT156175

Context Info Confidence 0.50 First Reported 2009 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 5 Total Number 6 Disease Relevance 0.86 Pain Relevance 0.80

plasma membrane (Trpv4) cilium (Trpv4) transmembrane transport (Trpv4)

Anatomy Link Frequency growth cones 2 sensory nerves 2 vascular endothelium 2 Trpv4 (Rattus norvegicus)

Pain Link Frequency Relevance Heat Taxol 60 99.58 Kinase C 8 99.00 Hyperalgesia 11 89.76 imagery 24 77.44 agonist 12 69.76 Inflammation 3 60.20 Pain 27 56.32 member 8 1 49.04 dorsal root ganglion 32 27.76 qutenza 2 10.00

Disease Link Frequency Relevance Heat Stress 10 99.66 Hyperalgesia 11 67.84 Adhesions 6 62.40 Increased Venous Pressure Under Development 4 60.56 INFLAMMATION 3 60.20 Pressure Volume 2 Under Development 4 57.20 Ganglion Cysts 32 27.76 Nociception 28 5.00 Pain 24 5.00 Neuropathic Pain 10 5.00

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Cell culture and in vivo studies demonstrate that an FSS- or a 4alphaPDD-induced activation of Trpv4 leads to an active proliferation of vascular cells and finally triggers collateral growth.

Positive_regulation (induced) of Positive_regulation (activation) of Trpv4 associated with stress

1) Confidence 0.50 Published 2009 Journal J. Cell. Mol. Med. Section Abstract Doc Link 19017361 Disease Relevance 0.38 Pain Relevance 0

To detect the roles of various vasodilating factors released by vascular endothelium in the hypotensive effect induced by TRPV4 activation, the corresponding inhibitors/blockers, including indomethacin (a cyclooxygenase inhibitor, 10 mg/kg, i.v.), Nomega-nitro-L-arginine (L-NA, a nitric oxide synthase inhibitor, 20 mg/kg, i.v.), apamin [a blocker of small conductance Ca2+-activated K+ (MaxiK) channels, 50 microg/kg, i.v.] combined with charybdotoxin (a blocker of intermediate and large conductance MaxiK channels, 50 microg/kg, i.v.), were used at various time before 4alpha-PDD injection.

Positive_regulation (induced) of Positive_regulation (activation) of TRPV4 in vascular endothelium

2) Confidence 0.49 Published 2010 Journal J. Hypertens. Section Body Doc Link 19996988 Disease Relevance 0.06 Pain Relevance 0

CONCLUSION: Our data show that the hypotensive effect induced by TRPV4 activation attributes to, at least in part, activation of MaxiK channels and CGRP receptors upon CGRP release from sensory nerves.

Positive_regulation (induced) of Positive_regulation (activation) of TRPV4 in sensory nerves

3) Confidence 0.49 Published 2010 Journal J. Hypertens. Section Body Doc Link 19996988 Disease Relevance 0 Pain Relevance 0

Activation of TRPV4 results in fast retraction of growth cones in F11 cell

Positive_regulation (results) of Positive_regulation (Activation) of TRPV4 in growth cones

4) Confidence 0.49 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2906515 Disease Relevance 0.18 Pain Relevance 0.07

Stabilization of microtubules by Taxol reduces Ca2+-influx through TRPV4 activation

Positive_regulation (through) of Positive_regulation (activation) of TRPV4 associated with taxol

5) Confidence 0.49 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2906515 Disease Relevance 0 Pain Relevance 0.12

Thus PKC, and possibly PKA, phosphorylate TRPV4 at Ser824 leading to the enhancement of TRPV4 channel function.

Positive_regulation (leading) of Positive_regulation (enhancement) of TRPV4 associated with kinase c

6) Confidence 0.40 Published 2010 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 20043876 Disease Relevance 0.24 Pain Relevance 0.61

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