Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Keeble, Julie; Russell, Fiona A.; Curtis, Bradley; Starr, Anna; Pintér, Erika; Brain, Susan D.

doi:10.1002/art.21297

Cited by 155 publications

(125 citation statements)

References 50 publications

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“…8 A). In TRPV1 Ϫ/Ϫ mice, withdrawal latencies under control saline injections were greater than in WT mice, consistent with previous observations (Keeble et al, 2005;PogatzkiZahn et al, 2005). In contrast to WT mice, activin injection into TRPV1 Ϫ/Ϫ null mice produced withdrawal latencies comparable with saline injection, and these latencies were not different from saline injections at any time examined.…”

Section: Inhibition Of Pkc But Not Pka Abrogates Activin A-induced supporting

confidence: 91%

Activin Acutely Sensitizes Dorsal Root Ganglion Neurons and Induces Hyperalgesia via PKC-Mediated Potentiation of Transient Receptor Potential Vanilloid I

Zhu¹,

Xu²,

Cuascut³

et al. 2007

J. Neurosci.

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Pain hypersensitivity is a cardinal sign of tissue damage, but how molecules from peripheral tissues affect sensory neuron physiology is incompletely understood. Previous studies have shown that activin A increases after peripheral injury and is sufficient to induce acute nociceptive behavior and increase pain peptides in sensory ganglia. This study was designed to test the possibility that the enhanced nociceptive responsiveness associated with activin involved sensitization of transient receptor potential vanilloid I (TRPV1) in primary sensory neurons. Activin receptors were found widely distributed among adult sensory neurons, including those that also express the capsaicin receptor. Whole-cell patch-clamp recording from sensory neurons showed that activin acutely sensitized capsaicin responses and depended on activin receptor kinase activity. Pharmacological studies revealed that the activin sensitization of capsaicin responses required PKC signaling, but not PI3K (phosphoinositide 3-kinase), ERK (extracellular signal-regulated protein kinase), PKA, PKC␣/␤, or Src. Furthermore, activin administration caused acute thermal hyperalgesia in wild-type mice, but not in TRPV1-null mice. These data suggest that activin signals through its own receptor, involves PKC signaling to sensitize the TRPV1 channel, and contributes to acute thermal hyperalgesia.

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Section: Inhibition Of Pkc But Not Pka Abrogates Activin A-induced supporting

confidence: 91%

Activin Acutely Sensitizes Dorsal Root Ganglion Neurons and Induces Hyperalgesia via PKC-Mediated Potentiation of Transient Receptor Potential Vanilloid I

Zhu¹,

Xu²,

Cuascut³

et al. 2007

J. Neurosci.

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“…Fur was removed from the knees of anesthetized mice using hair removal lotion (Nair; Church & Dwight Canada), and CFA (Sigma) was injected into the articular joint space via a 30G1/2-gauge needle, as previously described (14,15 (9). Additional mice were gavaged with 10 H diminuta cysticercoids that had been destroyed by sonication and boiled for 10 minutes.…”

Section: Methodsmentioning

confidence: 99%

Infection with an intestinal helminth parasite reduces Freund's complete adjuvant–induced monoarthritis in mice

Shi¹,

Wang²,

Prescott³

et al. 2011

Arthritis & Rheumatism

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Objective. Assessment of infection with helminth parasites in murine models of disease could identify antiinflammatory mechanisms that translate into treatments for arthritic disease. The aim of this study was to test the ability of infection with the tapeworm Hymenolepis diminuta to ameliorate Freund's complete adjuvant (CFA)-induced monoarthritis in mice.Methods. Mice received CFA with or without H diminuta, and knee swelling, pain, and measures of inflammation were assessed.Results. Injection of CFA resulted in rapid (within 24 hours) and sustained (lasting 20 days) knee swelling, a decreased pain threshold, increased blood flow to the knee, and increased production of tumor necrosis factor ␣ and interleukin-12p40 (IL-12p40). In mice that were infected with H diminuta 8 days prior to receiving CFA, the severity of arthritis was reduced as assessed by these indices of inflammation and infection 2 days after CFA injection and resulted in more rapid resolution of knee swelling. This antiarthritic effect required a viable infection and was dependent on adaptive immunity, because infection with H diminuta did not protect mice lacking T cells and B cells or the IL-4 receptor ␣ chain from CFA-induced inflammation. Interleukin-10 was of prime importance in the antiarthritic effect, because IL-10-knockout mice were not protected by infection, the antiarthritic effect was ablated by use of neutralizing IL-10 antibodies, and transfer of CD4؉ cells from infected wild-type mice but not IL-10-knockout mice significantly reduced CFAinduced knee swelling.Conclusion. In mice, the adaptive immune response to infection with H diminuta involves mobilization of IL-10, which has the concomitant advantage of dampening the innate immune responses that drive CFA-induced joint inflammation.

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“…Further, ASIC3 plays a role in normal visceral mechanosensation to stretch and in mechanical sensitization of primary afferents after visceral inflammation (Jones et al, 2005). In contrast, TRPV1 appears to mediate heat hyperalgesia associated with inflammation (Keeble et al, 2005;Honore et al, 2005;Caterina et al, 2000). Since in ASIC3−/− mice ASIC3 is removed from the entire animal it is not clear whether the reduction in mechanical hyperalgesia is a result of a loss of ASIC3 in muscle where the carrageenan is injected, or ASIC3 in paw where the mechanical hyperalgesia is tested.…”

Section: Introductionmentioning

confidence: 99%

ASIC3 in muscle mediates mechanical, but not heat, hyperalgesia associated with muscle inflammation

Sluka

Radhakrishnan

Benson

et al. 2007

Pain

166

160

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Peripheral initiators of muscle pain are virtually unknown, but likely key to development of chronic pain after muscle insult. The current study tested the hypothesis that ASIC3 in muscle is necessary for development of cutaneous mechanical, but not heat hyperalgesia induced by muscle inflammation. Using mechanical and heat stimuli, we assessed behavioral responses in ASIC3−/− and ASIC3+/+ mice after induction of carrageenan muscle inflammation. ASIC3−/−mice did not develop cutaneous mechanical hyperalgesia after muscle inflammation when compared to ASIC3+/ + mice; heat hyperalgesia developed similarly between groups. We then tested if the phenotype could be rescued in ASIC3−/− mice by using a recombinant herpes virus vector to express ASIC3 in skin (where testing occurred) or muscle (where inflammation occurred). Infection of mouse DRG neurons with ASIC3-encoding virus resulted in functional expression of ASICs. Injection of ASIC3-encoding virus into muscle or skin of ASIC3−/− mice resulted in ASIC3 mRNA in DRG and protein expression in DRG and the peripheral injection site. Injection of ASIC3-encoding virus into muscle, but not skin, resulted in development of mechanical hyperalgesia similar to that observed in ASIC3+/+ mice. Thus, ASIC3 in primary afferent fibers innervating muscle is critical to development of hyperalgesia that results from muscle insult.

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Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Cited by 155 publications

References 50 publications

Activin Acutely Sensitizes Dorsal Root Ganglion Neurons and Induces Hyperalgesia via PKC-Mediated Potentiation of Transient Receptor Potential Vanilloid I

Activin Acutely Sensitizes Dorsal Root Ganglion Neurons and Induces Hyperalgesia via PKC-Mediated Potentiation of Transient Receptor Potential Vanilloid I

Infection with an intestinal helminth parasite reduces Freund's complete adjuvant–induced monoarthritis in mice

ASIC3 in muscle mediates mechanical, but not heat, hyperalgesia associated with muscle inflammation

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