ganglion cysts/protease

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Capsaicin up-regulates protease-activated receptor-4 mRNA and protein in primary cultured dorsal root ganglion neurons.

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Previous study has shown that there is a functional link between the transient receptor potential vanilloid type 1 (TRPV1) receptor and protease-activated receptor-4 (PAR4) in modulation of inflammation and pain. Capsaicin activation of TRPV1 is involved in enhancement of the expression of TRPV1 in

Protease-dependent excitation of nodose ganglion neurons by commensal gut bacteria.

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The vagus nerve has been implicated in mediating behavioral effects of the gut microbiota on the central nervous system. This study examined whether the secretory products of commensal gut bacteria can modulate the excitability of vagal afferent neurons with cell bodies in nodose

Norrin attenuates protease-mediated death of transformed retinal ganglion cells.

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OBJECTIVE To investigate the effects of norrin, a nonconventional ligand for Wingless-Int (Wnt)-beta-catenin signaling pathway, on protease-mediated death of transformed rat retinal ganglion cells (RGC-5). METHODS Transformed RGC-5 cells were treated with 2.0 microM staurosporine (SS), a

Protease-activated receptor 4 activation increases the expression of calcitonin gene-related peptide mRNA and protein in dorsal root ganglion neurons.

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Accumulating evidence demonstrates that nociceptor activation evokes a rapid change in mRNA and protein levels of calcitonin gene-related peptide (CGRP) in dorsal root ganglion (DRG) neurons. Although the colocalization of CGRP and protease-activated receptor-4 (PAR4), a potent modulator of pain

Two types of protease-activated receptors (PAR-1 and PAR-2) mediate calcium signaling in rat retinal ganglion cells RGC-5.

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Protease-activated receptors (PARs), G-protein-coupled receptors, are widely expressed in various tissues, where they participate in physiological and pathological processes, such as hemostasis, proliferation, tissue repair, and inflammation. Recently, we found that PARs were upregulated in the rat

Capsaicin-induced neurotoxicity in cultured dorsal root ganglion neurons: involvement of calcium-activated proteases.

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We examined the mechanism by which capsaicin produces its toxic effects on cultures of rat sensory neurons. Capsaicin caused a robust increase in [Ca2+]i in a subpopulation of cultured rat dorsal root ganglion neurons. Similarly, a brief exposure to capsaicin resulted in delayed degeneration of a

Interleukin-1β increased the expression of protease-activated receptor 4 mRNA and protein in dorsal root ganglion neurons.

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Protease-activated receptor-4 (PAR4) is localized in primary sensory neurons and is believed to implicate in the modulation of nociceptive mechanisms. The pro-inflammatory cytokine interleukin-1β (IL-1β) is involved in the generation of hyperalgesia in pathological states such as neuropathy and

Inhibition of CPP32-like proteases rescues axotomized retinal ganglion cells from secondary cell death in vivo.

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The majority of retinal ganglion cells (RGCs) degenerate and die after transection of the optic nerve (ON) in the adult rat. This secondary cell death can primarily be ascribed to apoptosis. Recent work strongly suggests a decisive role for a family of cysteine proteases, termed caspases, as

The emerging role of proteases in retinal ganglion cell death.

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Retinal ganglion cell (RGC) death is an important issue in Primary Open Angle-Glaucoma (POAG) in terms of both vision loss and health care costs. Yet, the pathophysiology underlying RGC death in glaucoma is unclear. A growing body of evidence indicates that proteases that modulate the extracellular

Protease-activated receptor 2 in dorsal root ganglion contributes to peripheral sensitization of bone cancer pain.

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BACKGROUND Treating bone cancer pain continues to be a major clinical challenge, and the underlying mechanisms of bone cancer pain remain elusive. Protease-activated receptor 2 (PAR2) has been reported to be involved in neurogenic inflammation, nociceptive pain and hyperalgesia. Here, we

Properties of acetylcholinesterase and non-specific cholinesterase in rat superior cervical ganglion and plasma.

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Amphiphile dependency, solubility in aqueous solutions, and sensitivity to proteolysis of acetylcholinesterase (AChE) and nonspecific cholinesterase (nsChE) in the rat superior cervical ganglion were studied and compared to properties of soluble plasma cholinesterases. Ganglion AChE shows strong

Inhibition of plasminogen activators attenuates the death of differentiated retinal ganglion cells and stabilizes their neurite network in vitro.

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OBJECTIVE Although previous studies have indicated that elevated levels of the tissue plasminogen activator (tPA) and the urokinase plasminogen activator (uPA) associate with the death of retinal ganglion cells (RGCs), it was unclear whether these proteases directly cause cell death. With the use of

Distribution of acid protease activity in the squid nervous system.

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Acid protease activity was measured in homogenized stellate ganglion, axoplasm extruded from the squid giant axon, homogenized fin nerves, and in lysed synaptosomes prepared from the optic lobe of the squid. At least two different acid protease classes were distinguished on the bases of their

Decreased TNF Levels and Improved Retinal Ganglion Cell Survival in MMP-2 Null Mice Suggest a Role for MMP-2 as TNF Sheddase.

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Matrix metalloproteinases (MMPs) have been designated as both friend and foe in the central nervous system (CNS): while being involved in many neurodegenerative and neuroinflammatory diseases, their actions appear to be indispensable to a healthy CNS. Pathological conditions in the CNS are therefore

Calpain-mediated degradation of rapidly and slowly axonally transported proteins in retinal ganglion cells.

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Labelled axonally transported proteins belonging to four different phases of transport in the retinal ganglion cells of the rabbit were used as substrates in order to study proteolytic degradation in axons and nerve terminals. Proteins of both rapidly and slowly transported phases of axonal

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