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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Pecze, László Blum, Walter Schwaller, Beat |
| Description | Author Affiliation: Pecze L ( Department of Medicine, University of Fribourg, Fribourg, Switzerland.) |
| Abstract | Transient receptor potential vanilloid subtype 1 (TRPV1) receptor is a pain-sensing, ligand-gated, non-selective cation channel expressed in peripheral sensory neurons. Prolonged activation of TRPV1 by capsaicin leads to cell swelling and formation of membrane blebs in rat dorsal root ganglion (DRG) neurons. Similar results were obtained in NIH3T3 fibroblast cells stably expressing TRPV1. Here, we assessed the contribution of $Ca^{2 +}$ and $Na^{+}$ ions to TRPV1-mediated changes. Cell swelling was caused by a substantial influx of extracellular $Na^{+}$ via TRPV1 channels, causing concomitant transport of water. In the absence of extracellular $Na^{+},$ the membrane blebbing was completely inhibited, but $Ca^{2 +}$ influx did not change under these conditions. $Na^{+}$ influx was modulated by the intracellular $Ca^{2 +}$ concentration $([Ca^{2 +}]_{i}).$ Elevation of $[Ca^{2 +}]_{i}$ by ionomycin sensitized/activated TRPV1 channels causing cell swelling in TRPV1-positive cells. In the absence of extracellular $Ca^{2 +},$ capsaicin caused only little increase in $[Ca^{2 +}]_{i}$ indicating that the increase in $[Ca^{2 +}]_{i}$ observed after capsaicin application is derived essentially from extracellular $Ca^{2 +}$ and not from internal $Ca^{2 +}$ stores. In the absence of extracellular $Ca^{2 +}$ also the process of cell swelling was considerably slower. Calretinin is a $Ca^{2 +}$ buffer protein, which is expressed in a subset of TRPV1-positive neurons. Calretinin decreased the amplitude, but slowed down the decay of $Ca^{2 +}$ signals evoked by ionomycin. Cells co-expressing TRPV1 and calretinin were less sensitive to TRPV1-mediated, capsaicin-induced volume increases. In TRPV1-expressing NIH3T3 cells, calretinin decreased the capsaicin-induced $Ca^{2 +}$ and $Na^{+}$ influx. Swelling and formation of membrane blebs resulted in impaired plasma membrane integrity finally leading to cell death. Our results hint towards a mechanistic explanation for the apoptosis-independent capsaicin-evoked neuronal loss and additionally reveal a protective effect of calretinin; we propose that the $Ca^{2 +}-buffering$ capacity of calretinin reduces the susceptibility of calretinin-expressing DRG neurons against cell swelling/death caused by overstimulation of TRPV1 channels. This article is part of a Special Issue entitled:12th European Symposium on Calcium. |
| ISSN | 00063002 |
| Journal | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |
| Issue Number | 7 |
| Volume Number | 1833 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2013-07-01 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Calcium Metabolism Capsaicin Toxicity Cell Membrane Pathology Neurons Pain S100 Calcium Binding Protein G Sodium TRPV Cation Channels Animals Blotting, Western Calbindin 2 Drug Effects Cell Size Ganglia, Spinal Cytology Immunoenzyme Techniques Mice NIH 3T3 Cells Drug Therapy Sensory System Agents Research Support, Non-U.S. Gov't Biochemistry |
| Content Type | Text |
| Resource Type | Article |
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