De novo expression of Trpm4 initiates secondary hemorrhage in spinal cord injury

Nature Medicine

Volumn 15, Issue 2, 2009, Pages 185-191

  Gerzanich, Volodymyr ^a   Woo, S Kyoon ^a   Vennekens, Rudi ^b   Tsymbalyuk, Orest ^a   Ivanova, Svetlana ^a   Ivanov, Alexander ^a   Geng, Zhihua ^a   Chen, Zheng ^a   Nilius, Bernd ^b   Flockerzi, Veit ^c   Freichel, Marc ^c   Simard, J Marc ^a  

^a UNIVERSITY OF MARYLAND SCHOOL OF MEDICINE   (United States)

^b LABORATORY OF MOLECULAR AND CELLULAR SIGNALING   (Belgium)

^c SAARLAND UNIVERSITY   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATE; CLUSTERIN; MESSENGER RNA; OLIGODEOXYNUCLEOTIDE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BLEEDING; CANCER MORTALITY; CELL DEATH; CELL STRAIN COS7; CONTROLLED STUDY; DISEASE COURSE; FEMALE; FRAGMENTATION REACTION; GENE REPRESSION; NONHUMAN; OUTCOME ASSESSMENT; PETECHIA; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; SPINAL CORD INJURY; SWELLING;

ANIMALS; BASE SEQUENCE; CELL DEATH; DISEASE MODELS, ANIMAL; DNA PRIMERS; FEMALE; GENE EXPRESSION REGULATION; HEMORRHAGE; IMMUNOHISTOCHEMISTRY; MICE; MICE, KNOCKOUT; OLIGONUCLEOTIDES, ANTISENSE; RATS; RATS, LONG-EVANS; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; SPINAL CORD INJURIES; TRPM CATION CHANNELS;

MUS; RATTUS; RODENTIA;

EID: 59649105028     PISSN: 10788956     EISSN: 1546170X     Source Type: Journal    
DOI: 10.1038/nm.1899     Document Type: Article

References (44)

1. Nilius, B., Owsianik, G., Voets, T. & Peters, J.A. Transient receptor potential cation channels in disease. Physiol. Rev. 87, 165-217 (2007).
2. Venkatachalam, K. & Montell, C. TRP channels. Annu. Rev. Biochem. 76, 387-417 (2007).
3. 2+-activated nonselective cation channel mediating cell membrane depolarization. Cell 109, 397-407 (2002).
4. Launay, P. et al. TRPM4 regulates calcium oscillations after T cell activation. Science 306, 1374-1377 (2004).
5. Vennekens, R. et al. Increased IgE-dependent mast cell activation and anaphylactic responses in mice lacking the calcium-activated nonselective cation channel TRPM4. Nat. Immunol. 8, 312-320 (2007).
6. Nilius, B. TRP channels in disease. Biochim. Biophys. Acta 1772, 805-812 (2007).
7. 2+ entry through TRPM7 channels and anoxic neuronal death. Cell 115, 768-770 (2003).
8. Aarts, M. et al. A key role for TRPM7 channels in anoxic neuronal death. Cell 115, 863-877 (2003).
9. Oertel, M. et al. Progressive hemorrhage after head trauma: predictors and consequences of the evolving injury. J. Neurosurg. 96, 109-116 (2002).
10. Guth, L., Zhang, Z. & Steward, O. The unique histopathological responses of the injured spinal cord. Implications for neuroprotective therapy. Ann. NY Acad. Sci. 890, 366-384 (1999).
11. Griffiths, I.R., Burns, N. & Crawford, A.R. Early vascular changes in the spinal grey matter following impact injury. Acta Neuropathol. 41, 33-39 (1978).
12. Hayes, K.C. & Kakulas, B.A. Neuropathology of human spinal cord injury sustained in sports-related activities. J. Neurotrauma 14, 235-248 (1997).
13. Tator, C.H. & Koyanagi, I. Vascular mechanisms in the pathophysiology of human spinal cord injury. J. Neurosurg. 86, 483-492 (1997).
14. Tator, C.H. & Fehlings, M.G. Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J. Neurosurg. 75, 15-26 (1991).
15. Regan, R.F. & Guo, Y. Toxic effect of hemoglobin on spinal cord neurons in culture. J. Neurotrauma 15, 645-653 (1998).
16. Wang, X., Mori, T., Sumii, T. & Lo, E.H. Hemoglobin-induced cytotoxicity in rat cerebral cortical neurons: caspase activation and oxidative stress. Stroke 33, 1882-1888 (2002).
17. Simard, J.M. et al. Endothelial sulfonylurea receptor 1-regulated NC Ca-ATP channels mediate progressive hemorrhagic necrosis following spinal cord injury. J. Clin. Invest. 117, 2105-2113 (2007).
18. Swartz, K.R. et al. Gender differences in spinal cord injury are not estrogen-dependent. J. Neurotrauma 24, 473-480 (2007).
19. Zhao, Q. et al. Cellular distribution of phosphorothioate oligonucleotide following intravenous administration in mice. Antisense Nucleic Acid Drug Dev. 8, 451-458 (1998).
20. Pena, F. & Ordaz, B. Nonselective cation channel blockers: potential use in nervous system basic research and therapeutics. Mini Rev. Med. Chem. 8, 812-819 (2008).
21. Vennekens, R. & Nilius, B. Insights into TRPM4 function, regulation and physiological role. Handb. Exp. Pharmacol. 179, 269-285 (2007).
22. Colak, A. et al. Neuroprotective effects of GYKI 52466 on experimental spinal cord injury in rats. J. Neurosurg. 98, 275-281 (2003).
23. Osterholm, J.L., Alderman, J.B., Triolo, A.J., D'Amore, B.R. & Williams, H.D. Oxygenated fluorocarbon nutrient solution in the treatment of experimental spinal cord injury. Neurosurgery 15, 373-380 (1984).
24. Anderson, D.K., Means, E.D., Waters, T.R. & Spears, C.J. Spinal cord energy metabolism following compression trauma to the feline spinal cord. J. Neurosurg. 53, 375-380 (1980).
25. Rivlin, A.S. & Tator, C.H. Objective clinical assessment of motor function after experimental spinal cord injury in the rat. J. Neurosurg. 47, 577-581 (1977).
26. Basso, D.M. et al. Basso Mouse Scale for locomotion detects differences in recovery after spinal cord injury in five common mouse strains. J. Neurotrauma 23, 635-659 (2006).
27. Kunert-Keil, C., Bisping, F., Kruger, J. & Brinkmeier, H. Tissue-specific expression of TRP channel genes in the mouse and its variation in three different mouse strains. BMC Genomics 7, 159 (2006).
28. Guinamard, R., Demion, M., Magaud, C., Potreau, D. & Bois, P. Functional expression of the TRPM4 cationic current in ventricular cardiomyocytes from spontaneously hypertensive rats. Hypertension 48, 587-594 (2006).
29. Zhang, Z., Okawa, H., Wang, Y. & Liman, E.R. Phosphatidylinositol 4,5-bisphosphate rescues TRPM4 channels from desensitization. J. Biol. Chem. 280, 39185-39192 (2005).
30. Nilius, B. & Droogmans, G. Ion channels and their functional role in vascular endothelium. Physiol. Rev. 81, 1415-1459 (2001).
31. Guinamard, R. & Bois, P. Involvement of transient receptor potential proteins in cardiac hypertrophy. Biochim. Biophys. Acta 1772, 885-894 (2007).
32. Tiruppathi, C., Minshall, R.D., Paria, B.C., Vogel, S.M. & Malik, A.B. Role of Ca2+ signaling in the regulation of endothelial permeability. Vascul. Pharmacol. 39, 173-185 (2002).
33. 2+ signaling, TRP channels, and endothelial permeability. Microcirculation 13, 693-708 (2006).
34. Nilius, B., Prenen, J., Voets, T. & Droogmans, G. Intracellular nucleotides and polyamines inhibit the Ca2+-activated cation channel TRPM4b. Pflugers Arch. 448, 70-75 (2004).
35. Nilius, B. et al. The Ca2+-activated cation channel TRPM4 is regulated by phosphatidylinositol 4,5-biphosphate. EMBO J. 25, 467-478 (2006).
36. Steward, O. et al. Genetic approaches to neurotrauma research: opportunities and potential pitfalls of murine models. Exp. Neurol. 157, 19-42 (1999).
37. Khan, M., Griebel, R., Rozdilsky, B. & Politis, M. Hemorrhagic changes in experimental spinal cord injury models. Can. J. Neurol. Sci. 12, 259-262 (1985).
38. Kawata, K. et al. Experimental study of acute spinal cord injury: a histopathological study. No Shinkei Geka 21, 45-51 (1993).
39. Balentine, J.D. Pathology of experimental spinal cord trauma. I. The necrotic lesion as a function of vascular injury. Lab. Invest. 39, 236-253 (1978).
40. Iizuka, H., Yamamoto, H., Iwasaki, Y., Yamamoto, T. & Konno, H. Evolution of tissue damage in compressive spinal cord injury in rats. J. Neurosurg. 66, 595-603 (1987).
41. Simard, J.M., Tarasov, K.V. & Gerzanich, V. Non-selective cation channels, transient receptor potential channels and ischemic stroke. Biochim. Biophys. Acta 1772, 947-957 (2007).
42. Hall, E.D. & Springer, J.E. Neuroprotection and acute spinal cord injury: a reappraisal. NeuroRx 1, 80-100 (2004).
43. Simard, J.M. et al. Newly expressed SUR1-regulated NC(Ca-ATP) channel mediates cerebral edema after ischemic stroke. Nat. Med. 12, 433-440 (2006).
44. Nikulina, E., Tidwell, J.L., Dai, H.N., Bregman, B.S. & Filbin, M.T. The phosphodiesterase inhibitor rolipram delivered after a spinal cord lesion promotes axonal regeneration and functional recovery. Proc. Natl. Acad. Sci. USA 101, 8786-8790 (2004).