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TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler

Year 2010, Volume: 27 Issue: 2, 42 - 45, 21.01.2011

Mustafa Saygın , Mustafa Nazıroğlu

Abstract

Transient receptor potential (TRP) kanalları ilk olarak 1998 yılında Drosophila türü sirke sineklerinin göz hücrelerinde bulunmuştur. TRP kanallarının başlıca 6 familyası vardır. Bunların da kendi aralarında alt grupları vardır. Örneğin, beyin ve nöron hücrelerinde daha ziyade bulunan TRP Melastatindir. TRP kanalları (TRPM2) Ca2+ için spesifik değildir . TRPM kanallarının dört alt grubu vardır. Bu kanalların aktivasyon mekanizmaları ve bulundukları organlar farklıdır. Özellikle oksidatif stres ürünleriyle aktive olabildiğinden TRPM2 kanalları ile ilgilenmekteyiz. Oksidatif stres artışı ve antioksidan sistemin zayıfladığı durumlarda DNA tahribi ve NAD den PARP ve sonrasında PARG aktivasyonları ile ADP-Riboz (ADPR) oluşumu artmaktadır. Hem ADPR ve NAD hem de oksidatif stres ürünlerinden olan H2O2 nin TRPM2 kanallarını aktive ettiğine dair bildirimler mevcuttur. Fakat bu kanalların oksidatif stres ve ADPR ile doğrudan veya dolaylı aktive olduğuna dair zıt bildirimler mevcuttur. Günümüzde TRPM2 kanallarını doğrudan bloke eden kimyasal veya ilaç mevcut değildir.

Keywords

TRP channelsTRPM2 cation channelElectrophysiology

References

  • Akyol, O., Zoroglu, S.S., Armutcu, F., Sahin, S., Gurel, A. 2004. Nitric oxide as a physiopathological factor in neuropsychiatric disorders. In Vivo. 18, 377–390.
  • Altindag, O., Celik, H. 2006. Total antioxidant capacity and the severity of the pain in patients with fibromyalgia. Redox Rep. 11, 131-135.
  • Birnbaumer, L. 2009. The TRPC class of ion channels: a critical review of their roles in slow, sustained increases in intracellular Ca(2+) concentrations. Annu Rev. Pharmacol. Toxicol. 49, 395–426.
  • Clapham, D.E. 2003.TRP channels as cellular sensors. Nature. 426, 517-524.
  • Clapham, D.E. 2007. Snapshot: mammalian TRP channels. Cell. 129, 220.
  • Frei, B., England, L., Ames, B.N., 1989. Ascorbate is an outstanding antioxidant in human blood plasma. Proc. Natl. Acad. Sci. USA. 86, 6377-6381.
  • Gasser, A., Glassmeier, G., Fliegert, R., Langhorst, M.F., Meinke, S., Hein, D., Kruger, S., Weber, K., Heiner, I., Oppenheimer, N., Schwarz, J.R., Guse, A.H. 2006. Activation of T cell calcium influx by the second messenger ADP-ribose. J. Biol. Chem. 281, 2489–2496.
  • Halliwell, B. 2006. Oxidative stress and neurodegeneration: where are we now? J. Neurochem. 97, 16341658.
  • Hara, Y., Wakamori, M., Ishii, M., Maeno, E., Nishida, M., Yoshida, T., Yamada, H., Shimizu, S., Mori, E., Kudoh, J., Shimizu, N., Kurose, H., Okada, Y., Imoto, K., Mori, Y. 2002. LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death. Mol. Cell. 9, 163–73.
  • Heiner, I., Eisfeld, J., Warnstedt, M., Radukina, N., Jungling, E., Luckhoff, A. 2006. Endogenous ADP-ribose enables calcium-regulated cation currents through TRPM2 channels in neutrophil granulocytes. Biochem. J. 398, 225-232.
  • Kovacic, P., Somanathan, R. 2008. Unifying Mechanism for Eye Toxicity: Electron Transfer, Reactive Oxygen Species, Antioxidant Benefits, Cell Signaling and Cell Membranes. Cell Membr. Free Radic. Res. 2, 56–69.
  • Miller, B.A. 2006, The role of TRP channels in oxidative stress-induced cell death. J. Membr. Biol. 209, 3141.
  • Naziroglu, M. 2007. Molecular Mechanisms of vitamin E on intracellular signaling pathways in brain. In: Reactive Oxygen Species and Diseases. Ed.; Laszlo Goth, Research Signpost Press: Kerala, India. 239-256.
  • Naziroglu, M., Lückhoff, A. 2008. Effects of antioxidants on calcium influx through TRPM2 channels in transfected cells activated by hydrogen peroxide. J. Neurolog.Sci. 15, 152-158.
  • Naziroglu, M., Lückhoff, A. 2008. A calcium influx pathway regulated separately by oxidative stress and ADP- ribose in TRPM2 channels: Single channel events. Neurochem. Res. 33, 1256-1262.
  • Naziroglu, M. 2007. New molecular mechanisms on the activation of TRPM2 channels by oxidative stress and ADP-ribose. Neurochem. Res. 32, 1990-2001.
  • Nilius, B., Owsianik, G., Voets, T., Peters, J,A. 2007. Transient Receptor Potential cation channels in disease. Physiol. Rev. 87, 165–217.
  • Perraud, A.L., Fleig, A., Dunn, C.A., Bagley, L.A., Launay, P., Schmitz, C., Stokes, A.J., Zhu, Q., Bessman, M.J., Penner, R., Kinet, J.P., Scharenberg, A.M. 2001. ADP-ribose gating of the calcium-permeable LTRPC2 channel revealed by Nudix motif homology. Nature. 411, 595–599.
  • Perraud, A.L., Takanishi, C.L., Shen, B., Kang, S., Smith, M.K., Schmitz, C., Knowles, H.M., Ferraris, D., Li, W., Zhang, J., Stoddard, B.L., Scharenberg, A.M. 2005. Accumulation of free ADP-ribose from mitochondria mediates oxidative stress-induced gating of TRPM2 cation channels. J. Biol. Chem. 280, 6138–6148.
  • Rayman, M.P. 2000. The importance of selenium to human health. Lancet. 356, 233-241.
  • Szabo, C. 2005. Roles of poly (ADP-ribose) polymerase activation in the pathogenesis of diabetes mellitus and its complications. Pharmacol. Res. 52, 60–71.
  • Wehage, E., Eisfeld, J., Heiner, I., Jüngling, E., Zitt, C., Lückhoff, A. 2002. Activation of the cation channel long transient receptor potential channel 2 (LTRPC2) by hydrogen peroxide. A splice variant reveals a mode of activation independent of ADP- ribose. J. Biol. Chem. 277, 23150–23156.

Year 2010, Volume: 27 Issue: 2, 42 - 45, 21.01.2011

Mustafa Saygın , Mustafa Nazıroğlu

Abstract

References

  • Akyol, O., Zoroglu, S.S., Armutcu, F., Sahin, S., Gurel, A. 2004. Nitric oxide as a physiopathological factor in neuropsychiatric disorders. In Vivo. 18, 377–390.
  • Altindag, O., Celik, H. 2006. Total antioxidant capacity and the severity of the pain in patients with fibromyalgia. Redox Rep. 11, 131-135.
  • Birnbaumer, L. 2009. The TRPC class of ion channels: a critical review of their roles in slow, sustained increases in intracellular Ca(2+) concentrations. Annu Rev. Pharmacol. Toxicol. 49, 395–426.
  • Clapham, D.E. 2003.TRP channels as cellular sensors. Nature. 426, 517-524.
  • Clapham, D.E. 2007. Snapshot: mammalian TRP channels. Cell. 129, 220.
  • Frei, B., England, L., Ames, B.N., 1989. Ascorbate is an outstanding antioxidant in human blood plasma. Proc. Natl. Acad. Sci. USA. 86, 6377-6381.
  • Gasser, A., Glassmeier, G., Fliegert, R., Langhorst, M.F., Meinke, S., Hein, D., Kruger, S., Weber, K., Heiner, I., Oppenheimer, N., Schwarz, J.R., Guse, A.H. 2006. Activation of T cell calcium influx by the second messenger ADP-ribose. J. Biol. Chem. 281, 2489–2496.
  • Halliwell, B. 2006. Oxidative stress and neurodegeneration: where are we now? J. Neurochem. 97, 16341658.
  • Hara, Y., Wakamori, M., Ishii, M., Maeno, E., Nishida, M., Yoshida, T., Yamada, H., Shimizu, S., Mori, E., Kudoh, J., Shimizu, N., Kurose, H., Okada, Y., Imoto, K., Mori, Y. 2002. LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death. Mol. Cell. 9, 163–73.
  • Heiner, I., Eisfeld, J., Warnstedt, M., Radukina, N., Jungling, E., Luckhoff, A. 2006. Endogenous ADP-ribose enables calcium-regulated cation currents through TRPM2 channels in neutrophil granulocytes. Biochem. J. 398, 225-232.
  • Kovacic, P., Somanathan, R. 2008. Unifying Mechanism for Eye Toxicity: Electron Transfer, Reactive Oxygen Species, Antioxidant Benefits, Cell Signaling and Cell Membranes. Cell Membr. Free Radic. Res. 2, 56–69.
  • Miller, B.A. 2006, The role of TRP channels in oxidative stress-induced cell death. J. Membr. Biol. 209, 3141.
  • Naziroglu, M. 2007. Molecular Mechanisms of vitamin E on intracellular signaling pathways in brain. In: Reactive Oxygen Species and Diseases. Ed.; Laszlo Goth, Research Signpost Press: Kerala, India. 239-256.
  • Naziroglu, M., Lückhoff, A. 2008. Effects of antioxidants on calcium influx through TRPM2 channels in transfected cells activated by hydrogen peroxide. J. Neurolog.Sci. 15, 152-158.
  • Naziroglu, M., Lückhoff, A. 2008. A calcium influx pathway regulated separately by oxidative stress and ADP- ribose in TRPM2 channels: Single channel events. Neurochem. Res. 33, 1256-1262.
  • Naziroglu, M. 2007. New molecular mechanisms on the activation of TRPM2 channels by oxidative stress and ADP-ribose. Neurochem. Res. 32, 1990-2001.
  • Nilius, B., Owsianik, G., Voets, T., Peters, J,A. 2007. Transient Receptor Potential cation channels in disease. Physiol. Rev. 87, 165–217.
  • Perraud, A.L., Fleig, A., Dunn, C.A., Bagley, L.A., Launay, P., Schmitz, C., Stokes, A.J., Zhu, Q., Bessman, M.J., Penner, R., Kinet, J.P., Scharenberg, A.M. 2001. ADP-ribose gating of the calcium-permeable LTRPC2 channel revealed by Nudix motif homology. Nature. 411, 595–599.
  • Perraud, A.L., Takanishi, C.L., Shen, B., Kang, S., Smith, M.K., Schmitz, C., Knowles, H.M., Ferraris, D., Li, W., Zhang, J., Stoddard, B.L., Scharenberg, A.M. 2005. Accumulation of free ADP-ribose from mitochondria mediates oxidative stress-induced gating of TRPM2 cation channels. J. Biol. Chem. 280, 6138–6148.
  • Rayman, M.P. 2000. The importance of selenium to human health. Lancet. 356, 233-241.
  • Szabo, C. 2005. Roles of poly (ADP-ribose) polymerase activation in the pathogenesis of diabetes mellitus and its complications. Pharmacol. Res. 52, 60–71.
  • Wehage, E., Eisfeld, J., Heiner, I., Jüngling, E., Zitt, C., Lückhoff, A. 2002. Activation of the cation channel long transient receptor potential channel 2 (LTRPC2) by hydrogen peroxide. A splice variant reveals a mode of activation independent of ADP- ribose. J. Biol. Chem. 277, 23150–23156.
There are 22 citations in total.

Details

Primary Language TR
Journal Section Basic Medical Sciences
Authors

Mustafa Saygın

Mustafa Nazıroğlu

Publication Date January 21, 2011
Submission Date January 14, 2010
Published in Issue Year 2010 Volume: 27 Issue: 2

Cite

APA Saygın, M., & Nazıroğlu, M. (2011). TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler. Journal of Experimental and Clinical Medicine, 27(2), 42-45. https://doi.org/10.5835/jecm.v27i2.1139
AMA Saygın M, Nazıroğlu M. TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler. J. Exp. Clin. Med. January 2011;27(2):42-45. doi:10.5835/jecm.v27i2.1139
Chicago Saygın, Mustafa, and Mustafa Nazıroğlu. “TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler”. Journal of Experimental and Clinical Medicine 27, no. 2 (January 2011): 42-45. https://doi.org/10.5835/jecm.v27i2.1139.
EndNote Saygın M, Nazıroğlu M (January 1, 2011) TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler. Journal of Experimental and Clinical Medicine 27 2 42–45.
IEEE M. Saygın and M. Nazıroğlu, “TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler”, J. Exp. Clin. Med., vol. 27, no. 2, pp. 42–45, 2011, doi: 10.5835/jecm.v27i2.1139.
ISNAD Saygın, Mustafa - Nazıroğlu, Mustafa. “TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler”. Journal of Experimental and Clinical Medicine 27/2 (January 2011), 42-45. https://doi.org/10.5835/jecm.v27i2.1139.
JAMA Saygın M, Nazıroğlu M. TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler. J. Exp. Clin. Med. 2011;27:42–45.
MLA Saygın, Mustafa and Mustafa Nazıroğlu. “TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler”. Journal of Experimental and Clinical Medicine, vol. 27, no. 2, 2011, pp. 42-45, doi:10.5835/jecm.v27i2.1139.
Vancouver Saygın M, Nazıroğlu M. TRPM2 Katyon Kanallarının Aktivasyonunda Rol Oynayan Moleküler Mekanizmalardaki Son Gelişmeler. J. Exp. Clin. Med. 2011;27(2):42-5.
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