Skip to main content

Alteration of Intracellular Calcium and Its Modulator SLC24A6 After Experimental Intracerebral Hemorrhage

  • Conference paper
  • First Online:

Part of the book series: Acta Neurochirurgica Supplement ((NEUROCHIRURGICA,volume 118))

Abstract

Intracerebral hemorrhage (ICH) can lead to tragic disability and mortality. Accumulating evidence has shown that sodium calcium exchanger (NCX) may contribute to the secondary injury of a stroke. Recently, a novel member of NCX, SLC24A6, was discovered with knowledge of its abundant distribution in brain. In the present study, we examined the time course of expression of SLC24A6 and its mediated intracellular calcium concentration ([Ca2+]i) to investigate its potential roles in brain damage after ICH. An ICH model was established as previously reported. Real-time PCR and Western blotting were used to test the mRNA and protein levels of SLC24A6 on the hemorrhagic side and on the contralateral side caudate nucleus tissues at 6 h, and on days 1, 3, 5, and 7 after ICH. Immunohistochemistry was used to analyze the morphological changes. Fura-2/AM loaded, dual wavelength spectrophotofluorometry was used to test [Ca2+]i. The data presented a remarkable decrease in SLC24A6 early after ICH, along with a comparable increase in [Ca2+]i. Our results indicated that SLC24A6 presents specific and remarkable alterations in both mRNA and protein levels after ICH. Decreases in SLC24A6 level were correlated with [Ca2+]i elevation. These data suggest that SLC24A6-mediated calcium overload plays an important role in brain damage after ICH.

This is a preview of subscription content, log in via an institution.

Buying options

Chapter
USD   29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD   169.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD   279.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD   219.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Learn about institutional subscriptions

References

  1. Bano D, Young KW, Guerin CJ et al (2005) Cleavage of the plasma membrane Na/Ca2+ exchanger in excitotoxicity. Cell 120:275–285

    Article  PubMed  CAS  Google Scholar 

  2. Bano D, Nicotera P (2007) Ca2+ signals and neuronal death in brain ischemia. Stroke 38(2 Suppl):674–676

    Article  PubMed  CAS  Google Scholar 

  3. Cai XJ, Lytton J (2004) Molecular cloning of a sixth member of the K+-dependent Na+/Ca2+ exchanger gene family, NCKX6. J Biol Chem 279(7):5867–5876, 1999, 30(2):1167–1173

    Article  PubMed  CAS  Google Scholar 

  4. Cuomo O, Gala R, Pignataro G et al (2008) A critical role for the potassium-dependent sodium-calcium exchanger NCKX2 in protection against focal ischemic brain damage. J Neurosci 28(9):2053–2063

    Article  PubMed  CAS  Google Scholar 

  5. Gong Y, Xi GH, Keep RF et al (2005) Complement inhibition attenuates brain edema and neurological deficits induced by thrombin. Acta Neurochir Suppl 95:389–392

    Article  PubMed  CAS  Google Scholar 

  6. Gong Y, Xi GH et al (2008) Increase in brain thrombin activity after experimental intracerebral hemorrhage. Acta Neurochir Suppl 105:47–50

    Article  PubMed  CAS  Google Scholar 

  7. Matsuda T, Arakawa N, Takuma K et al (2001) SEA0400, a novel and selective inhibitor of the Na+-Ca2+ exchanger, attenuates reperfusion injury in the in vitro and in vivo cerebral ischemic models. J Pharmacol Exp Ther 298(1):249–256

    PubMed  CAS  Google Scholar 

  8. Palty R, Ohana E, Hershfinkel M et al (2004) Lithium-calcium exchange is mediated by a distinct potassium-independent sodium-calcium exchanger. J Biol Chem 279(24):25234–25240

    Article  PubMed  CAS  Google Scholar 

  9. Xi G, Hua Y, Bhasin RR (2001) Mechanisms of edema formation after intracerebral hemorrhage, effects of extravasated red blood cells on blood flow and blood-brain barrier integrity. Stroke 32(12):2932–2938

    Article  PubMed  CAS  Google Scholar 

  10. Zazulia AR, Diringer MN, Derdeny CP et al (1999) Progression of mass effect after intracerebral hemorrhage. Stroke 30(6):1167–1173

    Article  PubMed  CAS  Google Scholar 

  11. Zhang X, Li H, Hu S et al (2006) Brain edema after intracerebral hemorrhage in rats: the role of inflammation. Neurol India 54(4):402–407

    Article  PubMed  Google Scholar 

Download references

Acknowledgments

This study was supported by Grant No. 08411965100 from the Science and Technology Commission of Shanghai Municipality, and Grant Nos. 30872675 and 30901549 from the National Natural Science Foundation of China.

Conflict of InterestWe declare that we have no conflict of interest.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Ye Gong .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2013 Springer-Verlag Wien

About this paper

Cite this paper

Zheng, M. et al. (2013). Alteration of Intracellular Calcium and Its Modulator SLC24A6 After Experimental Intracerebral Hemorrhage. In: Katayama, Y., Maeda, T., Kuroiwa, T. (eds) Brain Edema XV. Acta Neurochirurgica Supplement, vol 118. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1434-6_31

Download citation

  • DOI: https://doi.org/10.1007/978-3-7091-1434-6_31

  • Published:

  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-7091-1433-9

  • Online ISBN: 978-3-7091-1434-6

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics