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.
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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.
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© 2013 Springer-Verlag Wien
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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
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DOI: https://doi.org/10.1007/978-3-7091-1434-6_31
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