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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Masahiro Sakurai Permission Requests Citing Articles Citing Articles via HighWire Google Scholar Articles by Sakurai, M. PubMed Articles by Sakurai, M. Related Collections Cerebral protection

Letters to the Editor

Which cell does apoptosis induce?

Department of Cardiovascular Surgery, National Hospital Organization Sendai Medical Center, 2-8-8, Miyagino, Miyagino-ku, Sendai 983-8520, Japan

Received 30 April 2009; accepted 5 June 2009.

^_* Corresponding author. Tel.: +81 22 293 1111; fax: +81 22 291 8114. (Email: sakuraim{at}snh.go.jp).

Key Words: Cell damage • Temporal profile

We read with interest the article by Pastuszko and associates titled ‘The effect of hypothermia on neuronal viability following cardiopulmonary bypass and circulatory arrest in newborn piglets’ [1]. We agree that the protection by hypothermia was observed in the striatum by decreasing the expression of Bax and caspase3. However, it is unclear whether each of these protein was induced in the neurons. In the experimental model of brain protection, the main concern has been the selective vulnerability of neurons. Therefore, a histological study is important and some researchers have counted the number of neurons following ischaemia [2,3]. In addition, the authors have described only the results of the Western blot analysis. However, there are several components in the central nervous system, such as the neurone, glia and vessels. Yanagisawa et al. demonstrated the protective effects of DJ1 following brain ischaemia with temporal profiles of nytrotyrosine [2]. Furthermore, our previous report has demonstrated that local cooling enhanced and prolonged the HSP72 protein levels in motor neurons, and saved the neuronal cells from lethal ischaemia [3]. Both quantitative and qualitative analyses are essential for evaluating brain damage. Therefore, the authors should demonstrate the temporal profiles of Bax, caspase3 and Bcl2 in histochemical study or in an in situ hybridisation study.

References

1. Pastuszko P, Pirzadeh A, Reade E, Kubin J, Mendoza A, Schears GJ, Greeley WJ, Pastuszko A. The effect of hypothermia on neuronal viability following cardiopulmonary bypass and circulatory arrest in newborn piglets. Eur J Cardiothorac Surg 2009;35:577-581.[Abstract/Free Full Text]
2. Yanagisawa D, Kitamura Y, Inden M, Takata K, Taniguchi T, Morikawa S, Morita M, Inubushi T, Tooyama I, Taira T, Iguchi-Ariga SM, Akaie A, Ariga H. DJ-1 protects against neurodegeneration caused by focal cerebral ischemia and reperfusion in rats. J Cereb Blood Flow Metab 2008;28:563-578.[CrossRef][Medline]
3. Motoyoshi N, Sakurai M, Hayashi T, Aoki M, Abe K, Itoyama Y, Tabayashi K. Establishment of local cooling model against spinal cord ischemia representing prolonged heat shock protein induction. J Thorac Cardiovasc Surg 2001;122:351-357.[Abstract/Free Full Text]

This article has been cited by other articles:

				P. Pastuszko, W. J. Greeley, D. F. Wilson, and A. Pastuszko Reply to Sakurai. Brain injury in cardiopulmonary bypass surgery Eur. J. Cardiothorac. Surg., October 1, 2009; 36(4): 782 - 783. [Full Text] [PDF]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Masahiro Sakurai Permission Requests Citing Articles Citing Articles via HighWire Google Scholar Articles by Sakurai, M. PubMed Articles by Sakurai, M. Related Collections Cerebral protection