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Immediately transcripted genes in various hepatic ischemia models

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ÃÖ°­±¹ ( Choi Kang-Kook ) 
Sungkyunkwan University School of Medicine Samsung Medical Center Department of Surgery

Á¶Áø¾Æ ( Cho Jin-A ) 
Gachon University of Medicine and Science Department of Surgery
±è¼¼ÈÆ ( Kim Se-Hoon ) 
Yonsei University College of Medicine Department of Pathology
ÀÌ»ó¿ì ( Lee Sang-Woo ) 
Yonsei University College of Medicine Department of Surgery
¹Î¼±¿Á ( Min Seon-Ok ) 
Yonsei University College of Medicine Department of Surgery
±è°æ½Ä ( Kim Kyung-Sik ) 
Yonsei University College of Medicine Department of Surgery

Abstract


Purpose: To elucidate the characteristic gene transcription profiles among various hepatic ischemia conditions, immediately transcribed genes and the degree of ischemic injury were compared among total ischemia (TI), intermittent clamping (IC), and ischemic preconditioning (IPC).

Methods: Sprague-Dawley rats were equally divided into control (C, sham-operated), TI (ischemia for 90 minutes), IC (ischemia for 15 minutes and reperfusion for 5 minutes, repeated six times), and IPC (ischemia for 15 minutes, reperfusion for 5 minutes, and ischemia again for 90 minutes) groups. A cDNA microarray analysis was performed using hepatic tissues obtained by partial hepatectomy after occluding hepatic inflow.

Results: The cDNA microarray revealed the following: interleukin (IL)-1¥â expression was 2-fold greater in the TI group than in the C group. In the IC group, IL-1¥á/¥â expression increased by 2.5-fold, and Na+/K+ ATPase ¥â1 expression decreased by 2.4-fold. In the IPC group, interferon regulatory factor-1, osteoprotegerin, and retinoblastoma-1 expression increased by approximately 2-fold compared to that in the C group, but the expression of Na+/K+ ATPase ¥â1 decreased 3-fold.

Conclusion: The current findings revealed characteristic gene expression profiles under various ischemic conditions. However, additional studies are needed to clarify the mechanism of protection against IPC.

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Reperfusion injury; Ischemic preconditioning; Necrosis; Apoptosis; Microarray analysis

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