Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

¸ð·¡ÁãÀÇ ÀÏ°ú¼º Àü³ú ÇãÇ÷ ÈÄ Çظ¶ÀÇ c-fos, p53, Transforming Growth Factor-¥â1, Glial Fibrillary Acidic ProteinÀÇ ¹ßÇö Expression of c-fos, p53, Transforming Growth Factor-¥â1 and Glial Fibrillary Acidic Protein in Hippocampus Following Transient Forebrain Ischemia in Mongolian Gerbil

´ëÇѺ´¸®ÇÐȸÁö 2001³â 35±Ç 1È£ p.60 ~ 70
ÀÌÀçÈ­, Çã¹æ,
¼Ò¼Ó »ó¼¼Á¤º¸
ÀÌÀçÈ­ ( Lee Jae-Hwa ) 
°í½Å´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç

Çã¹æ ( Huh Bang ) 
°í½Å´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç

Abstract


Background: Recent studies have shown that delayed neuronal death is closely associated with early gene (c-fos or c-jun)-related apoptosis in addition to hypoxia-induced energy deficiency in the hippocampus.

Methods: To elucidate the role of c-fos, p53, TGF- 1 and glial fibrillary acidic protein (GFAP) and their interactions, cellular expression with immunohistochemistry was examined during the time period of 10-minute hypoxia with variable reperfusion intervals in the mongolian gerbil hippocampus.

Results: Hippocampal CA1 shows progressive and delayed neuronal damage beginning from the 24-hour reperfusion, while CA2-3 reveals non-progressive, eosinophilic inclusion body within the neuron throughout the time period. CA1 neurons show short-term expressions of c-fos prior to significant cellular damage. However, CA2-3 neurons show persistent expressions by 3-day reperfusion. In both CA1 and CA2-3, p53 is expressed for the short-term period of the early time points. However, its intensity and duration are much less in CA2-3 than in CA1. While TGF- 1 is transiently expressed at 24-hour reperfusion in CA1, its expression in CA2-3 is persistent in late time points. Early expression of GFAP is observed in the pyramidal layer of CA1 prior to neuronal damage and progressively increased in the late time points.

Conclusion: These results suggest that c-fos and TGF- 1 may play a role in neuronal viability in the early- and late time points. Astrocytes may also be responsible for the active protective mechanism to neuronal death, as well as reactive gliosis. The hypoxia-induced neuronal damage is, in part, a p53- dependent process in the CA1 neurons.

Å°¿öµå

Hippocampus;c-fos;p53;Transforming growth factor-¥â1;Glial fibrillary acidic protein

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

  

µîÀçÀú³Î Á¤º¸

KCI
KoreaMed
KAMS