Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0381920060360030165
Korean Journal of Microscopy
2006 Volume.36 No. 3 p.165 ~ p.172
Increased Protein of the Secretory Leukocyte Protease Inhibitor (SLPI) and the Expression of Growth Factors in NIH3T3 Cells by LPS Stimulation
Lee Sang-Hwa

Kim Byung-Ok
Jeong Moon-Jin
Park Ju-Cheol
Jeong Soon-Jeong
Lim Do-Seon
Choi Baik-Dong
Jang Hyun-Seon
Wang Guan-lin
Abstract
Secretory leukocyte protease inhibitor (SLPI) involves tissue protection against the destructive action of neutrophil elastase at the site of inflammation. Several studies on new functions of SLPI have demonstrated that SLPI may play a primary role in innate immunity than protease inhibitor. To identify the function of SLPI by lipopolysaccharide (LPS) stimulation in the embryonic fibroblast (NIH3T3) cells, we studied the expression of SLPI compared to other growth factors involving the LPS treatment. To address this, we performed the reverse transcriptase polymerase chain reaction (RT-PCR) and Western blots for the detection of mRNA and protein expression of the SLPI and some growth factors such as VEGF, bFGF, and PDGF-BB after LPS stimulation. NIH3T3 cells were exposed 100 ng/mL Escherichia coli LPS for 30 min, 60 min, 90 min, 24 h, and 48 h, respectively. The result of RT-PCR showed that SLPI and VEGF mRNA was expressed strongly in NIH3T3 without related to LPS stimulation. mRNA of bFGF was weakly expressed such as the expression of the control. PDGF mRNA expression gradually increased follows at time course. However, SLPI protein level was increased in lysates and culture medium by LPS stimulation. Phase contrast microscopic and scanning electron microscopic observation showed that the increased cell number and cytoplasmic enlargement of the NIH3T3 cells. Therefore, it suggests that the LPS upregulates SLPI expression in NIH3T3 cells. Moreover, secreted SLPI may stimulate cell proliferation and migration.
KEYWORD
Growth factors, Lipopolysaccharide, NIH3T3, Secretory leukocyte protease inhibitor (SLPI)
FullTexts / Linksout information
 
Listed journal information
ÇмúÁøÈïÀç´Ü(KCI)