사람별아교세포주에서의 단백분해효소 활성 수용체-2를 매개한 TNF-alpha의 분비
Secretion of TNF-alpha via Proteinase-Activated Receptor-2 in Human Astrocyte Cell Line
김미선, 김진아, 강옥화, 백옥선, 엄재영, 이진무, 윤기중, 김형민, 이영미,
소속 상세정보
김미선 ( Kim Mi-Sun )
원광대학교 약학대학 한약학과
김진아 ( Kim Jin-Ah )
원광대학교 약학대학 한약학과
강옥화 ( Kang Ok-Hwa )
원광대학교 약학대학 한약학과
백옥선 ( Baek Ok-Seon )
원광대학교 약학대학 한약학과
엄재영 ( Um Jae-Young )
원광대학교 약학대학 한약학과
이진무 ( Yi Jin-Mu )
원광대학교 약학대학 한약학과
윤기중 ( Yun Ki-Jung )
원광대학교 의과대학 병리학교실
김형민 ( Kim Hyung-Min )
원광대학교 약학대학 한약학과
이영미 ( Lee Young-Mi )
원광대학교 약학대학 한약학과
KMID : 0357920030370030159
Abstract
Background: Proteinase-activated receptor 2 (PAR2) is cleaved, and it is activated by trypsin or mast cell tryptase. PAR2 plays an important role in inflammation. The aim of this study is to examine the potential of PAR2 agonists to modulate TNF-alpha secretion from the human astrocytoma cell line CCF-STTG1.
Methods: PAR2 expression in CCF-STTG1 was examined using reverse transcriptase polymerase chain reaction and immunocytochemistry. The potential of PAR2 agonists to modulate TNF-alpha secretion from CCF-STTG1 was examined by enzyme-linked immunosorbent assays.
Results: CCF-STTG1 expresses PAR2. PAR2 agonists such as trypsin, mast cell tryptase, and activating peptide SLIGKV-NH2 (corresponding to the PAR2 tethered ligand) directly signal CCF-STTG1 to induce the secretion of TNF-alpha, but not in the case of the soybean trypsin inhibitor (SBTI) or VKGILS-NH(2) (control peptide). Furthermore, the secretion of TNF-alpha was significantly reduced in CCF-STTG1 cells pre-treated with either 50 micro M PD98059 (mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) inhibitor) or 1 micro M SB203580 (p38 MAPK inhibitor) 30 min before trypsin stimulation.
Conclusion: These results show that trypsin may induce TNF-alpha secretion through the activation of MEK and p38 MAPK via PAR2 in astrocytoma cell line CCF-STTG1.
키워드
Proteinase;Activated Receptor 2;Trypsin;Tumor Necrosis Factor;alpha-Cytokines;Astrocytoma Cell Line
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