http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Wagley, Yadav (검색결과 4 건)
- 무료
- 기관 내 무료
- 유료
-
-
-
Yadav Wagley,Jae-Wook Oh(오재욱) 대한체질인류학회 2008 대한체질인류학회지 Vol.21 No.3
중추신경계에서 교세포의 대다수를 차지하는 Astrocytes는, 사이토카인 TNF-α 등의 자극으로 여러 혈관 세포유착인자들 중, vascular cell adhesion molecule-l (VCAM-l)의 발현을 증가시킨다. 이렇게 증가된 YCAM-l의 발현은 중추신경계의 염증과정에서 중요한 역할을 수행한다. Astrocyte cells 이 apo E 등을 포함하는 HDL-like lipoprotein particles을 분비함이 최근에 밝혀졌기 때문에, 우리는 astroglioma 세포를 가지고 YCAM-1 발현변화에 초점을 두고 인체 혈장에서 분리된 HDL, YLDL 그리고 LDL 등 다른 lipoproteins들의 YCAM-l 발현 조절 가능성을 조사하였다. Astroglioma세포에 VLDL, LDL 그리고 HDL등의 단독처리는 VCAM-l 발현변화에 아무런 영향이 없었다. 그러나 Astroglioma세포에서 HDL이 흥미롭게도 농도의존성으로 TNF-α에 의해 증가된 VCAM-1 발현을 억제시켰다. 그러나 비슷한 구조를 갖는 VLDL, LDL은 이러한 억제성을 보여주질 못했다. 특이성 실험에서, TNF-α에 의해 증가된 VCAM-1 발현에 대한 HDL억제성은 HDL의 주요 apolipoprotein 구성원인 Apo A-1 항체의 전처리로 언해 다시 증가됨을 확인하였다. 이는 곧 HDL의 Apo A-1이 이러한 억제기능에 중요한 역할이 있음을 의미한다. 게다가 Reconstituted HDL (apo HDL과 DMPC의 discoidal complexes) 또한 VCAM-1 발현증가를 억제함을 알 수 있었다. RNase protection assay (RPA) 실험에서, TNF-α에 의해 증가된 VCAM-l mRNA 발현증가 역시 HDL에 의해 억제되었다. 이러한 결과들은 질환상태의 중추신경계에서 HDL-like particles이 면역억제기능을 수행할 수 있음을 제시한다. Astrocytes, the major glial cells in the central nervous system (CNS), can express vascular cell adhesion molecule-l (YCAM-l) in response to cytokines, such as TNF-a. In CNS, an increased YCAM-l expression may contribute to inflammatory processes. We, in the present study, have examined the effect of human plasma High Density Lipoproteins (HDL) and other lipoproteins on YCAM-l expression in astroglioma cells since astrocytes secrete HDL-like lipoprotein particles which contain apo E and cholesterol, phospholipid. The exposure of astroglioma cells to the major plasma lipoprotein fractions (YLDL, LDL and HDL) had no effect on the YCAM-l expression. However, TNF-a-induced YCAM-l was inhibited by HDL in a dose-dependent manner, but not by YLDL or LDL. The inhibitory effect of HDL on TNF-α-induced YCAM-l was reversed by the inclusion of Apo A-I antibody, the major apolipoprotein of HDL, demonstrating the specificity of this response. Reconstituted HDL (discoidal complex of apo HDL and DMPC), but not apo HDL or DMPC, was effective in suppressing the YCAM-l expression. RNase protection assay (RPA) revealed that TNF-ainduced YCAM-l mRNA expression was markedly inhibited by HDL (500㎍ cholesterol/㎖). These results indicate that HDL-like particles in the CNS may function as an immunosuppressive molecule in pathologic conditions of CNS.
-
Endale, Mehari,Kim, Sung Dae,Lee, Whi Min,Kim, Sangseop,Suk, Kyoungho,Cho, Jae Youl,Park, Hwa Jin,Wagley, Yadav,Kim, Suk,Oh, Jae-Wook,Rhee, Man Hee American Physiological Society 2010 American journal of physiology. Cell physiology Vol.298 No.3
<P>Regulator of G protein signaling (RGS) family members, such as RGS2, interact with Gα subunits of heterotrimeric G proteins, accelerating the rate of GTP hydrolysis and attenuating the intracellular signaling triggered by the G protein-coupled receptor-ligand interaction. They are also reported to regulate G protein-effector interactions and form multiprotein signaling complexes. Ischemic stress-induced changes in RGS2 expression have been described in astrocytes, and these changes are associated with intracellular signaling cascades, suggesting that RGS2 upregulation may be an important mechanism by which astrocytes may regulate RGS2 function in response to physiological stress. However, information on the functional roles of stress-induced modulation of RGS2 protein expression in astrocyte function is limited. We report the role of ischemic stress in RGS2 protein expression in rat C6 astrocytoma cells and primary mouse astrocytes. A marked increase in RGS2 occurred after ischemic stress induced by chemicals (sodium azide and 2-deoxyglucose) or oxygen-glucose deprivation (OGD, real ischemia). RGS2 mRNA expression was markedly enhanced by 1 h of exposure to chemical ischemia or 6 h of OGD followed by 2 or 6 h of recovery, respectively. This enhanced expression in primary astrocytes and C6 cells was restored to baseline levels after 12 h of recovery from chemically induced ischemic stress or 4-6 h of recovery from OGD. RGS2 protein was also significantly expressed at 12-24 h of recovery from ischemic insult. Ischemia-induced RGS2 upregulation was associated with enhanced apoptosis. It significantly increased annexin V-positive cells, cleaved caspase-3, and enhanced DNA ladder formation and cell cycle arrest. However, a small interfering RNA (siRNA)-mediated RGS2 knockdown reversed the apoptotic cell death associated with ischemia-induced RGS2 upregulation. Upregulated RGS2 was significantly inhibited by SB-203580, a p38 MAPK inhibitor. Rottlerin, a potent inhibitor of PKCδ, completely abrogated the increased RGS2 expression. We also examine whether ischemia-induced RGS2-mediated apoptosis is affected by siRNA-targeted endogenous PKCδ downregulation or its phosphorylation. Although RGS2 upregulation was not affected, siRNA transfection significantly suppressed endogenous PKCδ mRNA and protein expressions. Ischemia-induced PKCδ phosphorylation and caspase-3 cleavage were dose dependently inhibited by PKCδ knockdown, and this endogenous PKCδ suppression reversed ischemia-induced annexin V-positive cells. This study suggests that ischemic stress increases RGS2 expression and that this condition contributes to enhanced apoptosis in C6 cells and primary astrocytes. The signaling it follows may involve PKCδ and p38 MAPK pathways.</P>
KCI연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
