뇌 염증 반응에서 phosphatidylinositol 4-phosphat 5-kinases 의 조절 기능

Alternative Title
Regulatory role of phosphatidylinositol 4-phosphate 5-kinases in brain inflammation
Author(s)
Kim Bo Kyoung
Alternative Author(s)
Bo Kyoung Kim
Advisor
주일로, 이상윤
Department
일반대학원 의생명과학과
Publisher
The Graduate School, Ajou University
Publication Year
2010-08
Language
eng
Keyword
PIP5KIPI(45)P2astrocyteGmixbrain inflammaion
Alternative Abstract
Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], mainly produced by the type I phosphatidylinositol 4-phosphate 5-kinase (PIP5KI) family members, PIP5KIα, PIP5KIβ and PIP5KIγ, is an important regulator of diverse cellular processes at the cell surface, such as cell survival, cell proliferation, phagocytosis, macropinocytosis membraned ruffles, ion channels transporters, cytoskeletal regulation and intracellular vesicle trafficking. Recently, it was reported that PI(4,5)P2 was important for neurodegenerative diseases. Nevertheless, expression and regulatory role of PIP5KIs in rat primary glia cell remain poorly understood. This present study has shown that PIP5KIα and PIP5KIγ are significantly upregulated in response to ganglioside mixture (Gmix) and lipopolysaccharide that are well known inflammatory stimulators. c-Jun N-terminal Kinase, phosphoinositide 3-kinase/Akt and extracellular signal-regulated kinase signaling pathways were responsible for the upregulation of PIP5KIα and PIP5KIγ. In addition, we have examined whether gene knockdown of PIP5KIα plays a role in the nuclear factor kappa B (NF-κB) signaling pathway. We found that PIP5KIα knockdown could inhibit the phosphorylation of NF-κB p65 in response to Gmix, leading to decrease in Gmix-induced proinflammatory cytokines, tumor necrosis factor α and interleukin-1β.These results suggest that PIP5KIα may act as a regulator of brain inflammation by modulating NF-κB signaling.
URI
https://dspace.ajou.ac.kr/handle/2018.oak/17612
Fulltext

Appears in Collections:
Graduate School of Ajou University > Department of Biomedical Sciences > 3. Theses(Master)
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse