Induction of lipopolysaccharide-binding protein gene expression in cultured rat pulmonary artery smooth muscle cells by interleukin 1 beta.
Induction of lipopolysaccharide-binding protein gene expression in cultured rat pulmonary artery smooth muscle cells by interleukin 1 beta.
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白细胞介素1β诱导培养的大鼠肺动脉平滑肌细胞中脂多糖结合蛋白基因的表达。
DOI:
10.1165/ajrcmb.12.4.7695925
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发表时间:
1995
期刊:
影响因子:
--
通讯作者:
Wang,SC
中科院分区:
文献类型:
--
作者:
Wong,HR;Pitt,BR;Su,GL;Rossignol,DP;Steve,AR;Billiar,TR;Wang,SC
Lipopolysaccharide (LPS)-binding protein (LBP) binds with high affinity to LPS, and the LBP-LPS complex enhances cellular inflammatory responses to LPS. Although it is present in normal serum, LBP is also induced as part of the acute phase response. Synthesis of LBP is though to be limited to the liver, but we have recently reported significant extrahepatic (including pulmonary) LBP mRNA expression in in vivo rat models of sepsis and inflammation. In the present study, we tested the hypothesis that a cellular source of pulmonary LBP in the rat may be vascular smooth muscle, by exposing cultured rat pulmonary artery smooth muscle cells (RPASMC) to cytokines and LPS. Treatment of RPASMC for 4 and 24 h with a combination of tumor necrosis factor alpha, interleukin 1 beta (IL-1 beta), interferon gamma, and LPS resulted in significant LBP mRNA expression. Of this mixture, IL-1 beta alone was sufficient to induce LBP mRNA expression in both a time- and dose-dependent manner. The effects of IL-beta on LBP mRNA expression were significantly antagonized by IL-1 receptor antagonist protein. Furthermore, supernatants from RPASMC treated with IL-1 beta enhanced the binding of [125I]ASD-LPS by the macrophage cell line RAW 264.7, indicative of LBP bioactivity. We conclude that pulmonary artery smooth muscle cells stimulated with IL-1 beta produce a transcript for LBP or a homologous product in vitro. Local production of LBP could play an important role in the pulmonary response to inflammation and sepsis.
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DOI:
10.1165/ajrcmb/7.3.239
发表时间:
1992-09
影响因子:
6.4
作者:
P. Tobias;J. Mathison;Douglas N. Mintz;J. D. Lee;V. Kravchenko;K. Kato;J. Pugin;R. Ulevitch
通讯作者:
P. Tobias;J. Mathison;Douglas N. Mintz;J. D. Lee;V. Kravchenko;K. Kato;J. Pugin;R. Ulevitch
影响因子:
56.9
作者:
SCHUMANN, RR;LEONG, SR;ULEVITCH, RJ
通讯作者:
ULEVITCH, RJ
DOI:
--
发表时间:
1992
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Mathison,JC;Tobias,PS;Wolfson,E;Ulevitch,RJ
通讯作者:
Ulevitch,RJ
影响因子:
4.4
作者:
G. Su;P. Freeswick;D. Geller;Qi Wang;R. Shapiro;Y. Wan;T. Billiar;D. Tweardy;R. L. Simmons
通讯作者:
G. Su;P. Freeswick;D. Geller;Qi Wang;R. Shapiro;Y. Wan;T. Billiar;D. Tweardy;R. L. Simmons
DOI:
--
发表时间:
1990
期刊:
The Journal of trauma
影响因子:
--
作者:
Ulevitch,RJ;Mathison,JC;Schumann,RR;Tobias,PS
通讯作者:
Tobias,PS