Tumor necrosis factor-alpha inhibits expression of pulmonary surfactant protein.

Tumor necrosis factor-alpha inhibits expression of pulmonary surfactant protein.
复制标题

肿瘤坏死因子-α 抑制肺表面活性蛋白的表达。

DOI:
10.1172/jci114929
复制
发表时间:
1990
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Whitsett,JA
Whitsett,JA
中科院分区:
--
文献类型:
--
作者:
Wispe,JR;Clark,JC;Warner,BB;Fajardo,D;Hull,WE;Holtzman,RB;Whitsett,JA

文献摘要

参考文献

被引文献

相似文献

肿瘤坏死因子- α (tnf - α)降低肺表面活性蛋白SP-A和SP-B在人肺腺癌细胞中的表达。TNF α对肺腺癌细胞H441-4中SP-A含量和mRNA的影响具有浓度和时间依赖性。TNF α使SP-A的细胞含量降低至对照组的10%以下。TNF - α降低SP-A的新生合成,减少SP-A在培养基中的积累。SP-A mRNA在加入TNF α后12 h内减少,24 h后SP-A mRNA几乎完全丧失。TNF α对SP-A mRNA的抑制作用与25 ng/ml TNF α对SP-A mRNA的几乎完全抑制呈剂量相关。TNF α对SP-A的作用与干扰素γ的作用不同,干扰素γ使H441-4细胞中SP-A含量增加约两倍。TNF α也降低SP-B mRNA的含量。与TNF α对SP-A和SP-B mRNA的抑制作用相反,TNF α增加了编码人锰超氧化物歧化酶(Mn-SOD)的mRNA。TNF α在两种细胞系中均未抑制生长、改变细胞活力或β -肌动蛋白mRNA。这些体外研究表明,细胞因子TNF α对肺表面活性蛋白SP-A和SP-B的表达具有显著的翻译前抑制作用。结果支持巨噬细胞来源的细胞因子可能控制表面活性剂蛋白表达的概念。图片
Tumor necrosis factor-alpha (TNF-alpha) decreased the expression of pulmonary surfactant proteins SP-A and SP-B in human pulmonary adenocarcinoma cell lines. The effect of TNF alpha on SP-A content and mRNA in the pulmonary adenocarcinoma cell line, H441-4, was concentration and time dependent. TNF alpha decreased the cellular content of SP-A to less than 10% of control 48 h after addition. TNF alpha decreased de novo synthesis of SP-A and decreased the accumulation of SP-A in media. SP-A mRNA was decreased within 12 h of addition of TNF alpha, with nearly complete loss of SP-A mRNA observed after 24 h. Inhibitory effects of TNF alpha on SP-A mRNA were dose-related with nearly complete inhibition of SP-A mRNA caused by 25 ng/ml TNF alpha. The effects of TNF alpha on SP-A were distinct from the effects of interferon gamma which increased SP-A content approximately twofold in H441-4 cells. TNF alpha also decreased the content of SP-B mRNA. In contrast to the inhibitory effect of TNF alpha on SP-A and SP-B mRNA, TNF alpha increased mRNA encoding human manganese superoxide dismutase (Mn-SOD). TNF alpha did not inhibit growth, alter cell viability or beta-actin mRNA in either cell line. These in vitro studies demonstrate the marked pretranslational inhibitory effects of the cytokine, TNF alpha, on the expression of pulmonary surfactant proteins, SP-A and SP-B. The results support the concept that macrophage-derived cytokines may control surfactant protein expression.Images
正常和恶性 T 细胞中 T 细胞抗原受体的基因。
DOI: --
发表时间: 1987
影响因子: 29.7
作者:
B. Toyonaga;T. Mak
通讯作者: T. Mak
DOI: 10.1002/eji.1830160706
发表时间: 1986-07-01
影响因子: 5.4
作者:
LYNCH, DH;COLE, BC;HODES, RJ
通讯作者: HODES, RJ
葡萄球菌肠毒素 B 诱导正常淋巴细胞释放巨噬细胞迁移抑制因子。
DOI: --
发表时间: 1972
影响因子: 4.3
作者:
J. Kaplan
通讯作者: J. Kaplan
DOI: 10.1038/333858a0
发表时间: 1988-06-30
期刊: NATURE
影响因子: 64.8
作者:
CHELLY, J;KAPLAN, JC;KAHN, A
通讯作者: KAHN, A
DOI: --
发表时间: 1988
影响因子: 4.4
作者:
R. Abe;R. Hodes
通讯作者: R. Hodes