Reduced IL-10 production in fetal type II epithelial cells exposed to mechanical stretch is mediated via activation of IL-6-SOCS3 signaling pathway.
Reduced IL-10 production in fetal type II epithelial cells exposed to mechanical stretch is mediated via activation of IL-6-SOCS3 signaling pathway.
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DOI：
10.1371/journal.pone.0059598
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Sanchez-Esteban J
中科院分区：
文献类型：
--
作者：
Hokenson MA;Wang Y;Hawwa RL;Huang Z;Sharma S;Sanchez-Esteban J
An imbalance between pro-inflammatory and anti-inflammatory cytokines is a key factor in the lung injury of premature infants exposed to mechanical ventilation. Previous studies have shown that lung cells exposed to stretch produces reduced amounts of the anti-inflammatory cytokine IL-10. The objective of these studies was to analyze the signaling mechanisms responsible for the decreased IL-10 production in fetal type II cells exposed to mechanical stretch. Fetal mouse type II epithelial cells isolated at embryonic day 18 were exposed to 20% stretch to simulate lung injury. We show that IL-10 receptor gene expression increased with gestational age. Mechanical stretch decreased not only IL-10 receptor gene expression but also IL-10 secretion. In contrast, mechanical stretch increased release of IL-6. We then investigated IL-10 signaling pathway-associated proteins and found that in wild-type cells, mechanical stretch decreased activation of JAK1 and TYK2 and increased STAT3 and SOCS3 activation. However, opposite effects were found in cells isolated from IL-10 knockout mice. Reduction in IL-6 secretion by stretch was observed in cells isolated from IL-10 null mice. To support the idea that stretch-induced SOCS3 expression via IL-6 leads to reduced IL-10 expression, siRNA-mediated inhibition of SOCS3 restored IL-10 secretion in cells exposed to stretch and decreased IL-6 secretion. Taken together, these studies suggest that the inhibitory effect of mechanical stretch on IL-10 secretion is mediated via activation of IL-6-STAT3-SOCS3 signaling pathway. SOCS3 could be a therapeutic target to increase IL-10 production in lung cells exposed to mechanical injury.
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影响因子：
14.2
作者：
Saadane, A;Soltys, J;Berger, M
通讯作者：
Berger, M
DOI：
10.1159/000071446
发表时间：
2003-01-01
期刊：
BIOLOGY OF THE NEONATE
影响因子：
--
作者：
Schultz, C;Tautz, J;Möller, JC
通讯作者：
Möller, JC
影响因子：
4.6
作者：
Schultz, C;Temming, P;Härtel, C
通讯作者：
Härtel, C
影响因子：
3.6
作者：
Garingo, Arlene;Tesoriero, Linda;Minoo, Parviz
通讯作者：
Minoo, Parviz
影响因子：
32.4
作者：
Karaghiosoff, M;Neubauer, H;Müller, M
通讯作者：
Müller, M