Protection from lipopolysaccharide-induced pulmonary microvascular endothelial cell injury by activation of hedgehog signaling pathway |
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Authors: | Yu Yang Qi Li Zhaoxia Deng Zhiyuan Zhang Jiancheng Xu Guisheng Qian Guansong Wang |
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Institution: | (1) Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China; |
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Abstract: | Pulmonary microvascular endothelial cells (PMVECs) are critically involved in the pathogenesis of acute lung injury. Hedgehog
signaling pathway plays a fundamental role in embryonic development as well as adult morphogenesis and carcinogenesis. As
the priming protein of hedgehog signaling pathway, sonic hedgehog (Shh) may recently be advantage for decreasing endothelial
injury and promoting the repair of endothelial barrier function. To investigate the expression and role of hedgehog signal
pathway in PMVECs injured by lipopolysaccharide (LPS), cells were divided into six groups: control group, LPS group, rhShh
group, LPS + rhShh group, rhShh + cyclopamine group, and LPS + rhShh + cyclopamine group. Real time RT-PCR and Western blotting
were used to detect the mRNA and protein expression of hedgehog signal molecules including Shh, Patched-1 (Ptc-1) and Gli1
in nucleus. The activity of PMVECs was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.
In this study, we found that Shh, Ptch1, and Gli1 were expressed in rat PMVECs and their expression decreased when cells were
treated by LPS. In the other hand, LPS inhibited the activity of rat PMVECs and caused the cells injury. Activation of Hedgehog
signaling pathway by Shh could elevate the activity of PMVECs with pretreatment by LPS. Therefore, hedgehog signaling pathway
should play a protective role on injury PMVECs by LPS. |
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