Apolipoprotein M Protects Against Lipopolysaccharide-Induced Acute Lung Injury via Sphingosine-1-Phosphate Signaling
(2018) In Inflammation 41(2). p.643-653- Abstract
Abstract: It had been demonstrated that apolipoprotein M (apoM) is an important carrier of sphingosine-1-phosphate (S1P) in blood, and the S1P has critical roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In the present study, we investigated whether apoM has beneficial effects in a mouse model after lipopolysaccharide (LPS)-induced ALI. Forty-eight mice were divided into two groups: male C57BL/6 wild-type (apoM+/+) group (n = 24) and apoM gene-deficient (apoM−/−) group (n = 24) and then randomly subdivided into four subgroups (n = 6 each) according to different intraperitoneal (i.p.) injection: control group, W146 group, LPS group, and LPS + W146 group. Serum levels of interleukin-1 beta... (More)
Abstract: It had been demonstrated that apolipoprotein M (apoM) is an important carrier of sphingosine-1-phosphate (S1P) in blood, and the S1P has critical roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In the present study, we investigated whether apoM has beneficial effects in a mouse model after lipopolysaccharide (LPS)-induced ALI. Forty-eight mice were divided into two groups: male C57BL/6 wild-type (apoM+/+) group (n = 24) and apoM gene-deficient (apoM−/−) group (n = 24) and then randomly subdivided into four subgroups (n = 6 each) according to different intraperitoneal (i.p.) injection: control group, W146 group, LPS group, and LPS + W146 group. Serum levels of interleukin-1 beta (IL-1β) and mRNA levels of IL-1β, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), lung histology, wet/dry weight ratio, and immunohistochemistry were measured at 3 h after the baseline and compared in each group. Our results clearly demonstrated that IL-1β mRNA levels and other inflammatory biomarkers were significantly increased in the lungs of LPS-induced ALI apoM−/− mice compared to those of the apoM+/+ mice. Moreover, when apoM+/+ mice were treated with W146, a S1P receptor (S1PR1) antagonist, these inflammatory biomarkers could be significantly upregulated by LPS-induced ALI. Therefore, it suggests that apoM-S1P-S1PR1 signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS-induced ALI.
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- author
- Zhu, Bin ; Luo, Guang hua ; Feng, Yue hua ; Yu, Miao mei ; Zhang, Jun ; Wei, Jiang ; Yang, Chun ; Xu, Ning LU and Zhang, Xiao ying
- organization
- publishing date
- 2018-03
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Inflammation
- volume
- 41
- issue
- 2
- pages
- 643 - 653
- publisher
- Springer
- external identifiers
-
- pmid:29260347
- scopus:85038370633
- ISSN
- 0360-3997
- DOI
- 10.1007/s10753-017-0719-x
- language
- English
- LU publication?
- yes
- id
- e7d7e85b-36bc-4aa1-b086-9d5a11f62eda
- date added to LUP
- 2018-01-03 12:13:51
- date last changed
- 2024-07-08 05:44:55
@article{e7d7e85b-36bc-4aa1-b086-9d5a11f62eda, abstract = {{<p>Abstract: It had been demonstrated that apolipoprotein M (apoM) is an important carrier of sphingosine-1-phosphate (S1P) in blood, and the S1P has critical roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In the present study, we investigated whether apoM has beneficial effects in a mouse model after lipopolysaccharide (LPS)-induced ALI. Forty-eight mice were divided into two groups: male C57BL/6 wild-type (apoM<sup>+/+</sup>) group (n = 24) and apoM gene-deficient (apoM<sup>−/−</sup>) group (n = 24) and then randomly subdivided into four subgroups (n = 6 each) according to different intraperitoneal (i.p.) injection: control group, W146 group, LPS group, and LPS + W146 group. Serum levels of interleukin-1 beta (IL-1β) and mRNA levels of IL-1β, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), lung histology, wet/dry weight ratio, and immunohistochemistry were measured at 3 h after the baseline and compared in each group. Our results clearly demonstrated that IL-1β mRNA levels and other inflammatory biomarkers were significantly increased in the lungs of LPS-induced ALI apoM<sup>−/−</sup> mice compared to those of the apoM<sup>+/+</sup> mice. Moreover, when apoM<sup>+/+</sup> mice were treated with W146, a S1P receptor (S1PR1) antagonist, these inflammatory biomarkers could be significantly upregulated by LPS-induced ALI. Therefore, it suggests that apoM-S1P-S1PR1 signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS-induced ALI.</p>}}, author = {{Zhu, Bin and Luo, Guang hua and Feng, Yue hua and Yu, Miao mei and Zhang, Jun and Wei, Jiang and Yang, Chun and Xu, Ning and Zhang, Xiao ying}}, issn = {{0360-3997}}, language = {{eng}}, number = {{2}}, pages = {{643--653}}, publisher = {{Springer}}, series = {{Inflammation}}, title = {{Apolipoprotein M Protects Against Lipopolysaccharide-Induced Acute Lung Injury via Sphingosine-1-Phosphate Signaling}}, url = {{http://dx.doi.org/10.1007/s10753-017-0719-x}}, doi = {{10.1007/s10753-017-0719-x}}, volume = {{41}}, year = {{2018}}, }