Abstract：
:Inflammation has an essential role in regulating the pathogenesis of acute respiratory distress syndrome (ARDS). The serine/threonine kinase PIM2 is highly expressed in human macrophages, and exhibits regulatory role in inflammatory response. However, its effect on ARDS progression has not been investigated and still remains unclear. In the study, we attempted to investigate the potential of PIM2 during ARDS progression, and to reveal the underlying molecular mechanisms. Here, we found that PIM2 expression was dramatically up-regulated in lipopolysaccharide (LPS)-exposed murine macrophages through a dose- and time-dependent manner. Additionally, we found that PIM2 knockdown greatly alleviated LPS-triggered activation of Caspase-1, interleukin (IL)-1β, NOD-like receptor pyrin domain 3 (NLRP3) and apoptosis-associated speck-like protein (ASC) in macrophages, along with suppressed inflammatory response. Importantly, we identified that PIM2 could directly interact with NLRP3. PIM2 over-expression could further promote LPS-triggered inflammation and NLRP3 inflammasome in macrophages. Furthermore, PIM2 knockout significantly alleviated the severity of ARDS in LPS-challenged mice. Evidently decreased inflammatory response and NLRP3 inflammasome were detected in pulmonary tissues of LPS-treated mice with PIM2 deficiency. Together, our findings demonstrated that PIM2 as a promising therapeutic target for ARDS treatment through regulating NLRP3 inflammasome.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Wang F,Xu L,Dong G,Zhu M,Liu L,Wang Bdoi
10.1016/j.bbrc.2020.08.109subject
Has Abstractpub_date
2020-12-17 00:00:00pages
1419-1426issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(20)31714-9journal_volume
533pub_type
杂志文章abstract：:Elevations in intracellular Ca(2+) ([Ca(2+)](i)) initiate insulin secretion from pancreatic beta-cells, but the secretory responses become rapidly desensitised to maintained elevations in [Ca(2+)](i). We have investigated the mechanisms underlying the Ca(2+) desensitization of insulin secretion using electrically perm...
journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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