https://scholars.lib.ntu.edu.tw/handle/123456789/615910
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Wu, Yu-Chih | en_US |
dc.contributor.author | Hsu, Sung-Po | en_US |
dc.contributor.author | MENG-CHUN HU | en_US |
dc.contributor.author | Lan, Yu-Ting | en_US |
dc.contributor.author | Yeh, Edward T H | en_US |
dc.contributor.author | Yang, Feng-Ming | en_US |
dc.date.accessioned | 2022-07-27T08:16:03Z | - |
dc.date.available | 2022-07-27T08:16:03Z | - |
dc.date.issued | 2022 | - |
dc.identifier.issn | 2296-858X | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/615910 | - |
dc.description.abstract | Acute lung injury (ALI) is a severe inflammatory lung disease associated with macrophages. Somatic nuclear autoantigenic sperm protein (sNASP) is a negative regulator of Toll-like receptor (TLR) signaling that targets tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) in macrophages, which is required to maintain homeostasis of the innate immune response. In the present study, we generated a cell permeable PEP-sNASP peptide using the sNASP protein N-terminal domain, and examined its potential therapeutic effect in a mouse model of ALI induced by the intranasal administration of lipopolysaccharide (LPS) and elucidated the underlying molecular mechanisms in RAW 264.7 cells. In vivo, PEP-sNASP peptide treatment markedly ameliorated pathological injury, reduced the wet/dry (W/D) weight ratio of the lungs and the production of proinflammatory cytokines (interleukin (IL)-1β, IL-6, and TNF-α). In vitro, we demonstrated that when the PEP-sNASP peptide was transduced into RAW 264.7 cells, it bound to TRAF6, which markedly decreased LPS-induced proinflammatory cytokines by inhibiting TRAF6 autoubiquitination, nuclear factor (NF)-κB activation, reactive oxygen species (ROS) and cellular nitric oxide (NO) levels. Furthermore, the PEP-sNASP peptide also inhibited NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. Our results therefore suggest that the PEP-sNASP may provide a potential protein therapy against oxidative stress and pulmonary inflammation via selective TRAF6 signaling. | en_US |
dc.language.iso | en | en_US |
dc.publisher | FRONTIERS MEDIA SA | en_US |
dc.relation.ispartof | Frontiers in medicine | en_US |
dc.subject | NASP; TLR4; TRAF6; acute lung injury; inflammation | en_US |
dc.title | PEP-sNASP Peptide Alleviates LPS-Induced Acute Lung Injury Through the TLR4/TRAF6 Axis | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.3389/fmed.2022.832713 | - |
dc.identifier.pmid | 35386914 | - |
dc.identifier.scopus | 2-s2.0-85127976980 | - |
dc.identifier.isi | WOS:000779693800001 | - |
dc.identifier.url | https://api.elsevier.com/content/abstract/scopus_id/85127976980 | - |
dc.relation.journalvolume | 9 | en_US |
item.openairetype | journal article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.fulltext | no fulltext | - |
item.grantfulltext | none | - |
crisitem.author.dept | Physiology | - |
crisitem.author.orcid | 0000-0002-2783-5687 | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 生理學科所 |
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