Change of surfactant protein D and A after renal ischemia reperfusion injury
DC Field | Value | Language |
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dc.contributor.author | Imtiazul, Islam Md | - |
dc.contributor.author | Asma, Redwan | - |
dc.contributor.author | Lee, Ji-Hye | - |
dc.contributor.author | Cho, Nam-Jun | - |
dc.contributor.author | Park, Samel | - |
dc.contributor.author | Song, Ho-Yeon | - |
dc.contributor.author | Gil, Hyo-Wook | - |
dc.date.accessioned | 2021-08-11T08:43:57Z | - |
dc.date.available | 2021-08-11T08:43:57Z | - |
dc.date.issued | 2019-12-26 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/3739 | - |
dc.description.abstract | Acute kidney injury (AKI) is associated with widespread effects on distant organs, including the lungs. Surfactant protein (SP)-A and SP-D are members of the C-type lectin family, which plays a critical role in host defense and regulation of inflammation in a variety of infections. Serum levels of SP-A and SP-D are markers to reflect lung injury in acute respiratory distress syndrome, idiopathic pulmonary fibrosis, and sarcoidosis. We investigated the change of lung-specific markers, including SP-A and SP-D in an AKI mice model. We studied C57BL/6J mice 4 and 24 hours after an episode of ischemic AKI (23 min of renal pedicle clamping and then reperfusion); numerous derangements were present, including SP-A, SP-D, and lung tight-junction protein. Neutrophil infiltration and apoptosis in the lungs increased in ischemic AKI. Receptor for advanced glycation end products (RAGE) in the lungs, a marker of pneumocyte I, was not changed. Lung tight-junction proteins, particularly claudin-4, claudin-18, and anti-junctional adhesion molecule 1 (JAMA-1), were reduced in 24 hours after AKI. Serum SP-A and SP-D significantly increased in ischemic AKI. SP-A and SP-D in the lungs did not increase in ischemic AKI. The immunohistochemistry showed that the expression of SP-A and SP-D was intact in ischemic AKI. SP-A and SP-D in the kidneys were significantly higher in AKI than in the sham. These patterns of SP-A and SP-D in the kidneys were similar to those of serum. AKI induces apoptosis and inflammation in the lungs. Serum SP-A and SP-D increased in ischemic AKI, but these could have originated from the kidneys. So serum SP-A and SP-D could not reflect lung injury in AKI. Further study is needed to reveal how a change in lung tight-junction protein could influence the prognosis in patients with AKI. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Public Library of Science | - |
dc.title | Change of surfactant protein D and A after renal ischemia reperfusion injury | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1371/journal.pone.0227097 | - |
dc.identifier.scopusid | 2-s2.0-85077260915 | - |
dc.identifier.wosid | 000515084600060 | - |
dc.identifier.bibliographicCitation | PLoS ONE, v.14, no.12 | - |
dc.citation.title | PLoS ONE | - |
dc.citation.volume | 14 | - |
dc.citation.number | 12 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | ACUTE KIDNEY INJURY | - |
dc.subject.keywordPlus | REPLACEMENT THERAPY | - |
dc.subject.keywordPlus | LUNG INJURY | - |
dc.subject.keywordPlus | FAILURE | - |
dc.subject.keywordAuthor | 의약학 | - |
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