Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions
- Authors
- Jung, Hyun Jin; Kang, Ju-Hee; Pak, Seongwon; Lee, Keunwook; Seong, Je Kyung; Oh, Seung Hyun
- Issue Date
- 2-Jan-2020
- Publisher
- MDPI
- Keywords
- Ninjurin1; myeloid cells; IL1 beta; IBD; inflammation
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.21, no.2
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Volume
- 21
- Number
- 2
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/26155
- DOI
- 10.3390/ijms21020614
- ISSN
- 1661-6596
- Abstract
- Nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a cell-surface adhesion molecule that regulates cell migration and attachment. This study demonstrates the increase in Ninj1 protein expression during development of intestinal inflammation. Ninj1-deficient mice exhibited significantly attenuated bodyweight loss, shortening of colon length, intestinal inflammation, and lesser pathological lesions than wild-type mice. Although more severe inflammation and serious lesions are observed in wild-type mice than Ninj1-deficient mice, there were no changes in the numbers of infiltrating macrophages in the inflamed tissues obtained from WT and Ninj1-deficient mice. Ninj1 expression results in activation of macrophages, and these activated macrophages secrete more cytokines and chemokines than Ninj1-deficient macrophages. Moreover, mice with conditional deletion of Ninj1 in myeloid cells (Ninj1(fl/fl); Lyz-Cre+) alleviated experimental colitis compared with wild-type mice. In summary, we propose that the Ninj1 in myeloid cells play a pivotal function in intestinal inflammatory conditions.
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