Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 한중수 | - |
dc.date.accessioned | 2019-12-08T04:24:16Z | - |
dc.date.available | 2019-12-08T04:24:16Z | - |
dc.date.issued | 2018-05 | - |
dc.identifier.citation | EXPERIMENTAL AND MOLECULAR MEDICINE, v. 50, Article no. 55 | en_US |
dc.identifier.issn | 1226-3613 | - |
dc.identifier.issn | 2092-6413 | - |
dc.identifier.uri | https://www.nature.com/articles/s12276-018-0083-4 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/118741 | - |
dc.description.abstract | Asthma is a chronic lung disease that causes airflow obstruction due to airway inflammation. However, its therapeutics remain inadequate. We previously reported that phospholipase D1 (PLD1) is a key enzyme involved in the production of pro-inflammatory cytokines in airway inflammation induced by the house dust mite allergen Dermatophagoides farinae 2 (Der f 2). We also revealed that PLD1 is specifically inactivated by AP180 (assembly protein, 180 kDa) and identified the PLD1-specific binding motif (TVTSP) of AP180. Therefore, the aims of this study were to develop a novel anti-asthmatic agent that could suppress airway inflammation by inhibiting PLD1 and examine its acute and chronic toxicity. We designed TAT-TVTSP, a PLD1-inhibitory peptide fused with a cell-penetrating peptide (CPP) delivery system. TAT-TVTSP was efficiently delivered to bronchial epithelial cells and significantly reduced Der f 2-induced PLD activation and Interleukin 13 (IL-13) production. Intranasally administered TAT-TVTSP was also efficiently transferred to airway tissues and ameliorated airway inflammation in a Der f 2-induced allergic asthma mouse model. Moreover, we investigated the safety of TAT-TVTSP as a therapeutic agent through single-and repeated-dose toxicity studies in a mouse model. Taken together, these results indicated that a PLD1-inhibitory peptide fused with a cell-penetrating peptide may be useful for treating allergic inflammatory asthma induced by house dust mites (HDMs). | en_US |
dc.description.sponsorship | We thank Dr. Je-Min Choi (Hanyang University, Seoul, Republic of Korea) for the CPP design and Dr. Ju-Seop Kang (Hanyang University, Seoul, Republic of Korea) for helpful discussions on the entire toxicity study. This work was supported by the National Research Foundation of Korea (NRF) grants funded by the Korean government (MSIP) (NRF-2013R1A2A2A03067895 and NRF-2016R1A2B4015358) and the Bio & Medical Technology Development Program of the NRF funded by the Korean government, MSIP (2017M3A9D8063627). | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | NATURE PUBLISHING GROUP | en_US |
dc.subject | NEURAL STEM-CELLS | en_US |
dc.subject | PROTEIN-KINASE-C | en_US |
dc.subject | EPITHELIAL-CELLS | en_US |
dc.subject | NEURONAL DIFFERENTIATION | en_US |
dc.subject | ASTHMA-TREATMENT | en_US |
dc.subject | CANCER | en_US |
dc.subject | TRANSDUCTION | en_US |
dc.subject | ACTIVATION | en_US |
dc.subject | DELIVERY | en_US |
dc.subject | PATHOGENESIS | en_US |
dc.title | Therapeutic potential of a phospholipase D1 inhibitory peptide fused with a cell-penetrating peptide as a novel anti-asthmatic drug in a Der f 2-induced airway inflammation model | en_US |
dc.type | Article | en_US |
dc.relation.volume | 50 | - |
dc.identifier.doi | 10.1038/s12276-018-0083-4 | - |
dc.relation.page | 55-65 | - |
dc.relation.journal | EXPERIMENTAL AND MOLECULAR MEDICINE | - |
dc.contributor.googleauthor | Lee, Yun Young | - |
dc.contributor.googleauthor | Lee, So Young | - |
dc.contributor.googleauthor | Park, Shin-Young | - |
dc.contributor.googleauthor | Choi, Hye-Jin | - |
dc.contributor.googleauthor | Kim, Eung-Gook | - |
dc.contributor.googleauthor | Han, Joong-Soo | - |
dc.relation.code | 2018002394 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jshan | - |
dc.identifier.orcid | http://orcid.org/0000-0002-0875-6158 | - |
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