한빛사논문
- 조회466
Yohan Han1, Yin Zhu1, Sultan Almuntashiri1,2, Xiaoyun Wang1, Payaningal R. Somanath1,4,5, Caroline A. Owen3, Duo Zhang1,4
1Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA
2Department of Clinical Pharmacy, College of Pharmacy, University of Hail, Hail 55473, Saudi Arabia
3Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA
4Vascular Biology Center, Augusta University, Augusta, GA 30912, USA
5Georgia Cancer Center, Augusta University, Augusta, GA 30912, USA
To whom correspondence should be addressed. : Duo Zhang
Abstract
Acute lung injury (ALI) is still associated with high mortality. Growing evidence suggests that Club Cell Protein 16 (CC16) plays a protective role against ALI. However, the doses of recombinant CC16 (rCC16) used in preclinical studies are supraphysiological for clinical applications. Extracellular vesicles (EVs) are nanovesicles endogenously generated by mammalian cells. Our study demonstrated that CC16 is released via small EVs and EV-encapsulated CC16 (sEV-CC16) has anti-inflammatory activities, which protect mice from lipopolysaccharide (LPS) or bacteria-induced ALI. Additionally, sEV-CC16 can activate the DNA damage repair signaling pathways. Consistent with this activity, we observed more severe DNA damage in lungs from Cc16 knockout (KO) than wild-type (WT) mice. Mechanistically, we elucidated that CC16 suppresses NF-κB signaling activation by binding to Heat Shock Protein 60 (HSP60). We concluded that sEV-CC16 could be a potential therapeutic agent for ALI by inhibiting the inflammatory and DNA damage responses by reducing NF-κB signaling.
논문정보
- Research article
- 2023년 01월 (BRIC 등록일 2023-01-19)
- 국외 연구진
- 의약학 > 약학
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