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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Human Umbilical Cord Mesenchymal Stem Cell-derived Mitochondria (PN-101) Attenuate LPS-Induced Inflammatory Responses by Inhibiting the NFリB Signaling Pathway
Shin-Hye Yu 1 (Senior Research Scientist), Soomin Kim 1 (Assistant Research Scientist), Yujin Kim 1 (Senior Research Scientist), Seo-Eun Lee 1 (Assistant Research Scientist), Jong Hyeok Park 1 (Assistant Research Scientist), Gayoung Cho 1 (Assistant Research Scientist), Jong-Cheon Ha1 (Principle Scientist), Hahnsun Jung1 (Principle Scientist), Sang-Min Lim1 (VP), Kyuboem Han1 (CEO), Hong Kyu Lee1 (Scientific advisor), Young Cheol Kang 1 (Principle Scientist), Chun-Hyung Kim 1,* (Executive VP)
1Biopharmaceutical Research Institute, Paean Biotechnology, Inc.
Inflammation is one of the body’s natural responses to injury and illness as part of the healing process. However, persistent inflammation can lead to chronic inflammatory diseases or multi-organ failure. Altered mitochondrial function has been implicated in several acute and chronic inflammatory diseases through induction of an abnormal inflammatory response. Therefore, treating inflammatory diseases through recovery of mitochondrial function may be a potential therapeutic approach. Recently, mitochondrial transplantation proved beneficial in hyperinflammatory animal models. However, it is unclear how mitochondrial transplantation attenuates inflammatory responses induced by external stimuli. Here, we isolated mitochondria from umbilical cord-derived mesenchymal stem cells, referred as to a PN-101. We demonstrated that PN-101 significantly reduced LPS-induced mortality in mice. In addition, in phorbol 12-myristate 13-acetate (PMA)-treated THP-1 macrophages, PN-101 attenuated the LPS-induced increase production of pro-inflammatory cytokines. Furthermore, we showed that anti-inflammatory effect of PN-101 is mediated by blockade of the phosphorylation, nuclear translocation, and trans-activity of NFリB. Taken together, our results demonstrate the therapeutic potential to attenuate pathological inflammatory responses using PN-101.
Abstract, Accepted Manuscript(in press) [Submitted on June 28, 2021, Accepted on August 9, 2021]
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