TY - JOUR
T1 - Lipid-encapsulated siRNA for hepatocyte-directed treatment of advanced liver disease
AU - Woitok, Marius Maximilian
AU - Zoubek, Miguel Eugenio
AU - Doleschel, Dennis
AU - Bartneck, Matthias
AU - Mohamed, Mohamed Ramadan
AU - Kiessling, Fabian
AU - Lederle, Wiltrud
AU - Trautwein, Christian
AU - Cubero, Francisco Javier
N1 - Funding Information:
This work was supported by the Deutsche Forschungsgemeinschaft (DFG) in the framework of the Research Training Group 2375 “Tumor-targeted Drug Delivery” grant 331065168, the SFB/TRR 57, DFG Tr 10-1, the German Krebshilfe Grant Nr. 361209, the i3tm SF_15-5-17 und Step2Project, the MINECO Retos SAF2016-78711, EXOHEP-CM S2017/BMD-3727, NanoLiver-CM Y2018/NMT-4949, ERAB Ref. EA 18/14, AMMF 2018/117, UCM-25-2019, the BMBF (German Federal Ministry of Education and Research) Project LiSyM (Grant No. 031L0041) and COST Action CA17112. F.J.C. is a Ramón y Cajal Researcher RYC-2014-15242 affiliated to the UCM group “Lymphocyte Immunobiology”, No. 920631 (imas12-associated, Ref. IBL-6) and a Gilead Liver Research Scholar. Bettina Jansen and Sonja Strauss provided essential technical support with mice genotyping, providing histological sections of livers and performing H&E and Sirius red stainings. In addition, the authors gratefully acknowledge Chris Pak from Molecular Targeting Technologies, Inc., for providing the Duramycin-NIR790 conjugate, Felix Gremse and Marek Weiler for the reconstruction of the FMT/µCT data and for the supply of the software Imalytics preclinical 2.0 (Gremse-IT GmbH Aachen). This work was supported by the “Immunohistochemistry Facility”, a core facility of the Interdisciplinary Center for Clinical Research (IZKF) Aachen within the Faculty of Medicine at RWTH-Aachen University. We thank Axolabs (LGC group) for generation of LNP.
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/5/11
Y1 - 2020/5/11
N2 - Lipid-based RNA nanocarriers have been recently accepted as a novel therapeutic option in humans, thus increasing the therapeutic options for patients. Tailored nanomedicines will enable to treat chronic liver disease (CLD) and end-stage liver cancer, disorders with high mortality and few treatment options. Here, we investigated the curative potential of gene therapy of a key molecule in CLD, the c-Jun N-terminal kinase-2 (Jnk2). Delivery to hepatocytes was achieved using a lipid-based clinically employable siRNA formulation that includes a cationic aminolipid to knockdown Jnk2 (named siJnk2). After assessing the therapeutic potential of siJnk2 treatment, non-invasive imaging demonstrated reduced apoptotic cell death and improved hepatocarcinogenesis was evidenced by improved liver parenchyma as well as ameliorated markers of hepatic damage, reduced fibrogenesis in 1-year-old mice. Strikingly, chronic siJnk2 treatment reduced premalignant nodules, indicative of tumor initiation. Furthermore, siJnk2 treatment led to a significant activation of the immune cell compartment. In conclusion, Jnk2 knockdown in hepatocytes ameliorated hepatitis, fibrogenesis, and initiation of hepatocellular carcinoma (HCC), and hence might be a suitable therapeutic option, to define novel molecular targets for precision medicine in CLD.
AB - Lipid-based RNA nanocarriers have been recently accepted as a novel therapeutic option in humans, thus increasing the therapeutic options for patients. Tailored nanomedicines will enable to treat chronic liver disease (CLD) and end-stage liver cancer, disorders with high mortality and few treatment options. Here, we investigated the curative potential of gene therapy of a key molecule in CLD, the c-Jun N-terminal kinase-2 (Jnk2). Delivery to hepatocytes was achieved using a lipid-based clinically employable siRNA formulation that includes a cationic aminolipid to knockdown Jnk2 (named siJnk2). After assessing the therapeutic potential of siJnk2 treatment, non-invasive imaging demonstrated reduced apoptotic cell death and improved hepatocarcinogenesis was evidenced by improved liver parenchyma as well as ameliorated markers of hepatic damage, reduced fibrogenesis in 1-year-old mice. Strikingly, chronic siJnk2 treatment reduced premalignant nodules, indicative of tumor initiation. Furthermore, siJnk2 treatment led to a significant activation of the immune cell compartment. In conclusion, Jnk2 knockdown in hepatocytes ameliorated hepatitis, fibrogenesis, and initiation of hepatocellular carcinoma (HCC), and hence might be a suitable therapeutic option, to define novel molecular targets for precision medicine in CLD.
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KW - NANOPARTICLES
KW - INFLAMMATION
KW - DELIVERY
KW - DELETION
U2 - 10.1038/s41419-020-2571-4
DO - 10.1038/s41419-020-2571-4
M3 - Article
C2 - 32393755
SN - 2041-4889
VL - 11
JO - Cell Death & Disease
JF - Cell Death & Disease
IS - 5
M1 - 343
ER -