Human Stem Cells Promote Liver Regeneration After Partial Hepatectomy in BALB/C Nude Mice.


Journal

The Journal of surgical research
ISSN: 1095-8673
Titre abrégé: J Surg Res
Pays: United States
ID NLM: 0376340

Informations de publication

Date de publication:
07 2019
Historique:
received: 25 09 2018
revised: 16 01 2019
accepted: 05 02 2019
pubmed: 8 3 2019
medline: 25 1 2020
entrez: 8 3 2019
Statut: ppublish

Résumé

Mesenchymal stem cells (MSCs) have been suggested to augment liver regeneration after surgically and pharmacologically induced liver failure. To further investigate this we processed human bone marrow-derived MSC according to good manufacturing practice (GMP) and tested those cells for their modulatory capacities of metabolic alterations and liver regeneration after partial hepatectomy in BALB/c nude mice. Human MSCs were obtained by bone marrow aspiration of healthy donors as in a previously described GMP process. Transgenic GFP-MSCs were administered i.p. 24 h after 70% hepatectomy in BALB/c nude mice, whereas control mice received phosphate-buffered saline. Mice were sacrificed 2, 3, and 5 d after partial hepatectomy. Blood and organs were harvested and metabolic alterations as well as liver regeneration subsequently assessed by liver function tests, multianalyte profiling immunoassays, histology, and immunostaining. Hepatocyte and sinusoidal endothelial cell proliferation were significantly increased after partial hepatectomy in mice receiving MSC compared to control mice (Hepatocyte postoperative day 3, P < 0.01; endothelial cell postoperative day 5, P < 0.05). Hepatocyte fat accumulation correlated inversely with hepatocyte proliferation (r Human bone marrow-derived MSC attenuate metabolic alterations and improve liver regeneration after partial hepatectomy in BALB/c nude mice. Obtained results using GMP-processed human MSC suggest functional links between fat accumulation and hepatocyte proliferation, without any evidence for cellular homing. This study using GMP-proceeded MSC has important regulatory implications for an urgently needed translation into a clinical trial.

Sections du résumé

BACKGROUND
Mesenchymal stem cells (MSCs) have been suggested to augment liver regeneration after surgically and pharmacologically induced liver failure. To further investigate this we processed human bone marrow-derived MSC according to good manufacturing practice (GMP) and tested those cells for their modulatory capacities of metabolic alterations and liver regeneration after partial hepatectomy in BALB/c nude mice.
METHODS
Human MSCs were obtained by bone marrow aspiration of healthy donors as in a previously described GMP process. Transgenic GFP-MSCs were administered i.p. 24 h after 70% hepatectomy in BALB/c nude mice, whereas control mice received phosphate-buffered saline. Mice were sacrificed 2, 3, and 5 d after partial hepatectomy. Blood and organs were harvested and metabolic alterations as well as liver regeneration subsequently assessed by liver function tests, multianalyte profiling immunoassays, histology, and immunostaining.
RESULTS
Hepatocyte and sinusoidal endothelial cell proliferation were significantly increased after partial hepatectomy in mice receiving MSC compared to control mice (Hepatocyte postoperative day 3, P < 0.01; endothelial cell postoperative day 5, P < 0.05). Hepatocyte fat accumulation correlated inversely with hepatocyte proliferation (r
CONCLUSIONS
Human bone marrow-derived MSC attenuate metabolic alterations and improve liver regeneration after partial hepatectomy in BALB/c nude mice. Obtained results using GMP-processed human MSC suggest functional links between fat accumulation and hepatocyte proliferation, without any evidence for cellular homing. This study using GMP-proceeded MSC has important regulatory implications for an urgently needed translation into a clinical trial.

Identifiants

pubmed: 30844633
pii: S0022-4804(19)30086-1
doi: 10.1016/j.jss.2019.02.010
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

191-200

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Simon Wabitsch (S)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany. Electronic address: simon.wabitsch@charite.de.

Christian Benzing (C)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Felix Krenzien (F)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Katrin Splith (K)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Philipp Konstantin Haber (PK)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Alexander Arnold (A)

Departement of Pathology, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Maximilian Nösser (M)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Can Kamali (C)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Felix Hermann (F)

Apceth Biopharma GmbH, Munich, Germany.

Christiane Günther (C)

Apceth Biopharma GmbH, Munich, Germany.

Daniela Hirsch (D)

Apceth Biopharma GmbH, Munich, Germany.

Igor M Sauer (IM)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Johann Pratschke (J)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

Moritz Schmelzle (M)

Department of Surgery, Campus Charité Mitte and Campus Virchow-Klinikum, Charité - Universitaetsmedizin, Berlin, Germany.

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