Primary allogeneic mitochondrial mix (PAMM) transfer/transplant by MitoCeption to address damage in PBMCs caused by ultraviolet radiation.
Artificial mitochondria transfer / transplant (AMTT)
Cell repair
Cellular damage
MitoCeption
Mitochondria
Primary allogeneic mitochondrial mix (PAMM)
Primary immune cells
Ultraviolet radiation (UVR)
p53
Journal
BMC biotechnology
ISSN: 1472-6750
Titre abrégé: BMC Biotechnol
Pays: England
ID NLM: 101088663
Informations de publication
Date de publication:
28 06 2019
28 06 2019
Historique:
received:
14
11
2018
accepted:
14
06
2019
entrez:
30
6
2019
pubmed:
30
6
2019
medline:
14
1
2020
Statut:
epublish
Résumé
Artificial Mitochondrial Transfer or Transplant (AMT/T) can be used to reduce the stress and loss of viability of damaged cells. In MitoCeption, a type of AMT/T, the isolated mitochondria and recipient cells are centrifuged together at 4 °C and then co-incubated at 37 °C in normal culture conditions, inducing the transfer. Ultraviolet radiation (UVR) can affect mitochondria and other cell structures, resulting in tissue stress, aging, and immunosuppression. AMT/T could be used to repair UVR cellular and mitochondrial damage. We studied if a mitochondrial mix from different donors (Primary Allogeneic Mitochondrial Mix, PAMM) can repair UVR damage and promote cell survival. Using a simplified adaption of the MitoCeption protocol, we used peripheral blood mononuclear cells (PBMCs) as the recipient cell model of the PAMM in order to determine if this protocol could repair UVR damage. Our results showed that when PBMCs are exposed to UVR, there is a decrease in metabolic activity, mitochondrial mass, and mtDNA sequence stability as well as an increase in p53 expression and the percentage of dead cells. When PAMM MitoCeption was used on UVR-damaged cells, it successfully transferred mitochondria from different donors to distinct PBMCs populations and repaired the observed UVR damage. Our results represent an advancement in the applications of MitoCeption and other AMT/T. We showed that PBMCs could be used as a PAMM source of mitochondria. We also showed that these mitochondria can be transferred in a mix from different donors (PAMM) to UVR-damaged, non-adherent primary cells. Additionally, we decreased the duration of the MitoCeption protocol.
Sections du résumé
BACKGROUND
Artificial Mitochondrial Transfer or Transplant (AMT/T) can be used to reduce the stress and loss of viability of damaged cells. In MitoCeption, a type of AMT/T, the isolated mitochondria and recipient cells are centrifuged together at 4 °C and then co-incubated at 37 °C in normal culture conditions, inducing the transfer. Ultraviolet radiation (UVR) can affect mitochondria and other cell structures, resulting in tissue stress, aging, and immunosuppression. AMT/T could be used to repair UVR cellular and mitochondrial damage. We studied if a mitochondrial mix from different donors (Primary Allogeneic Mitochondrial Mix, PAMM) can repair UVR damage and promote cell survival.
RESULTS
Using a simplified adaption of the MitoCeption protocol, we used peripheral blood mononuclear cells (PBMCs) as the recipient cell model of the PAMM in order to determine if this protocol could repair UVR damage. Our results showed that when PBMCs are exposed to UVR, there is a decrease in metabolic activity, mitochondrial mass, and mtDNA sequence stability as well as an increase in p53 expression and the percentage of dead cells. When PAMM MitoCeption was used on UVR-damaged cells, it successfully transferred mitochondria from different donors to distinct PBMCs populations and repaired the observed UVR damage.
CONCLUSION
Our results represent an advancement in the applications of MitoCeption and other AMT/T. We showed that PBMCs could be used as a PAMM source of mitochondria. We also showed that these mitochondria can be transferred in a mix from different donors (PAMM) to UVR-damaged, non-adherent primary cells. Additionally, we decreased the duration of the MitoCeption protocol.
Identifiants
pubmed: 31253149
doi: 10.1186/s12896-019-0534-6
pii: 10.1186/s12896-019-0534-6
pmc: PMC6599354
doi:
Substances chimiques
DNA, Mitochondrial
0
Reactive Oxygen Species
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
42Références
Cytotechnology. 2008 Mar;56(3):145-9
pubmed: 19002852
Sci Rep. 2018 Mar 22;8(1):5014
pubmed: 29568084
Oncogene. 2013 Oct 24;32(43):5129-43
pubmed: 23416979
Stem Cells. 2011 May;29(5):812-24
pubmed: 21433223
J Exp Med. 2017 Apr 3;214(4):1111-1128
pubmed: 28351984
Nature. 2016 Oct 12;538(7624):183-192
pubmed: 27734871
Proc Natl Acad Sci U S A. 2015 Aug 18;112(33):10437-42
pubmed: 26216948
Sci Rep. 2016 May 17;6:26057
pubmed: 27184109
Nature. 1982 Feb 18;295(5850):605-7
pubmed: 7057918
Cell Death Differ. 2015 Jul;22(7):1181-91
pubmed: 25571977
Clin Transl Med. 2016 Mar;5(1):16
pubmed: 27130633
Mitochondrion. 2019 Sep;48:16-30
pubmed: 30771504
Sci Rep. 2018 Feb 20;8(1):3330
pubmed: 29463809
Oncotarget. 2017 Mar 7;8(10):17002-17011
pubmed: 28199983
Sci Rep. 2015 Mar 13;5:9073
pubmed: 25766410
Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1283-8
pubmed: 16432190
Cell Metab. 2016 Sep 13;24(3):376-378
pubmed: 27626198
Mol Biol Cell. 2015 Nov 15;26(23):4197-208
pubmed: 26399294
J Thorac Cardiovasc Surg. 2017 Jul;154(1):286-289
pubmed: 28283239
J Cell Mol Med. 2014 Aug;18(8):1694-703
pubmed: 24912369
Nat Biotechnol. 2017 Jun 7;35(6):520-521
pubmed: 28591119
Biotechnol Prog. 1993 Nov-Dec;9(6):671-4
pubmed: 7764357
Free Radic Res. 2006 Nov;40(11):1138-48
pubmed: 17050167
Br J Dermatol. 2013 Jul;169 Suppl 2:9-14
pubmed: 23786615
Methods Mol Biol. 2015;1264:117-31
pubmed: 25631009
Cell Death Discov. 2017 Jun 19;3:17030
pubmed: 28835855
Biochem Biophys Res Commun. 2011 Aug 19;412(1):1-7
pubmed: 21703239
Semin Cell Dev Biol. 2016 Apr;52:119-31
pubmed: 26868759
Trends Immunol. 2015 Aug;36(8):494-502
pubmed: 26169254
Stem Cells. 2016 Aug;34(8):2210-23
pubmed: 27059413
Nat Med. 2012 Apr 15;18(5):759-65
pubmed: 22504485
Int J Biochem Cell Biol. 2014 Aug;53:141-6
pubmed: 24842105
Stem Cells Int. 2017;2017:7610414
pubmed: 28751917
Leukemia. 2018 Sep;32(9):2073-2077
pubmed: 30030506
J Cell Biochem. 2000 Oct 20;80(2):216-22
pubmed: 11074592