-
Je něco špatně v tomto záznamu ?
Platelets Facilitate the Wound-Healing Capability of Mesenchymal Stem Cells by Mitochondrial Transfer and Metabolic Reprogramming
J. Levoux, A. Prola, P. Lafuste, M. Gervais, N. Chevallier, Z. Koumaiha, K. Kefi, L. Braud, A. Schmitt, A. Yacia, A. Schirmann, B. Hersant, M. Sid-Ahmed, S. Ben Larbi, K. Komrskova, J. Rohlena, F. Relaix, J. Neuzil, AM. Rodriguez
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NV17-30138A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
NLK
Cell Press Free Archives
od 2005-01-01 do Před 1 rokem
Free Medical Journals
od 2005 do Před 1 rokem
- MeSH
- hojení ran MeSH
- mezenchymální kmenové buňky metabolismus MeSH
- mitochondrie metabolismus MeSH
- myši inbrední C57BL MeSH
- myši transgenní MeSH
- myši MeSH
- trombocyty metabolismus MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Platelets are known to enhance the wound-healing activity of mesenchymal stem cells (MSCs). However, the mechanism by which platelets improve the therapeutic potential of MSCs has not been elucidated. Here, we provide evidence that, upon their activation, platelets transfer respiratory-competent mitochondria to MSCs primarily via dynamin-dependent clathrin-mediated endocytosis. We found that this process enhances the therapeutic efficacy of MSCs following their engraftment in several mouse models of tissue injury, including full-thickness cutaneous wound and dystrophic skeletal muscle. By combining in vitro and in vivo experiments, we demonstrate that platelet-derived mitochondria promote the pro-angiogenic activity of MSCs via their metabolic remodeling. Notably, we show that activation of the de novo fatty acid synthesis pathway is required for increased secretion of pro-angiogenic factors by platelet-preconditioned MSCs. These results reveal a new mechanism by which platelets potentiate MSC properties and underline the importance of testing platelet mitochondria quality prior to their clinical use.
Department of Zoology Faculty of Science Charles University 128 44 Prague 2 Czech Republic
EnvA IMRB 94700 Maisons Alfort France
Etablissement Français du Sang 94017 Créteil France
Institute of Biotechnology Czech Academy of Sciences 252 50 Prague West Prague Czech Republic
School of Medical Science Griffith University Southport QLD 4222 Australia
Université de Paris Institut Cochin INSERM CNRS 75014 Paris France
Université Paris Est Créteil INSERM IMRB 94010 Créteil France
Citace poskytuje Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc22004630
- 003
- CZ-PrNML
- 005
- 20220127145113.0
- 007
- ta
- 008
- 220113s2021 xxu f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1016/j.cmet.2020.12.006 $2 doi
- 035 __
- $a (PubMed)33400911
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Levoux, Jennyfer $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France
- 245 10
- $a Platelets Facilitate the Wound-Healing Capability of Mesenchymal Stem Cells by Mitochondrial Transfer and Metabolic Reprogramming / $c J. Levoux, A. Prola, P. Lafuste, M. Gervais, N. Chevallier, Z. Koumaiha, K. Kefi, L. Braud, A. Schmitt, A. Yacia, A. Schirmann, B. Hersant, M. Sid-Ahmed, S. Ben Larbi, K. Komrskova, J. Rohlena, F. Relaix, J. Neuzil, AM. Rodriguez
- 520 9_
- $a Platelets are known to enhance the wound-healing activity of mesenchymal stem cells (MSCs). However, the mechanism by which platelets improve the therapeutic potential of MSCs has not been elucidated. Here, we provide evidence that, upon their activation, platelets transfer respiratory-competent mitochondria to MSCs primarily via dynamin-dependent clathrin-mediated endocytosis. We found that this process enhances the therapeutic efficacy of MSCs following their engraftment in several mouse models of tissue injury, including full-thickness cutaneous wound and dystrophic skeletal muscle. By combining in vitro and in vivo experiments, we demonstrate that platelet-derived mitochondria promote the pro-angiogenic activity of MSCs via their metabolic remodeling. Notably, we show that activation of the de novo fatty acid synthesis pathway is required for increased secretion of pro-angiogenic factors by platelet-preconditioned MSCs. These results reveal a new mechanism by which platelets potentiate MSC properties and underline the importance of testing platelet mitochondria quality prior to their clinical use.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a trombocyty $x metabolismus $7 D001792
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a mezenchymální kmenové buňky $x metabolismus $7 D059630
- 650 _2
- $a myši $7 D051379
- 650 _2
- $a myši inbrední C57BL $7 D008810
- 650 _2
- $a myši transgenní $7 D008822
- 650 _2
- $a mitochondrie $x metabolismus $7 D008928
- 650 _2
- $a hojení ran $7 D014945
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Prola, Alexandre $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France; EnvA, IMRB, 94700 Maisons-Alfort, France
- 700 1_
- $a Lafuste, Peggy $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France
- 700 1_
- $a Gervais, Marianne $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France
- 700 1_
- $a Chevallier, Nathalie $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France; Etablissement Français du Sang, 94017, Créteil, France
- 700 1_
- $a Koumaiha, Zeynab $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France
- 700 1_
- $a Kefi, Kaouthar $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France
- 700 1_
- $a Braud, Laura $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France
- 700 1_
- $a Schmitt, Alain $u Université de Paris, Institut Cochin, INSERM, CNRS, 75014, Paris, France
- 700 1_
- $a Yacia, Azzedine $u Université de Paris, Institut Cochin, INSERM, CNRS, 75014, Paris, France
- 700 1_
- $a Schirmann, Aurélie $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France
- 700 1_
- $a Hersant, Barbara $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France; AP-HP, Hôpital Henri Mondor, A. Chenevier, Service de chirurgie plastique et maxillo-faciale, Créteil, France
- 700 1_
- $a Sid-Ahmed, Mounia $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France; AP-HP, Hôpital Henri Mondor, A. Chenevier, Service de chirurgie plastique et maxillo-faciale, Créteil, France
- 700 1_
- $a Ben Larbi, Sabrina $u Institut NeuroMyoGène, Université Claude Bernard - Lyon 1, University Lyon, CNRS UMR 5310, INSERM U1217, Lyon, France
- 700 1_
- $a Komrskova, Katerina $u Institute of Biotechnology, Czech Academy of Sciences, 252 50 Prague-West, Prague, Czech Republic; Department of Zoology, Faculty of Science, Charles University, 128 44 Prague 2, Czech Republic
- 700 1_
- $a Rohlena, Jakub $u Institute of Biotechnology, Czech Academy of Sciences, 252 50 Prague-West, Prague, Czech Republic
- 700 1_
- $a Relaix, Frederic $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France; EnvA, IMRB, 94700 Maisons-Alfort, France; APHP, Hôpitaux Universitaires Henri Mondor & Centre de Référence des Maladies Neuromusculaires GNMH, 94000, Créteil, France
- 700 1_
- $a Neuzil, Jiri $u Institute of Biotechnology, Czech Academy of Sciences, 252 50 Prague-West, Prague, Czech Republic; School of Medical Science, Griffith University, Southport, QLD 4222, Australia
- 700 1_
- $a Rodriguez, Anne-Marie $u Université Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France. Electronic address: anne-marie.rodriguez@inserm.fr
- 773 0_
- $w MED00008684 $t Cell metabolism $x 1932-7420 $g Roč. 33, č. 2 (2021), s. 283-299.e9
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/33400911 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y p $z 0
- 990 __
- $a 20220113 $b ABA008
- 991 __
- $a 20220127145110 $b ABA008
- 999 __
- $a ok $b bmc $g 1751939 $s 1155779
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2021 $b 33 $c 2 $d 283-299.e9 $e 20210104 $i 1932-7420 $m Cell metabolism $n Cell Metab $x MED00008684
- GRA __
- $a NV17-30138A $p MZ0
- LZP __
- $a Pubmed-20220113