Megakaryocytes form linear podosomes devoid of digestive properties to remodel medullar matrix.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
15 04 2022
Historique:
received: 25 08 2021
accepted: 01 04 2022
pubmed: 17 4 2022
medline: 20 4 2022
entrez: 16 4 2022
Statut: epublish

Résumé

Bone marrow megakaryocytes (MKs) undergo a maturation involving contacts with the microenvironment before extending proplatelets through sinusoids to deliver platelets in the bloodstream. We demonstrated that MKs assemble linear F-actin-enriched podosomes on collagen I fibers. Microscopy analysis evidenced an inverse correlation between the number of dot-like versus linear podosomes over time. Confocal videomicroscopy confirmed that they derived from each-other. This dynamics was dependent on myosin IIA. Importantly, MKs progenitors expressed the Tks4/5 adaptors, displayed a strong gelatinolytic ability and did not form linear podosomes. While maturing, MKs lost Tks expression together with digestive ability. However, those MKs were still able to remodel the matrix by exerting traction on collagen I fibers through a collaboration between GPVI, ß1 integrin and linear podosomes. Our data demonstrated that a change in structure and composition of podosomes accounted for the shift of function during megakaryopoiesis. These data highlight the fact that members of the invadosome family could correspond to different maturation status of the same entity, to adapt to functional responses required by differentiation stages of the cell that bears them.

Identifiants

pubmed: 35428815
doi: 10.1038/s41598-022-10215-x
pii: 10.1038/s41598-022-10215-x
pmc: PMC9012751
doi:

Substances chimiques

Collagen Type I 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

6255

Informations de copyright

© 2022. The Author(s).

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Auteurs

Antoine Oprescu (A)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France.

Déborah Michel (D)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France.

Adrien Antkowiak (A)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France.

Elodie Vega (E)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France.

Julien Viaud (J)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France.

Sara A Courtneidge (SA)

Department of Cell, Development and Cancer Biology, Oregon Health & Science University, Oregon, USA.

Anita Eckly (A)

INSERM, UMR_S1255, Université de Strasbourg, Etablissement Français du Sang-GEST, Strasbourg, France.

Henri de la Salle (H)

INSERM, UMR_S1255, Université de Strasbourg, Etablissement Français du Sang-GEST, Strasbourg, France.

Gaëtan Chicanne (G)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France.

Catherine Léon (C)

INSERM, UMR_S1255, Université de Strasbourg, Etablissement Français du Sang-GEST, Strasbourg, France.

Bernard Payrastre (B)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France.
CHU de Toulouse, laboratoire d'Hématologie, Toulouse, France.

Frédérique Gaits-Iacovoni (F)

INSERM, UMR1297, Université Toulouse III, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France. frgaits@gmail.com.
Molecular, Cellular and Developmental Biology Department (MCD, UMR5077), Centre de Biologie Intégrative (CBI, FR3743), University of Toulouse, CNRS, UPS, 31062, Toulouse, France. frgaits@gmail.com.

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