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Tytuł pozycji:

BMP4 signaling plays critical roles in self-renewal of R2i mouse embryonic stem cells.

Tytuł:
BMP4 signaling plays critical roles in self-renewal of R2i mouse embryonic stem cells.
Autorzy:
Taleahmad S; Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Salari A; Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Samadian A; Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Chae SH; Korea Brain Bank, Korea Brain Research Institute, Daegu, Republic of Korea.
Hwang D; School of Biological Sciences, Seoul National University, Seoul, Republic of Korea.
Lee B; Lee Gil Ya Cancer and Diabetes Institute, School of Medicine, Gachon University, Incheon, Republic of Korea.
Bayarsaikhan D; Lee Gil Ya Cancer and Diabetes Institute, School of Medicine, Gachon University, Incheon, Republic of Korea.
Bayarsaikhan G; Lee Gil Ya Cancer and Diabetes Institute, School of Medicine, Gachon University, Incheon, Republic of Korea.
Lee J; Department of Chemistry, Seoul National University, Seoul, Republic of Korea.
Park JH; Department of Chemistry, Seoul National University, Seoul, Republic of Korea.
Hassani SN; Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Baharvand H; Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran; Department of Developmental Biology, School of Basic Sciences and Advanced Technologies in Biology, University of Science and Culture, Tehran, Iran. Electronic address: .
Hosseini Salekdeh G; Department of Molecular Sciences, Macquarie University, Sydney, NSW, Australia. Electronic address: .
Źródło:
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2022 Aug 20; Vol. 617 (Pt 1), pp. 8-15. Date of Electronic Publication: 2022 May 14.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: <2002- >: San Diego, CA : Elsevier
Original Publication: New York, Academic Press.
MeSH Terms:
Mouse Embryonic Stem Cells*/metabolism
Signal Transduction*
Animals ; Bone Morphogenetic Protein 4/metabolism ; Bone Morphogenetic Proteins/metabolism ; Cell Differentiation ; MAP Kinase Signaling System ; Mice ; Transforming Growth Factor beta/metabolism
Contributed Indexing:
Keywords: Apoptosis; BMP4; Cell adhesion; RNA-Seq; Self-renewal; mESCs
Substance Nomenclature:
0 (Bmp4 protein, mouse)
0 (Bone Morphogenetic Protein 4)
0 (Bone Morphogenetic Proteins)
0 (Transforming Growth Factor beta)
Entry Date(s):
Date Created: 20220606 Date Completed: 20220621 Latest Revision: 20220725
Update Code:
20240105
DOI:
10.1016/j.bbrc.2022.05.036
PMID:
35660877
Czasopismo naukowe
Mouse embryonic stem cells (mESCs) can be maintained in a pluripotent state under R2i culture conditions that inhibit the TGF-β and ERK signaling pathways. BMP4 is another member of the TGF-β family that plays a crucial role in maintaining the pluripotency state of mESCs. It has been reported that inhibition of BMP4 caused the death of R2i-grown cells. In this study, we used the loss-of-function approach to investigate the role of BMP4 signaling in mESC self-renewal. Inhibition of this pathway with Noggin and dorsomorphin, two bone morphogenetic protein (BMP) antagonists, elicited a quick death of the R2i-grown cells. We showed that the canonical pathway of BMP4 (BMP/SMAD) was dispensable for self-renewal and maintaining pluripotency of these cells. Transcriptome analysis of the BMPi-treated cells revealed that the p53 signaling and two adhesion (AD) and apoptotic mitochondrial change (MT) pathways could be involved in the cell death of the BMPi-treated cells. According to our results, inhibition of BMP4 signaling caused a decrease in cell adhesion and ECM detachment, which triggered anoikis in the R2i-grown cells. Altogether, these findings demonstrate that endogenous BMP signaling is required for the survival of mESCs under the R2i condition.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Hossein Baharvand reports financial support was provided by Iranian Council of Stem Cell Research and Technology. Hossein Baharvand reports financial support was provided by Iran National Science Foundation. Hossein Baharvand reports financial support was provided by Iran Science Elites Federation.
(Copyright © 2022. Published by Elsevier Inc.)

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