Evidence map›Paper›PMID 38956646›Full record

ArticleStem cell research & therapy2024

Autophagy modulation effect on homotypic transfer of intracellular components via tunneling nanotubes in mesenchymal stem cells.

Fatemeh Sadeghsoltani, Çığır Biray Avci, Parisa Hassanpour, Sanya Haiaty, Mohamad Rahmati, Ali Mota, Reza Rahbarghazi, Maryam Nemati, Mahdi Mahdipour, Mehdi Talebi and 3 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Fatemeh SadeghsoltaniStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Çığır Biray AvciDepartment of Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey.
Parisa HassanpourStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sanya HaiatyInfectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohamad RahmatiDepartment of Clinical Biochemistry and Laboratory Medicine, School of Medicine, Tabriz University of Medical Sciences, Tabriz, 5166614766, Iran.
Ali Mota *Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. mota.biomed@gmail.com.
Reza Rahbarghazi *Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. rahbarghazir@tbzmed.ac.ir.ORCID 0000-0003-3864-9166
Maryam NematiDepartment of Genetic, Tabriz Branch, Islamic Azad University, Tabriz, Iran.
Mahdi MahdipourStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mehdi TalebiHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Leila Sabour TakanlouDepartment of Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey.
Maryam Sabour TakanlouDepartment of Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey.
Amir MehdizadehHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Funding

Stem Cell Research Center, Tabriz University of Medical Sciences 66522
6 · The paper itself

Abstract

backgroundRecent studies have proved the role of autophagy in mesenchymal stem cell (MSCs) function and regenerative properties. How and by which mechanism autophagy modulation can affect the juxtacrine interaction of MSCs should be addressed. Here, the role of autophagy was investigated in the formation of tunneling nanotubes (TNTs) and homotypic mitochondrial donation.

methodsMSCs were incubated with 15 µM Metformin (Met) and/or 3 µM 3-methyladenine (3-MA) for 48 h. The formation of TNTs was assessed using bright-field and SEM images. The mitochondria density and ΔΨ values were monitored using flow cytometry analysis. Using RT-PCR and protein array, the close interaction and shared mediators between autophagy, apoptosis, and Wnt signaling pathways were also monitored. The total fatty acid profile was assessed using gas chromatography.

resultData indicated the increase of TNT length and number, along with other cell projections after the induction of autophagy while these features were blunted in 3-MA-treated MSCs (p < 0.05). Western blotting revealed the significant reduction of Rab8 and p-FAK in 3-MA-treated MSCs (p < 0.05), indicating the inhibition of TNT assembly and vesicle transport. Likewise, the stimulation of autophagy increased autophagic flux and mitochondrial membrane integrity compared to 3-MA-treated MSCs. Despite these findings, protein levels of mitochondrial membrane Miro1 and 2 were unchanged after autophagy inhibition/stimulation (p > 0.05). We found that the inhibition/stimulation of autophagy can affect the protein, and transcription levels of several mediators related to Wnt and apoptosis signaling pathways involved in different cell bioactivities. Data confirmed the profound increase of mono and polyunsaturated/saturated fatty acid ratio in MSCs exposed to autophagy stimulator.

conclusionsIn summary, autophagy modulation could affect TNT formation which is required for homotypic mitochondrial donation. Thus, the modulation of autophagy creates a promising perspective to increase the efficiency of cell-based therapies.

Indexed as

AutophagyMesenchymal Stem CellsAdenineAnimalsApoptosisCell Membrane StructuresCells, CulturedHumansMetforminMitochondriaNanotubesWnt Signaling Pathway3-methyladenineAdenineMetforminTunneling NanotubesApoptosisAutophagyMesenchymal stem cellsMitochondrial donationTunneling nanotubesWnt signaling pathway

Identifiers

PMID38956646
PMCPMC11218273

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.