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Study of the Actin Cytoskeleton in Live Endothelial Cells Expressing GFP-Actin
Published on: November 18, 2011
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Actin cytoskeleton dynamics in stem cells from autistic individuals
Karina Griesi-Oliveira1,2, Angela May Suzuki3, Aline Yasuda Alves4
1Hospital Israelita Albert Einstein, São Paulo, Brazil. karina.griesi@einstein.br.
Scientific Reports
|July 26, 2018
Summary
Autism spectrum disorder (ASD) may involve impaired actin cytoskeleton dynamics in stem cells. This study found altered actin filament reconstruction in cells from over half of ASD patients, suggesting a potential cellular basis for neuronal abnormalities.
Area of Science:
- Neuroscience
- Cell Biology
- Genetics
Background:
- Cytoskeletal dynamics are crucial for neuronal development.
- Indirect evidence suggests compromised cytoskeletal function in autism spectrum disorders (ASD).
- No prior studies have functionally assessed cytoskeleton dynamics in cells from ASD patients.
Purpose of the Study:
- To investigate the functional regulation of actin cytoskeleton dynamics in stem cells from individuals with ASD.
- To determine if actin filament reconstruction is altered in cells derived from ASD patients.
Main Methods:
- Utilized stem cells from human exfoliated deciduous teeth (SHEDs) from 13 ASD patients and 8 controls.
- Induced actin filament depolymerization followed by measurement of repolymerization upon Rho GTPase activation (Rac, Cdc42, RhoA).
Main Results:
- Altered actin filament reconstruction dynamics were observed in stem cells from 7 out of 13 ASD individuals (53%).
- One patient's cells showed abnormalities consistent with previously observed neuronal cell defects (shortened, less arborized neurites).
- Potentially pathogenic genetic variants were identified that may correlate with observed actin repolymerization defects.
Conclusions:
- Actin polymerization dynamics are impaired in a significant subgroup of individuals with ASD.
- This impairment may contribute to the neuronal abnormalities observed in autism spectrum disorders.
- Findings suggest a potential cellular mechanism underlying ASD pathophysiology.
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