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Updated: May 10, 2026
Isolation, In Vitro Expansion, and Characterization of Mesenchymal Stem Cells from Mouse Epididymal Adipose Tissue
Published on: January 12, 2024
Systemic treatment with adipose-derived mesenchymal stem cells ameliorates clinical and pathological features in the
S Marconi1, M Bonaconsa1, I Scambi1
1Department of Neurological Sciences and Movement, University of Verona, Verona, Italy.
Abstract:
Therapeutic strategies for the fatal neurodegenerative disease amyotrophic lateral sclerosis (ALS) are actually minimally effective on patients' survival and quality of life. Although stem cell therapy has raised great expectations, information on the involved molecular mechanisms is still limited. Here we assessed the efficacy of the systemic administration of adipose-derived mesenchymal stem cells (ASC), a previously untested stem cell population, in superoxide-dismutase 1 (SOD1)-mutant transgenic mice, the animal model of familial ALS. The administration of ASC to SOD1-mutant mice at the clinical onset significantly delayed motor deterioration for 4-6 weeks, as shown by clinical and neurophysiological tests. Neuropathological examination of ASC-treated SOD1-mutant mice at day 100 (i.e. the time of their best motor performance) revealed a higher number of lumbar motorneurons than in phosphate-buffered saline-treated SOD1-mutant mice and a restricted number of undifferentiated green fluorescent protein-labeled ASC in the spinal cord. By examining the spinal cord tissue factors that may prolong neuronal survival, we found a significant up-regulation in levels of glial-derived neurotrophic factor (GDNF) and basic fibroblast growth factor (bFGF) after ASC treatment. Considering that ASC produce bFGF but not GDNF, these findings indicate that ASC may promote neuroprotection either directly and/or by modulating the secretome of local glial cells toward a neuroprotective phenotype. Such neuroprotection resulted in a strong and long-lasting effect on motor performance and encourages the use of ASC in human pathologies, in which current therapies are not able to maintain a satisfying neurological functional status.
Insights
Adipose-derived mesenchymal stem cells (ASC) significantly delayed motor decline in a mouse model of amyotrophic lateral sclerosis (ALS). This stem cell therapy enhanced motor neuron survival and may offer new hope for ALS patients.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Stem Cell Biology
Background:
- Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with limited effective treatments.
- Stem cell therapy shows promise for ALS, but underlying mechanisms require further investigation.
Purpose of the Study:
- To evaluate the efficacy of adipose-derived mesenchymal stem cells (ASC) in a mouse model of familial ALS (SOD1-mutant mice).
- To explore the neuroprotective mechanisms of ASC in ALS.
Main Methods:
- Systemic administration of ASC to SOD1-mutant mice at clinical onset.
- Assessment of motor function using clinical and neurophysiological tests.
- Neuropathological examination of spinal cord tissue, including motor neuron counts and analysis of neurotrophic factors.
Main Results:
- ASC treatment significantly delayed motor deterioration by 4-6 weeks in SOD1-mutant mice.
- ASC-treated mice showed increased lumbar motor neuron survival compared to controls.
- Elevated levels of glial-derived neurotrophic factor (GDNF) and basic fibroblast growth factor (bFGF) were observed in the spinal cord.
Conclusions:
- Systemic ASC administration demonstrates neuroprotective effects in a preclinical ALS model.
- ASC may promote neuroprotection directly or by modulating glial cell secretomes.
- ASC therapy holds potential for treating neurodegenerative diseases like ALS where current options are insufficient.
