Role of laminin-111 in neurotrophin-3 production of canine adipose-derived stem cells: involvement of Akt, mTOR, and p70S6K.
Park SS., Lee YJ., Han HJ., Kweon OK.
Animal Study, published in J Cell Physiol (2011) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Cell Physiol (2011)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 21321942
- DOI
- 10.1002/jcp.22686
- Citations
- 6
Abstract (original English)
Extracellular matrix (ECM) components play an important role in the regulation and maintenance of neural stem cells (NSCs). Laminin, an ECM component, is a key factor in promoting axonal regeneration and differentiation of NSCs. Since NSCs cannot be easily harvested with low morbidity, adipose-derived stem cells have been suggested for therapeutic applications of neural tissue damage. Therefore, the potential of laminin-111 to enhance the production of neurotrophin-3 (NT3) and its related signal pathways from canine adipose tissue-derived stem cells (cADSCs) was investigated. Laminin-111 enhanced NT3 production in neural induction medium (NIM). Treatment of NIM or laminin-111 on cADSCs distinctively changed integrin β1 mRNA and protein expression levels. In addition, laminin-111-induced Akt phosphorylation was inhibited by integrin β1 small interfering RNA (siRNA) and PI3K inhibitors (LY294002 and wortmannin). Furthermore, increased phosphorylations of mTOR and p70S6K by laminin-111 were blocked by inhibitors or specific siRNA, respectively. Moreover, laminin-111-induced NT3 production was blocked by these inhibitors. In experiments to induce the differentiation of cADSCs, laminin-111 increased the expression of neuronal markers β 3 tubulin, MAP2, and NeuN, and decreased the expression of the NSC markers nestin and vimentin. In conclusion, laminin-111 increases NT3 production t
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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