MiR-122 modification enhances the therapeutic efficacy of adipose tissue-derived mesenchymal stem cells against liver fibrosis.
Lou G., Yang Y., Liu F., Ye B., Chen Z., Zheng M.
Animal Study, published in J Cell Mol Med (2017) — 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 Mol Med (2017)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 28544786
- DOI
- 10.1111/jcmm.13208
Abstract (original English)
Mesenchymal stem cell (MSC) transplantation alone may be insufficient for treatment of liver fibrosis because of complicated histopathological changes in the liver. Given that miR-122 plays an essential role in liver fibrosis by negatively regulating the proliferation and transactivation of hepatic stellate cells (HSCs), this study investigated whether miR-122 modification can improve the therapeutic efficacy of adipose tissue-derived MSCs in treating liver fibrosis. MiR-122-modified AMSCs (AMSC-122) were constructed through lentivirus-mediated transfer of pre-miR-122. MiR-122-modified AMSCs expressed high level of miR-122, while they retained their phenotype and differentiation potential as naïve AMSCs. AMSC-122 more effectively suppressed the proliferation of and collagen maturation in HSCs than scramble miRNA-modified AMSCs. In addition, AMSC-derived exosomes mediated the miR-122 communication between AMSCs and HSCs, further affecting the expression levels of miR-122 target genes, such as insulin-like growth factor receptor 1 (IGF1R), Cyclin G(1) (CCNG1) and prolyl-4-hydroxylase α1 (P4HA1), which are involved in proliferation of and collagen maturation in HSCs. Moreover, miR-122 modification enhanced the therapeutic efficacy of AMSCs in the treatment of carbon tetrachloride (CCl 4 )-induced liver fibrosis by suppressing the activation of HSCs and alleviating collagen deposit
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.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.