Silencing the ADAM9 Gene through CRISPR/Cas9 Protects Mice from Alcohol-Induced Acute Liver Injury.
Yong-Yong ZhangSan-Qiang LiYing SongPing WangXiao-Gai SongWen-Feng ZhuDong-Mei WangPublished in: BioMed research international (2022)
Alcoholic liver injury is a major global public health concern at present. The ADAM9 gene plays a crucial role in the occurrence and development of various liver diseases, but its role in acute alcoholic liver injury remains ambiguous. In this study, a chimeric single-guide RNA targeting the genomic regions of mouse ADAM9 was designed using the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) technology. Next, the role of ADAM9 in acute alcoholic liver injury in vitro in cultured mouse cells and in vivo in a hydrodynamic injection-based alcoholic liver injury mouse model was documented. The findings of this study suggest that ADAM9 induces by regulating cell proliferation, apoptosis, and stress metabolism in mice. Thus, inhibiting the expression of ADAM9 gene using CRISPR/Cas9 can attenuate alcohol-induced acute liver injury in mice.
Keyphrases
- liver injury
- drug induced
- crispr cas
- genome editing
- genome wide
- public health
- copy number
- cell proliferation
- mouse model
- high fat diet induced
- cell cycle arrest
- liver failure
- endoplasmic reticulum stress
- oxidative stress
- induced apoptosis
- poor prognosis
- signaling pathway
- cell death
- stem cells
- long non coding rna
- insulin resistance
- alcohol consumption
- metabolic syndrome
- endothelial cells
- bone marrow
- respiratory failure
- drug delivery
- cancer therapy
- stress induced
- extracorporeal membrane oxygenation
- cell therapy
- mesenchymal stem cells