| Gene name: | FBP1 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HSC |
| Experiment: | SA-β-gal activity assay//Flow cytometry//γH2AX staining |
| Description: | Importantly, SA-β-Gal+ cells colocalized with those positive for α-SMA (an activated HSC maker), and IL6 (prominent SASP component), and significant percentage of α-SMA+?HSCs also expressed the DNA damage marker γ-H2AX, collectively supporting the presence of senescent HSCs. As DEN is not usually fibrogenic in mice22,24, we surmised that FBP1 deficiency in and of itself promotes HSC activation and senescence. Indeed, liver fibrosis was also detected in?non-DEN treated Cre livers, together with a population of α-SMA+and Ki67+/α-SMA+HSCs. |
| Target gene: | HMGB1 |
| Official symbol(s): | HMGB1 |
| R-AG-Target gene: | Upregulation |
| Subcategory: | Unclear |
| Target gene experiment: | IF//Immunoblotting |
| Target gene description: | We therefore treated DEN/GFP or DEN/Cre animals with inflachromene (ICM), a small molecule shown to block HMGB1 release45. ICM treatment greatly reduced not only surface tumours, but also microscopic lesions in DEN/Cre mice. ICM did not affect hepatic steatosis, based on comparable TG levels. As expected, cytosolic HMGB1 levels decreased while nuclear HMGB1 levels increased in ICM-treated livers. ICM also substantially reduced numbers of HSCs expressing SASP components. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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