Adipose tissue‑derived mesenchymal stem cells (ADSCs) have been considered to be attractive and readily available adult mesenchymal stem cells, and they are becoming increasingly popular for use in regenerative cell therapy, as they are readily accessible through minimally invasive techniques. The present study investigated whether autologous ADSC transplantation promoted liver regeneration following a repeat partial hepatectomy in rats. The rats were divided into three groups as follows: 70% partial hepatectomy (PH) group; repeat PH (R‑PH) group and R‑PH/ADSC group, subjected to R‑PH and treated with autologous ADSCs via portal vein injection. In each group, the rats were sacrificed at different time points postoperatively in order to evaluate the changes in liver function and to estimate the liver regenerative response. The expression of proliferating cell nuclear antigen (PCNA) labeling index in the liver was measured using immunohistochemistry. The expression levels of hepatocyte growth factor (HGF) mRNA were measured using reverse transcription polymerase chain reaction. The results showed that regeneration of the remaining liver following R‑PH was significantly promoted by ADSC transplantation, as shown by a significant increase in liver to body weight ratio and the PCNA labeling index at 24 h post‑hepatectomy. Additionally, ADSC transplantation markedly inhibited the elevation of serum levels of alanine aminotransferase, aspartate aminotransferase and total bilirubin, increased HGF content and also attenuated hepatic vacuolar degeneration 24 h postoperatively. Furthermore, the liver was found to almost fully recover from hepatocellular damage due to hepatectomy among the three groups at 168 h postoperatively. These results indicated that autologous ADSC transplantation enhanced the regenerative capacity of the remnant liver tissues in the early phase following R‑PH.

/pdf/autologous-adipose-tissue-derived-mesenchymal-stem-cells-are-3h2zkr4fyu.pdf

Autologous adipose tissue‑derived mesenchymal stem cells are involved in rat liver regeneration following repeat partial hepatectomy.

The update on transcriptional regulation of autophagy in normal and pathologic cells: A novel therapeutic target

Compound Kushen Injection intervenes metabolic reprogramming and epithelial-mesenchymal transition of HCC via regulating β-catenin/c-Myc signaling.

BACKGROUND & AIMS
To clarify the mechanism of persistent cholestasis after massive hepatectomy, the relationship between such cholestasis and the expression and localization of organic anion transporters for bile acids was examined in a rat model.


METHODS
Male Sprague-Dawley rats were subjected to 90% hepatectomy, and tissues were harvested at 0, 1, 3, and 7 days for microarray analysis, quantitative real-time polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemistry to examine the expression of multidrug resistance protein 4 (Mrp4), bile salt export pump (Bsep), and sodium-dependent taurocholate cotransporting polypeptide (Ntcp).


RESULTS
Persistently elevated levels of serum bile acids were observed at days 3 and 7. RT-PCR and Western blotting indicated that the expression of Mrp4, a bile acid export pump located in the basolateral membrane, was increased at day 3. The expression of Ntcp, a transporter used to uptake bile acids from the sinusoids, was significantly decreased throughout the period. The levels of Bsep, an export pump localized to the canalicular membrane, were unchanged. Immunohistochemistry revealed the localization of Mrp4 and Bsep in the basolateral and canalicular membranes, respectively. On the other hand, at days 3 and 7, Ntcp was localized in the cytoplasm and was hardly detected in the basolateral membrane.


CONCLUSIONS
These results suggested that the sustained repression and translocation of Ntcp and the expression of Mrp4 at the basolateral membrane seem to be responsible for the high blood bile acids levels after massive hepatectomy.

Sustained Repression and Translocation of NTCP and Expression of MRP4 for Cholestasis after Rat 90% Partial Hepatectomy [Innovation in Transplant and Regenerative Medicine. The 13th Meeting of Hirosaki International Forum of Medical Science. Communication Center of Hirosaki University School of Medicine. September 9, 2011, Hirosaki, Japan]

Background The Associating Liver Partition and Portal Ligation for Staged Hepatectomy (ALPPS) depends on a significant inter-stages kinetic growth rate (KGR) Liver regeneration is highly energy-dependent The metabolic adaptations in ALPPS are unknown Aims: i) Assess bioenergetics in both stages of ALPPS (T1 and T2) and compare them with control patients undergoing minor (miHp) and major hepatectomy (MaHp), respectively; ii) Correlate findings in ALPPS with volumetric data; iii) Investigate expression of genes involved in liver regeneration and energy metabolism Methods Five patients undergoing ALPPS, five controls undergoing miHp and five undergoing MaHp Assessment of remnant liver bioenergetics in T1, T2 and controls Analysis of gene expression and protein content in ALPPS Results Mitochondrial function was worsened in T1 versus miHp; and in T2 versus MaHp (p  Conclusion Metabolic capacity in ALPPS is worse than in controls, improves between stages and correlates with volumetric growth Bioenergetic adaptations in ALPPS could serve as surrogate markers of liver reserve and as target for energetic conditioning

Bioenergetic adaptations of the human liver in the ALPPS procedure - how liver regeneration correlates with mitochondrial energy status.

Construction of prediction model for prognosis of uterine corpus endometrial carcinoma based on pyroptosis gene

miR-22 expression in hepatocellular carcinoma: Correlation with E-cadherin and Vimentin expression

Bile acids, which are synthesized from cholesterol in the hepatocytes of the liver, are amphipathic molecules with a steroid backbone Studies have shown that bile acid exhibits important effects on liver regeneration However, the mechanism underlying these effects remains unclear The aim of the present study was to investigate the effect of bile acid and the farnesoid X receptor (FXR) on hepatic regeneration and lipid metabolism Rats were fed with 02% bile acid or glucose for 7 days and then subjected to a 50 or 70% hepatectomy Hepatic regeneration rate, serum and liver levels of bile acid, and expression of FXR and Caveolin‑1, were detected at 24, 48 or 72 h following hepatectomy The expression of proliferating cell nuclear antigen (PCNA) in the liver was measured using immunohistochemistry at the end of the study Hepatocytes isolated from rats were treated with bile acid, glucose, FXR agonist and FXR antagonist, separately or in combination Lipid metabolism, the expression of members of the FXR signaling pathway and energy metabolism‑related factors were measured using ELISA kits or western blotting Bile acid significantly increased the hepatic regeneration rate and the expression of FXR, Caveolin‑1 and PCNA Levels of total cholesterol and high density lipoprotein were increased in bile acid‑ or FXR agonist‑treated hepatocytes in vitro Levels of triglyceride, low density lipoprotein and free fatty acid were decreased In addition, bile acid and FXR agonists increased the expression of bile salt export pump and small heterodimer partner, and downregulated the expression of apical sodium‑dependent bile acid transporter, Na+/taurocholate cotransporting polypeptide and cholesterol 7α‑hydroxylase These results suggested that physiological concentrations of bile acid may promote liver regeneration via FXR signaling pathways, and may be associated with energy metabolism

/pdf/bile-acid-promotes-liver-regeneration-via-farnesoid-x-2enf2bqoit.pdf

Bile acid promotes liver regeneration via farnesoid X receptor signaling pathways in rats

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Papers

Construction of prediction model for prognosis of uterine corpus endometrial carcinoma based on pyroptosis gene

miR-22 expression in hepatocellular carcinoma: Correlation with E-cadherin and Vimentin expression

Bile acid promotes liver regeneration via farnesoid X receptor signaling pathways in rats