Postoperative Ileus Murine Model

Most patients experience postoperative ileus (POI) after surgery, which is associated with increased morbidity, mortality, and hospitalization time. POI ...

murine-model-for-selective-transection-of-intestinal-autonomic-nerves

Murine Model for Selective Transection of Intestinal Autonomic Nerves

Autonomic nerves comprise the sympathetic and parasympathetic systems, which act in a largely antagonistic manner to regulate diverse physiological ...

Capital Medical University

National Clinical Research Center for Digestive Diseases

Capital Medical University School of Stomatology

State Key Lab of Digestive Health

Beijing Key Laboratory of Cancer Invasion and Metastasis Research

Hepatic stellate cells (HSC) and hydrogen sulfide (HS) both play important roles in the development of hepatocellar carcinoma (HCC). Whereas, in the microenvironment of HCC, whether HSC participate in regulating the biological process of HCC cells by releasing HS remains elusive. In vitro, Flow cytometry (FCM), CCK-8, RNA-sequencing, Western blotting, RT-qPCR, immunofluorescence and ChIP assays were carried out in the HCC cells to investigate the effect of HS on biological functions and JNK/JunB-TNFSF14 signaling pathway. Specimens from HCC patients were analyzed by RT-qPCR and Western blotting assays for evaluating the expression of TNFSF14 and CSE. Statistical analysis was used to analyze the correlation between TNFSF14 expression and clinical data of HCC patients. Based on the FCM and CCK-8 results, we found the LX-2 cells were able to induce HCC cells apoptosis through releasing HS. RNA-sequencing, RT-qPCR, and Western blotting results showed that TNFSF14 gene was upregulated in both LX-2 and NaHS group. NaHS treated in HCC cells led to JNK/JunB signaling pathway activating and greater binding of p-JunB to its responsive elements on TNFSF14 promoter. Impairment of TNFSF14 induction alleviated LX-2 and NaHS induced apoptosis of HepG2 and PLC/PRF/5 cells. Furthermore, TNFSF14 expression in HCC tissues was lower than the adjacent tissue. HCC patients with low expression of TNFSF14 had higher malignant degree and poor prognosis. In summary, demonstration of the involvement of HSC-derived HS in JNK/JunB mediated expression of TNFSF14 gene strongly indicates HS palys an important role in the regulation of HCC apoptosis.

Hepatic stellate cell mediates transcription of TNFSF14 in hepatocellular carcinoma cells via HS/CSE-JNK/JunB signaling pathway.

Retraction Note: Hepatic stellate cell mediates transcription of TNFSF14 in hepatocellular carcinoma cells via HS/CSE-JNK/JunB signaling pathway.

In mammalian systems, hydrogen sulfide (HS)-one of the three known gaseous signaling molecules in mammals-has been found to have a variety of physiological functions. Existing studies have demonstrated that endogenous HS is produced through enzymatic and non-enzymatic pathways. The liver is the body's largest solid organ and is essential for HS synthesis and elimination. Mounting evidence suggests HS has essential roles in various aspects of liver physiological processes and pathological conditions, such as hepatic lipid metabolism, liver fibrosis, liver ischemia‒reperfusion injury, hepatocellular carcinoma, hepatotoxicity, and acute liver failure. In this review, we discuss the functions and underlying molecular mechanisms of HS in multiple liver pathophysiological conditions.

The double-edged role of hydrogen sulfide in the pathomechanism of multiple liver diseases.

This study sought to investigate risk factors for 6-week mortality of patients with decompensated liver cirrhosis associated esophagogastric variceal bleeding (EGVB) and clinical characteristics of myocardial injury in cirrhotic patients with EGVB. This retrospective cohort study included 249 patients with decompensated liver cirrhosis associated EGVB in the Department of Emergency. Patients were divided into two groups including liver cirrhosis associated EGVB without myocardial injury and liver cirrhosis associated EGVB with myocardial injury. Myocardial injury, recurrent bleeding, total bilirubin (TBIL) level and dyslipidemia are independent risk factors for 6-week mortality in liver cirrhosis associated EGVB. Among all patients with liver cirrhosis associated EGVB, 90 (36.2%) had myocardial injury and 159 individuals (63.8%) not. The 6-week mortality in the group with myocardial injury was 21%, which was significantly higher than that of 7% in the group without myocardial injury. More patients in the myocardial injury group smoked, had moderate to severe esophageal varices, liver failure, and Child-Pugh C liver function compared to the non-myocardial injury group. Myocardial injury, recurrent bleeding, TBIL level and dyslipidemia are independent risk factors for death within 6 weeks in liver cirrhosis associated EGVB. The 6-week mortality is considerably higher in patients with myocardial injury in liver cirrhosis associated EGVB than those without myocardial injury.

ArticleTotal : 2	Year
Publication title Cited by 4	2024
Publication title	2026

Article	Year
Hepatic stellate cell mediates transcription of TNFSF14 in hepatocellular carcinoma cells via HS/CSE-JNK/JunB signaling pathway. Cell death & disease\| PubMed ID: 35292636	2022
Retraction Note: Hepatic stellate cell mediates transcription of TNFSF14 in hepatocellular carcinoma cells via HS/CSE-JNK/JunB signaling pathway. Cell death & disease\| PubMed ID: 36450708	2022
The double-edged role of hydrogen sulfide in the pathomechanism of multiple liver diseases. Frontiers in pharmacology\| PubMed ID: 36588686	2022
Myocardial injury is a risk factor for 6-week mortality in liver cirrhosis associated esophagogastric variceal bleeding. Scientific reports\| PubMed ID: 37069298	2023

Bihan Liu

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