Mesenchymal stem cells (MSCs) are considered to be an ideal source for the cell therapy of end‑stage liver diseases. Umbilical cord (UC)‑MSCs can be obtained via a non‑invasive procedure and can be easily cultured, making them potentially superior candidates for cell transplantation when compared with MSCs from other sources. In the present study, UC‑MSCs were induced to differentiate into hepatocytes and were compared with bone marrow (BM)‑MSCs for their hepatic differentiation potential. UC‑MSCs showed significantly higher proliferation than BM‑MSCs. Under hepatic induction, UC‑MSCs and BM‑MSCs could differentiate into hepatocytes. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis revealed that a higher expression of the hepatocyte‑specific genes albumin, cytochrome P450 3A4 (CYP3A4), tyrosine‑aminotransferase, glucose‑6phosphate, α1 antitrypsin and α‑fetoprotein was detected in differentiated UC‑MSCs when compared with differentiated BM‑MSCs. The results of ELISA and western blotting were in accordance with those of RT‑qPCR. Theses results indicated that UC‑MSCs had higher hepatic differentiation potential than BM‑MSCs. Therefore, UC‑MSCs may be advantageous over BM‑MSCs for the treatment of end‑stage liver disease.
Remarkable progress has been achieved in the transplantation of mesenchymal stem cells (MSCs)for the treatment of liver injury and hepatic failure.However,there are obstacles such as low engraftment capacity,tumorigenesis,and a fibrogenic potential that all hamper the use of MSCs in clinical trials.Therefore,it is worthwhile to talk about the alternatives that will increase the safety and efficacy of MSCs therapy.To date,applications of MSCs-derived hepatocytes,genetically modified MSCs,or MSC-conditioned medium for promoting liver regeneration have shown encouraging results.This review summarizes the current applications of MSCs in the study of hepatic regeneration.
Key words:
Mesenchymal stem cells; Liver regeneration
Primary hepatocellular carcinoma progresses from liver fibrosis and cirrhosis to eventually result in liver failure and distant metastasis.Surgical resection is the preferred method of treatment for liver cancer while interventional treatment and liver transplantation are the choices to treat end-stage liver cancer.Unfortunately,partial hepatectomy and interventional treatment are not ideal due to the resulting consequence of hepatocyte dysfunction.Extensive clinical application of liver transplants is limited by the lack of available donors and high costs.Over the past decade,researches on bone marrow mesenchymal stem cells (BMSCs)have made remarkable achievements in the medical field.In this review,we summarize the recent progress of BMSCs in the treatment of liver diseases.
Key words:
Bone marrow mesenchymal stem cells; Liver cancer; Liver regeneration; Tumor metastasis
// Sun Yong 1 , Yu Yabin 1 , Zhou Bing 1 , Zhu Chuanrong 1 , Gu Dianhua 1 , Zhang Jianhuai 1 , Yuan Weidong 1 , Wang Shuming 1 and Liu Ling 1 1 Department of Hepatobiliary and Pancreatic Surgery, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, People's Republic of China Correspondence to: Liu Ling, email: liulingdoc_2002@aliyun.com Keywords: PDAC, DGCR5, miR-320a, lncRNA Received: March 13, 2017 Accepted: April 17, 2017 Published: June 06, 2017 ABSTRACT Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal malignancies. Long non-coding microRNAs (lncRNAs) are a newly discovered type of regulatory molecule with both diagnostic and prognostic value, but the role of lncRNA in PDAC has not been well investigated until now. Here, we present evidence that shows that the lncRNA DGCR5 is significantly reduced in PDAC tissues as well as in PDAC cell lines and that the downregulation of DGCR5 predicts poor prognosis. Ectopic expression of DGCR5 inhibits the proliferation and migration, and promotes 5-FU resistances of PDAC cells. Further experiments demonstrated that DGCR5 and miR-320a regulate each other in a reciprocal manner and that DGCR5 reverses the inhibition of PDCD4 by miR-320a, which is involved in the regulation of the PDAC cell phenotype and response to 5-FU. Our findings provide novel information about the functions of lncRNAs in PDAC, some of which might be beneficial to the precise diagnosis, prognosis and individualized therapy of patients with PDAC in the future.
Objective
To study the effectiveness and safety of prophylactic anticoagulation in the prevention of portal venous thrombosis (PVST) in patients after laparoscopic splenectomy.
Methods
A systematic search of the PubMed, Embase, Cochrane Library, Sinomed, Wangfang, Weipu and CNKI databases was performed to identify studies which compared outcomes in patients with or without prophylactic anticoagulation after laparoscopic splenectomy. The quality of the included studies was assessed using the Cochrane collaboration tool and the Newcastle-Ottawa Scale. Heterogeneity was evaluated using the χ2 and I2 tests. The primary outcome was the incidence of postoperative PVST.
Results
Five studies were included into this review, which involved 206 and 168 patients with or without prophylactic anticoagulation, respectively. The incidence of PVST was significantly reduced with prophylactic anticoagulation with an odds ratio (OR) of 0.32 [95% confidence interval (CI), 0.13~0.79, P<0.05].
Conclusion
Prophylactic anticoagulation resulted in a significant reduced incidence of PVST after laparoscopic splenectomy.
Key words:
Portal vein system thrombosis; Anticoagulants; Laparoscopic splenectomy; Meta-analysis
Previous studies have shown that long noncoding RNAs (lncRNAs) are capable of regulating cell differentiation and pluripotency. The objective of the present study was to explore the effect of lncRNA cancer upregulated drug resistant (CUDR) on the hepatic differentiation of human umbilical cord mesenchymal stem cells (HuMSCs). HuMSCs were subjected to a hepatogenic differentiation protocol. The level of CUDR was monitored by reverse transcription‑quantitative PCR (RT‑qPCR) following certain stages of hepatic differentiation. Lentivirus transfection was used to achieve CUDR overexpression. The hepatocyte‑related proteins and mRNAs were then examined by immunofluorescence, ELISA and RT‑qPCR analyses. The results showed that CUDR was upregulated during the hepatic differentiation of HuMSCs. Upregulation of CUDR can improve hepatic differentiation of HuMSCs, including hepatocyte‑related genes and proteins. In addition, it was also found that liver‑enriched transcription factors were upregulated after CUDR overexpression. Moreover, there was an association between the Wnt/β‑catenin pathway and CUDR. In summary, these results demonstrated that the overexpression of CUDR could improve the hepatic differentiation of HuMSCs, therefore it could be an ideal source for regenerative therapy.
Background: With a poor prognosis for affected individuals, pancreatic adenocarcinoma (PAAD) is known as a complicated and diverse illness. Immunocytes have become essential elements in the development of PAAD. Notably, sphingolipid metabolism has a dual function in the development of tumors and the invasion of the immune system. Despite these implications, research on the predictive ability of sphingolipid variables for PAAD prognosis is strikingly lacking, and it is yet unclear how they can affect PAAD immunotherapy and targeted pharmacotherapy. Methods: The investigation process included SPG detection while also being pertinent to the prognosis for PAAD. Both the analytical capability of CIBERSORT and the prognostic capability of the pRRophetic R package were used to evaluate the immunological environments of the various HCC subtypes. In addition, CCK-8 experiments on PAAD cell lines were carried out to confirm the accuracy of drug sensitivity estimates. The results of these trials, which also evaluated cell survival and migratory patterns, confirmed the usefulness of sphingolipid-associated genes (SPGs). Results: As a result of this thorough investigation, 32 SPGs were identified, each of which had a measurable influence on the dynamics of overall survival. This collection of genes served as the conceptual framework for the development of a prognostic model, which was carefully assembled from 10 chosen genes. It should be noted that this grouping of patients into cohorts with high and low risk was a sign of different immune profiles and therapy responses. The increased abundance of SPGs was identified as a possible sign of inadequate responses to immune-based treatment approaches. The careful CCK-8 testing carried out on PAAD cell lines was of the highest importance for providing clear confirmation of drug sensitivity estimates. Conclusion: The significance of Sphingolipid metabolism in the complex web of PAAD development is brought home by this study. The novel risk model, built on the complexity of sphingolipid-associated genes, advances our understanding of PAAD and offers doctors a powerful tool for developing personalised treatment plans that are specifically suited to the unique characteristics of each patient.
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