LncRNA CamK-A Regulates Ca-Signaling-Mediated Tumor Microenvironment Remodeling.

Cancer cells entail metabolic adaptation and microenvironmental remodeling to survive and progress. Both calcium (Ca) flux and Ca-dependent signaling play a crucial role in this process, although the underlying mechanism has yet to be elucidated. Through RNA screening, we identified one long noncoding RNA (lncRNA) named CamK-A (lncRNA for calcium-dependent kinase activation) in tumorigenesis.

LncRNA wires up Hippo and Hedgehog signaling to reprogramme glucose metabolism.

The Hippo pathway plays essential roles in organ size control and cancer prevention via restricting its downstream effector, Yes-associated protein (YAP). Previous studies have revealed an oncogenic function of YAP in reprogramming glucose metabolism, while the underlying mechanism remains to be fully clarified. Accumulating evidence suggests long noncoding RNAs (lncRNAs) as attractive therapeutic targets, given their roles in modulating various cancer-related signaling pathways.

Low-molecular-weight fibroblast growth factor 2 attenuates hepatic fibrosis by epigenetic down-regulation of Delta-like1.

Unlabelled: Liver fibrosis, a major cause of end-stage liver diseases, is closely regulated by multiple growth factors and cytokines. The correlation of fibroblast growth factor 2 (FGF2) with chronic liver injury has been reported, but the exact functions of different FGF2 isoforms in liver fibrogenesis remain unclear. Here, we report on the differential expression patterns and functions of low- and high-molecular-weight FGF2 (namely, FGF2(lmw) and FGF2(hmw) , respectively) in hepatic fibrogenesis using a CCl4 -induced mouse liver fibrosis model.

Delta-like 1 serves as a new target and contributor to liver fibrosis down-regulated by mesenchymal stem cell transplantation.

Chronic liver injury always progresses to fibrosis and eventually to cirrhosis, a massive health care burden worldwide. Delta-like 1 (Dlk1) is well known as an inhibitor of adipocyte differentiation. However, whether it is involved in liver fibrosis remains unclear.

Identification of Treg-like cells in Tetraodon: insight into the origin of regulatory T subsets during early vertebrate evolution.

CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg cells) are critical for the maintenance of peripheral tolerance, and the suppression of autoimmune diseases and even tumors. Although Treg cells are well characterized in humans, little is known regarding their existence or occurrence in ancient vertebrates. In the present study, we report on the molecular and functional characterization of a Treg-like subset with the phenotype CD4-2(+)CD25-like(+)Foxp3-like(+) from a pufferfish (Tetraodon nigroviridis) model.

Identification of cytokines involved in hepatic differentiation of mBM-MSCs under liver-injury conditions.

Aim: To identify the key cytokines involved in hepatic differentiation of mouse bone marrow mesenchymal stem cells (mBM-MSCs) under liver-injury conditions.

Methods: Abdominal injection of CCl(4) was adopted to duplicate a mouse acute liver injury model. Global gene expression analysis was performed to evaluate the potential genes involved in hepatic commitment under liver-injury conditions.

Direct hepatic differentiation of mouse embryonic stem cells induced by valproic acid and cytokines.

Aim: To develop a protocol for direct hepatic lineage differentiation from early developmental progenitors to a population of mature hepatocytes.

Methods: Hepatic progenitor cells and then mature hepatocytes from mouse embryonic stem (ES) cells were obtained in a sequential manner, induced by valproic acid (VPA) and cytokines (hepatocyte growth factor, epidermal growth factor and insulin). Morphological changes of the differentiated cells were examined by phase-contrast microscopy and electron microscopy.

Recruitment of endogenous bone marrow mesenchymal stem cells towards injured liver.

Recent studies suggest that mesenchymal stem cells (MSCs) possess a greater differentiation potential than once thought and that they have the capacity to regenerate damaged tissues/organs. However, the evidence is insufficient, and the mechanism governing the recruitment and homing of MSCs to these injured sites is not well understood. We first examined the MSCs circulating in peripheral blood and then performed chemotaxis, wound healing and tubule-formation assays to investigate the migration capability of mouse bone marrow MSCs (mBM-MSCs) in response to liver-injury signals.

Induction of hepatic differentiation of mouse bone marrow stromal stem cells by the histone deacetylase inhibitor VPA.

Bone marrow stromal stem cells (BMSSCs) may have potential to differentiate in vitro and in vivo into hepatocytes. Here, we investigated the effects of valproic acid (VPA) involved in epigenetic modification, a direct inhibitor of histone deacetylase, on hepatic differentiation of mouse BMSSCs. Following the treatment of 2.

[Differentiation of adult mouse mesenchymal stem cells into hepatocytes cultured in a conditioned culture medium of injured hepatocytes].

Objective: To establish a method through which murine bone marrow mesenchymal stem cells (MSCs) can be induced into hepatocytes in vitro.

Methods: A conditioned medium of injured hepatocytes (with CCl4 in vivo) was used to culture the isolated MSCs. The differentiated cells were identified by morphological observation, reverse transcription polymerase chain reaction (RT-PCR), immunofluorescence assay (for AFP, Albumin, and CK18) and periodic acid schiff reaction (PAS) for glycogen.