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hepatic cells

Kelly Stevens Receives $1.3M Allen Distinguished Investigator Award to Study How Liver Develops

[University of Washington Department of Bioengineering] University of Washington bioengineer Kelly Stevens, whose research focuses on mapping human organs and engineering artificial human tissues, has received an Allen Distinguished Investigator Award to support her work to map and understand how human livers develop.

ECM1 Modified HF-MSCs Targeting HSC Attenuate Liver Cirrhosis by Inhibiting the TGF-β/Smad Signaling Pathway

[Cell Death Discovery] To improve the effectiveness of naïve hair follicle-derived-MSC (HF-MSC) treatments on liver cirrhosis (LC), the authors used bioinformatic tools to identify an exogenous gene targeting hepatic stellate cells (HSCs) among the differentially expressed genes in LC to modify HF-MSCs.

Temporal Analyses of Postnatal Liver Development and Maturation by Single-Cell Transcriptomics

[Developmental Cell] Researchers observed unexpectedly high levels of hepatocyte heterogeneity in the developing liver and the progressive construction of the zonated metabolic functions from pericentral to periportal hepatocytes, which was orchestrated with the development of sinusoid endothelial, stellate, and Kupffer cells.

PD-L1 Promotes Myofibroblastic Activation of Hepatic Stellate Cells by Distinct Mechanisms Selective for TGF-β Receptor I versus II

[Cell Reports] To determine the role of programmed death-ligand 1 (PD-L1) in myofibroblastic activation of hepatic stellate cells (HSCs), researchers disrupted PD-L1 of HSCs by shRNA or anti-PD-L1 antibody.

Endocan, a Soluble Marker of Endothelial Cell Activation Is a Molecular Marker of Disease Severity in Women with Preeclampsia

[Reproductive Sciences] Scientists hypothesized that women diagnosed with preeclampsia and/or fetal growth restriction have elevated circulating endocan concentrations in direct relationship with severity of clinical manifestations.

Cullin Neddylation Inhibitor Attenuates Hyperglycemia by Enhancing Hepatic Insulin Signaling through Insulin Receptor Substrate Stabilization

[Proceedings of the National Academy of Sciences of the United States of America] In vitro knockdown of either cullin 1 or cullin 3, but not other cullin members, attenuated insulin-induced insulin receptor substrate protein degradation and enhanced cellular insulin signaling activation.

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