Regulation of adipogenic differentiation and adipose tissue inflammation by interferon regulatory factor 3

Abstract: Dysfunction of adipocytes and adipose tissue is a primary defect in obesity and obesity-associated metabolic diseases. Interferon regulatory factor 3 (IRF3) has been implicated in adipogenesis. However, the role of IRF3 in obesity and obesity-associated disorders remains unclear. Here, we show that IRF3 expression in human adipose tissues is positively associated with insulin sensitivity and negatively associated with type 2 diabetes. In mouse pre-adipocytes, deficiency of IRF3 results in increased expression of PPARγ and PPARγ-mediated adipogenic genes, leading to increased adipogenesis and altered adipocyte functionality. The IRF3 knockout (KO) mice develop obesity, insulin resistance, glucose intolerance, and eventually type 2 diabetes with aging, which is associated with the development of white adipose tissue (WAT) inflammation. Increased macrophage accumulation with M1 phenotype which is due to the loss of IFNβ-mediated IL-10 expression is observed in WAT of the KO mice compared to that in wild-type mice. Bone-marrow reconstitution experiments demonstrate that the nonhematopoietic cells are the primary contributors to the development of obesity and both hematopoietic and nonhematopoietic cells contribute to the development of obesity-related complications in IRF3 KO mice. This study demonstrates that IRF3 regulates the biology of multiple cell types including adipocytes and macrophages to prevent the development of obesity and obesity-related complications and hence, could be a potential target for therapeutic interventions for the prevention and treatment of obesity-associated metabolic disorders

Startle habituation: a tool for assessing information processing deficits in zebrafish model of schizophrenia

Prepulse inhibition (PPI) and habituation of acoustic startle reflex have been extensively used to assess deficits in the sensorimotor functions of human patients and animal models of schizophrenia. These assays require expensive and sophisticated experimental setup for fine control of acoustic stimuli and sound attenuation. In this study, we investigate whether startle habituation assay based on mechanical (tap) stimuli can induce similar impairment in the habituation response in the schizophrenia model of larval zebrafish. For this purpose, a custom startle apparatus consisting of a 9 V push and pull solenoid and an Arduino Uno microcontroller was used to generate tap stimuli at desired intervals. Our results showed that tap stimuli at 1 Hz effectively evoked startle response in the control fishes which habituated after a few trials. The habituation response was significantly impaired in the MK801-induced schizophrenia model, similar to that elicited by acoustic startle stimuli in a previous study. We propose this simple and inexpensive method as an alternative tool for studying information processing and attention deficits in the pharmacological model of schizophrenia in zebrafish

PATZ1 (MAZR) Co-occupies Genomic Sites With p53 and Inhibits Liver Cancer Cell Proliferation via Regulating p27

10.3389/fcell.2021.586150Frontiers in Cell and Developmental Biology958615

Protective Function of Mitogen-Activated Protein Kinase Phosphatase 5 in Aging- and Diet-Induced Hepatic Steatosis and Steatohepatitis.

10.1002/hep4.1324Hepatol Commun36748-76

DUSP16 promotes cancer chemoresistance through regulation of mitochondria-mediated cell death

10.1038/s41467-021-22638-7NATURE COMMUNICATIONS12

Recent progress in metal-organic complexes for optoelectronic applications

10.1039/c3cs60449gChemical Society Reviews43103259-3302CSRV