Myricetin and myricitrin indirectly and directly increases uncoupling protein-1 mRNA expression in C3H10T1/2 beige adipocytes.

In thermogenic brown and beige adipocytes, the proton gradient formed by energy derived from nutrients such as lipids and carbohydrates is consumed by uncoupling protein-1 (UCP-1), resulting in thermogenesis without ATP production in the mitochondria. Accordingly, increased UCP-1 expression represents a crucial aspect of dietary management for individuals with overweight and obesity. Myricetin and its glycoside, myricitrin, are food-derived flavonoids that possess various beneficial effects.

Release of SMP30 in Extracellular Vesicles under Conditions of Ascorbic Acid Deficiency Is Involved with Acute Phase Response in ODS Rat.

Senescence marker protein-30 (SMP30) is a senescence marker molecule that exhibits lactonase activity in the ascorbic acid (AsA) biosynthesis pathway, except in primate mammals, including humans. Although numerous studies have shown that hepatic AsA deficiency causes acute-phase responses, details of the relationship between SMP30 expression and acute-phase responses in AsA-deficient conditions remain to be elucidated. Here, we investigated the effects of AsA deficiency on the relationship between SMP30 and acute liver injury in osteogenic disorder Shionogi (ODS) rats, which have a hereditary defect in AsA biosynthesis.

Resveratrol Upregulates Senescence Marker Protein 30 by Activating AMPK/Sirt1-Foxo1 Signals and Attenuating HO-Induced Damage in FAO Rat Liver Cells.

Resveratrol (RSV) is a polyphenol with numerous biological functions, including anti-inflammatory, antioxidant, and anti-aging activities. The novel senescence marker protein-30 (SMP30) indicates aging, and it suppresses hepatic oxidative stress. However, the effects of RSV on SMP30 expression regulation remain unclear.

CD9 protects the sperm from cytotoxic factors in the epididymis as extracellular components.

The mechanism by which seemingly normal sperm cause infertility is still under debate. Although CD9 is expressed in male reproductive tissues, its role in male fertility remains unclear. To address this, we investigated the role of CD9 in analyzing -deficient ( -KO) male mice.

Progesterone depletion results in Lamin B1 loss and induction of cell death in mouse trophoblast giant cells.

Trophoblast giant cells (TGCs), a mouse trophoblast subtype, have large amounts of cytoplasm and high ploidy levels via endocycles. The diverse functions and gene expression profiles of TGCs have been studied well, but their nuclear structures remain unknown. In this study, we focus on Lamin B1, a nuclear lamina, and clarify its expression dynamics, regulation and roles in TGC functions.

The Differentiation Potency of Trophoblast Stem Cells from Mouse Androgenetic Embryos.

In mice, trophoblast stem (TS) cells are derived from the polar trophectoderm of blastocysts. TS cells cultured in the presence of fibroblast growth factor 4 (Fgf4) are in an undifferentiated state and express undifferentiated marker genes such as Cdx2. After removing Fgf4 from the culture medium, TS cells drastically reduce the expression of undifferentiated marker genes, stop cell proliferation, and differentiate into all trophoblast cell subtypes.

Cell proliferation potency is independent of FGF4 signaling in trophoblast stem cells derived from androgenetic embryos.

We previously established trophoblast stem cells from mouse androgenetic embryos (AGTS cells). In this study, to further characterize AGTS cells, we compared cell proliferation activity between trophoblast stem (TS) cells and AGTS cells under fibroblast growth factor 4 (FGF4) signaling. TS cells continued to proliferate and maintained mitotic cell division in the presence of FGF4.