Splenocyte proliferation and anaphylaxis induced by BSA challenge in a D-galactose-induced aging mouse model.

We previously found a cross-reactive autoantibody that bound to bovine serum albumin generated in a D-galactose-induced aging mouse model. Also, we confirmed that other reducing sugars (glucose and fructose) could induce the formation of autoantibody, and only following subcutaneous injection, not oral or intraperitoneal administration. Mice that had never been exposed to bovine serum albumin produced an anti-bovine serum albumin autoantibody following repeated subcutaneous injection of D-galactose (D-gal).

The production of cross-reactive autoantibodies that bind to bovine serum albumin in mice administered reducing sugars by subcutaneous injection.

Introduction: In a previous study, we identified the formation of cross-reactive autoantibodies that bound to bovine serum albumin (BSA) in a D-galactose-induced aging mouse model.

Aim Of The Study: In this study, we investigated the effect of other reducing sugars (namely, glucose and fructose) on the formation of autoantibodies. The effects of concentration and route of administration on the formation of autoantibodies were examined in detail.

Subcutaneous administration of monosodium glutamate to pregnant mice reduces weight gain in pups during lactation.

Administering monosodium glutamate (MSG) to neonatal rodents induces obesity and type 2 diabetes. In addition, several studies have shown that MSG administered to pregnant animals can cross the placenta and reach the foetus. The present study was performed to investigate the effects of administering MSG to pregnant ICR mice on dam and neonatal growth.

Polycystic ovary syndrome (PCOS)-like phenotypes in the d-galactose-induced aging mouse model.

The D-galactose (D-gal)-induced animal model, which is established by consecutive subcutaneous d-gal injections for approximately 6weeks, has been frequently used for aging research. This animal model has been shown to accelerate aging of the brain, kidneys, liver, and blood cells. However, aging of the female reproductive organs in this animal model has not been reported.

Bone marrow-derived circulating progenitor cells fail to transdifferentiate into adipocytes in adult adipose tissues in mice.

Little is known about whether bone marrow-derived circulating progenitor cells (BMDCPCs) can transdifferentiate into adipocytes in adipose tissues or play a role in expanding adipocyte number during adipose tissue growth. Using a mouse bone marrow transplantation model, we addressed whether BMDCPCs can transdifferentiate into adipocytes under standard conditions as well as in the settings of diet-induced obesity, rosiglitazone treatment, and exposure to G-CSF. We also addressed the possibility of transdifferentiation to adipocytes in a murine parabiosis model.

Angiogenic role of LYVE-1-positive macrophages in adipose tissue.

Here we report the discovery of a characteristic dense vascular network (DVN) in the tip portion of epididymal adipose tissue in adult mice. The DVN is formed by angiogenesis rather than by vasculogenesis, and has functional blood circulation. This DVN and its subsequent branching may provide a new functional route for adipogenesis.

Oocyte-based screening of cytokinesis inhibitors and identification of pectenotoxin-2 that induces Bim/Bax-mediated apoptosis in p53-deficient tumors.

In this study, we demonstrate that a loss of p53 sensitizes tumor cells to actin damage. Using a novel oocyte-based screening system, we identified natural compounds that inhibit cytokinesis. Among these, pectenotoxin-2 (PTX-2), which was first identified as a cytotoxic entity in marine sponges, which depolymerizes actin filaments, was found to be highly effective and more potent to activate an intrinsic pathway of apoptosis in p53-deficient tumor cells compared to those with functional p53 both in vitro and in vivo.

Oocyte-based screening system for anti-microtubule agents.

Taxol and vinblastine have been widely used in cancer chemotherapy as anti-microtubule agents. However, there are on-going efforts to find new anti-microtubule agents with fewer of the side effects associated with these drugs, such as toxicity or the development of resistance. The standard method used to identify anti-microtubule agents has been the in vitro microtubule polymerization assay.

A phenotypic study of murine oocyte death in vivo.

Most studies of oocyte apoptosis have been performed in vitro and have employed the method of artificial induction of apoptosis by an anti-cancer agent. However, the process of oocyte death in vivo has not been clearly identified. To investigate the death process in unfertilized oocytes in vivo, we examined the cytochemical change of oocytes collected by oviduct flushing at various intervals after hCG injection.

Bcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing reactive oxygen species-dependent p38 activation.

In this study, we describe novel functions of the anti-apoptotic Bcl-2 family proteins. Bcl-x(L) and E1B-19K were found to inhibit p53-induced irreversible growth arrest and senescence, but not to inhibit transient growth arrest, implying that Bcl-x(L) and E1B-19K are specifically involved in senescence without participating in growth arrest. We provide several lines of evidences showing that the functions of Bcl-x(L) and E1B-19K to prevent generation of reactive oxygen species (ROS) are important to inhibit senescence induction.

Cdk2-dependent phosphorylation of the NF-Y transcription factor and its involvement in the p53-p21 signaling pathway.

Recent studies have suggested that the NF-Y transcription factor is involved in transcription repression of the cell cycle regulatory genes in a response to p53 induction or DNA damage. Here we demonstrate the cdk2-dependent phosphorylation of NF-Y and its involvement in transcription repression by the p53-p21 signaling pathway. Cdk2 phosphorylates two serine residues near the DNA-binding domain of the YA subunit of NF-Y.