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Transmission of Mouse Aapoaii Amyloidosis from Mother to Pups
Published in Gilles Grateau, Robert A. Kyle, Martha Skinner, Amyloid and Amyloidosis, 2004
T. Korenaga, X. Fu, M. Mori, J. Sawashita, H. Naiki, T. Matsushita, K. Higuchi
The R1.P1-Apoa2c, a congenic strain of mice that has amyloidogenic Apoa2c allele of the SAMP1 strains on the genetic background of the SAMR1 strain were raised under specific pathogen free (SPF) condition.
Macrophages in the reticuloendothelial system inhibit early induction stages of mouse apolipoprotein A-II amyloidosis
Published in Amyloid, 2023
Hiroki Miyahara, Jian Dai, Ying Li, Xiaoran Cui, Hibiki Takeuchi, Naomi Hachiya, Fuyuki Kametani, Masahide Yazaki, Masayuki Mori, Keiichi Higuchi
R1.P1-Apoa2c mice are a congenic strain with the amyloidogenic Apoa2c allele of the SAMP1 strain on the genetic background of the SAMR1 strain [27]. Homozygous ApoA-II knockout (129S4/SvJae-Apoa2tm1Bres) mice were purchased from Jackson Laboratory and crossbred for 10 generations to a pure C57BL/6 background in our laboratory (B6-Apoa2−/−). Mice were reared in the Division of Animal Research, Research Center for Support of Advanced Sciences, Shinshu University, under specific pathogen-free conditions at 24 ± 2 °C with a controlled light regimen (12-h light/dark cycle). A commercial diet (MF; Oriental Yeast, Tokyo, Japan) and tap water were available ad libitum. All experiments were performed with the approval of the Committee for Animal Experiments at Shinshu University.
The effects of coenzyme Q10 supplementation on gene expression related to insulin, lipid and inflammation in patients with polycystic ovary syndrome
Published in Gynecological Endocrinology, 2018
Elham Rahmani, Mehri Jamilian, Mansooreh Samimi, Maryam Zarezade Mehrizi, Esmat Aghadavod, Elmira Akbari, Omid Reza Tamtaji, Zatollah Asemi
This research demonstrated that CoQ10 supplementation for 12 weeks in subjects with PCOS upregulated PPAR-γ expression, but unchanged GLUT-1 expression. However, data on the effects of CoQ10 intake on gene expression of PPAR-γ and GLUT-1 are scarce; few studies have evaluated the effects of CoQ10 on gene expression related to insulin. Lee et al. [19] found that CoQ10 increased gene expression of PPAR-α at both the mRNA and protein levels in 3T3-L1preadipocytes. In addition, supplementation with CoQ10 induced gene expression of PPAR-α in SAMP1 mice [20]. In another study, CoQ10 supplementation increased p110β protein expression both liver and skeletal muscle [6]. This is consistent with prior studies indicating that administration of a much higher dose of CoQ10 (20 mg/kg) affects insulin sensitivity and had antidiabetic properties via increasing the activity of phosphatidylinositol kinase (PI-3Ks) in rats fed with a high-fat, high-fructose diet [7]. PPAR-γ is primarily present in adipocytes, which plays an important function in glucose and insulin metabolism [21]. CoQ10 intake may induce PPAR-γ expression thorough the calcium-mediated AMPK signal pathway and suppressing differentiation-induced adipogenesis [19].
E-cadherin activating antibodies limit barrier dysfunction and inflammation in mouse inflammatory bowel disease
Published in Tissue Barriers, 2021
Chirosree Bandyopadhyay, Leslayann Schecterson, Barry M Gumbiner
Epithelial barrier function plays an important role in gastrointestinal (GI) mucosal immunity and inflammation, and deficits in GI epithelial barrier function is etiologically linked with Inflammatory Bowel Disease (IBD).1–6 An intact GI barrier prevents leakage of antigens derived from intestinal flora and foodstuffs from the intestinal lumen into the interstitial space and the lamina propria where immune cells reside. It also regulates the migration of polymorphonuclear leukocytes (PMN) across the epithelium of the crypts into the lumen, a common occurrence in IBD that is associated with disease symptoms.7–9 Moreover, it regulates the functions of mucosal dendritic cells (DCs) and T-cells through their interactions with epithelial cells.2,10–15 Increased intestinal permeability is even observed in asymptomatic relatives of patients with IBD, suggesting that there may be a genetic component to the barrier defects.16–18 Increased paracellular permeability has also been strongly implicated in the development of IBD in animal models.,1,2,19,20 including SAMP1/YitFc (SAMP) mice, which develop ileitis spontaneously,1 and mice lacking the Interleukin-10 (IL-10) gene19 that develops colitis. The genetic basis for ileitis in the SAMP1 model is not fully known.21–23 Several inflammatory mediators, including TNFα and INFγ are known to increase intestinal epithelial permeability, and both early and late effects on permeability could also be important for promoting disease.24–27 Inflammatory mediators are induced by naïve T cells transferred from healthy donor into lymphophenic mice and adoptive T cell transfer is used as a model of colitis to study the onset and progression of chronic inflammation that mimics human IBD.28–30 Hence, IL10-/- and adoptive T cell transfer are commonly studied mouse models for barrier dysfunction investigation in IBD research.10,11,14,28,30–42