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Akita mice

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https://www.readbyqxmd.com/read/29348593/temporal-diabetes-induced-biochemical-changes-in-distinctive-layers-of-mouse-retina
#1
Ebrahim Aboualizadeh, Christine M Sorenson, Alex J Schofield, Miriam Unger, Nader Sheibani, Carol J Hirschmugl
To discover the mechanisms underlying the progression of diabetic retinopathy (DR), a more comprehensive understanding of the biomolecular processes in individual retinal cells subjected to hyperglycemia is required. Despite extensive studies, the changes in the biochemistry of retinal layers during the development of DR are not well known. In this study, we aimed to determine a more detailed understanding of the natural history of DR in Akita/+ (type 1 diabetes model) male mice with different duration of diabetes...
January 18, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29304075/%C3%AE-cell-specific-overexpression-of-adiponectin-receptor-1-does-not-improve-diabetes-mellitus-in-akita-mice
#2
Jungmi Choi, Hatasu Kobayashi, Hiroko Okuda, Kouji H Harada, Midori Takeda, Hiroyuki Fujimoto, Shunsuke Yamane, Daisuke Tanaka, Shohab Youssefian, Nobuya Inagaki, Akio Koizumi
Adiponectin, a metabolically-active cytokine secreted from adipose tissue, is reported to have anti-apoptotic effects on β-cells as well as anti-hyperglycemic effects through adiponectin receptor signaling. However, the anti-apoptotic effects of adiponectin on β-cells have not been confirmed in established diabetic models, and the anti-hyperglycemic effects and their associated signal cascades remain controversial. To investigate the effects of adiponectin on β-cell protection and its down-stream signaling events, we have generated β-cell-specific rat insulin promoter (RIP)-AdipoR1 transgenic mice (AdipoR1 mice), in which the adiponectin receptor, AdipoR1, is overexpressed in β-cells in a manner synchronous with insulin demand...
2018: PloS One
https://www.readbyqxmd.com/read/29211853/nrf2-deficiency-upregulates-intrarenal-angiotensin-converting-enzyme-2-and-angiotensin-1-7-receptor-expression-and-attenuates-hypertension-and-nephropathy-in-diabetic-mice
#3
Shuiling Zhao, Anindya Ghosh, Chao-Sheng Lo, Isabelle Chenier, James W Scholey, Janos G Filep, Julie R Ingelfinger, Shao-Ling Zhang, John S D Chan
We investigated the role of nuclear factor erythroid 2-related factor 2 (Nrf2) in renin-angiotensin system (RAS) gene expression in renal proximal tubule cells (RPTCs) and in the development of systemic hypertension and kidney injury in diabetic Akita mice. We used adult male Akita Nrf2 knockout (KO) mice and Akita mice treated with trigonelline (an Nrf2 inhibitor) or oltipraz (an Nrf2 activator). We also examined immortalized rat RPTCs (IRPTCs) stably transfected with control plasmids or plasmids containing rat angiotensinogen (Agt), angiotensin-converting enzyme (ACE), angiotensin-converting enzyme-2 (Ace2) or angiotensin 1-7 receptor (MasR) gene promoters...
December 1, 2017: Endocrinology
https://www.readbyqxmd.com/read/29203863/orai-channels-are-critical-for-receptor-mediated-endocytosis-of-albumin
#4
Bo Zeng, Gui-Lan Chen, Eliana Garcia-Vaz, Sunil Bhandari, Nikoleta Daskoulidou, Lisa M Berglund, Hongni Jiang, Thomas Hallett, Lu-Ping Zhou, Li Huang, Zi-Hao Xu, Viji Nair, Robert G Nelson, Wenjun Ju, Matthias Kretzler, Stephen L Atkin, Maria F Gomez, Shang-Zhong Xu
Impaired albumin reabsorption by proximal tubular epithelial cells (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the underlying molecular mechanisms. Here we find that ORAI1-3, are preferentially expressed in PTECs and downregulated in patients with DN. Hyperglycemia or blockade of insulin signaling reduces the expression of ORAI1-3. Inhibition of ORAI channels by BTP2 and diethylstilbestrol or silencing of ORAI expression impairs albumin uptake. Transgenic mice expressing a dominant-negative Orai1 mutant (E108Q) increases albuminuria, and in vivo injection of BTP2 exacerbates albuminuria in streptozotocin-induced and Akita diabetic mice...
December 4, 2017: Nature Communications
https://www.readbyqxmd.com/read/29203613/nfe2l1-silenced-insulinoma-cells-acquire-aggressiveness-and-chemo-resistance
#5
Jingqi Fu, Hongzhi Zheng, Qi Cui, Chengjie Chen, Simeng Bao, Jing Sun, Lu Li, Bei Yang, Huihui Wang, Yongyong Hou, Yuanyuan Xu, Yuanhong Xu, Qiang Zhang, Jingbo Pi
The transcription factor nuclear factor erythroid 2 like 1 (NFE2L1 or NRF1) is involved in various critical cell processes such as maintenance of ubiquitin-proteasome system and regulation of the cellular antioxidant response. We previously determined that pancreatic β-cell-specific Nfe2l1-knockout mice had hyperinsulinemia, and that silencing of Nfe2l1 in mouse islets or MIN6 insulinoma β-cells induced elevated basal insulin release and altered glucose metabolism. Hypoglycemia is a major issue with aggressive insulinomas, although a role of NFE2L1 in this pathology is not defined...
December 4, 2017: Endocrine-related Cancer
https://www.readbyqxmd.com/read/29186067/immunohistochemical-characterization-of-connexin43-expression-in-a-mouse-model-of-diabetic-retinopathy-and-in-human-donor-retinas
#6
Odunayo O Mugisho, Colin R Green, Jie Zhang, Nicolette Binz, Monica L Acosta, Elizabeth Rakoczy, Ilva D Rupenthal
Diabetic retinopathy (DR) develops due to hyperglycemia and inflammation-induced vascular disruptions in the retina with connexin43 expression patterns in the disease still debated. Here, the effects of hyperglycemia and inflammation on connexin43 expression in vitro in a mouse model of DR and in human donor tissues were evaluated. Primary human retinal microvascular endothelial cells (hRMECs) were exposed to high glucose (HG; 25 mM) or pro-inflammatory cytokines IL-1β and TNF-α (10 ng/mL each) or both before assessing connexin43 expression...
November 29, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29061652/progressive-renal-disease-established-by-renin-coding-adeno-associated-virus-driven-hypertension-in-diverse-diabetic-models
#7
Shannon M Harlan, Kathleen M Heinz-Taheny, John M Sullivan, Tao Wei, Hana E Baker, Dianna L Jaqua, Zhonghua Qi, Martin S Cramer, Tatiyana L Shiyanova, Matthew D Breyer, Josef G Heuer
Progress in research and developing therapeutics to prevent diabetic kidney disease (DKD) is limited by a lack of animal models exhibiting progressive kidney disease. Chronic hypertension, a driving factor of disease progression in human patients, is lacking in most available models of diabetes. We hypothesized that superimposition of hypertension on diabetic mouse models would accelerate DKD. To test this possibility, we induced persistent hypertension in three mouse models of type 1 diabetes and two models of type 2 diabetes by adeno-associated virus delivery of renin (ReninAAV)...
October 23, 2017: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/29043461/effect-of-anti-angiogenesis-induced-by-chemotherapeutic-monotherapy-chemotherapeutic-bisphosphonate-combination-therapy-and-anti-vegfa-mab-therapy-on-tooth-extraction-socket-healing-in-mice
#8
Yuri Akita, Shinichiro Kuroshima, Kazunori Nakajima, Hiroki Hayano, Riho Kanai, Muneteru Sasaki, Takashi Sawase
Osteonecrosis of the jaw (ONJ), which is a rare but severe adverse effect, mainly occurs in oncology patients receiving chemotherapeutic agents and bisphosphonates. However, the combined impact of chemotherapy and bisphosphonates on wound healing after tooth extraction remains unknown. The aim of this study was to determine the precise etiology of ONJ induced by chemotherapy and bisphosphonate combination therapy. Mice received zoledronate (ZA) monotherapy, cyclophosphamide (CY) monotherapy or CY/ZA combination therapy...
October 17, 2017: Journal of Bone and Mineral Metabolism
https://www.readbyqxmd.com/read/28883608/gyy4137-a-hydrogen-sulfide-donor-modulates-mir194-dependent-collagen-realignment-in-diabetic-kidney
#9
A M Sashi Papu John, Sourav Kundu, Sathnur Pushpakumar, Maura Fordham, Gregory Weber, Manas Mukhopadhyay, Utpal Sen
The relationship between hydrogen sulfide (H2S), microRNAs (miRs), matrix metalloproteinases (MMPs) and poly-ADP-ribose-polymerase-1 (PARP-1) in diabetic kidney remodeling remains mostly obscured. We aimed at investigating whether alteration of miR-194-dependent MMPs and PARP-1 causes renal fibrosis in diabetes kidney, and whether H2S ameliorates fibrosis. Wild type, diabetic Akita mice as well as mouse glomerular endothelial cells (MGECs) were used as experimental models, and GYY4137 as H2S donor. In diabetic mice, plasma H2S levels were decreased while ROS and expression of its modulator (ROMO1) were increased...
September 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28837672/cardiac-transcriptome-profiling-of-diabetic-akita-mice-using-microarray-and-next-generation-sequencing
#10
Varun Kesherwani, Hamid R Shahshahan, Paras K Mishra
Although diabetes mellitus (DM) causes cardiomyopathy and exacerbates heart failure, the underlying molecular mechanisms for diabetic cardiomyopathy/heart failure are poorly understood. Insulin2 mutant (Ins2+/-) Akita is a mouse model of T1DM, which manifests cardiac dysfunction. However, molecular changes at cardiac transcriptome level that lead to cardiomyopathy remain unclear. To understand the molecular changes in the heart of diabetic Akita mice, we profiled cardiac transcriptome of Ins2+/- Akita and Ins2+/+ control mice using next generation sequencing (NGS) and microarray, and determined the implications of differentially expressed genes on various heart failure signaling pathways using Ingenuity pathway (IPA) analysis...
2017: PloS One
https://www.readbyqxmd.com/read/28686632/autophagy-dependent-regulation-of-tumor-metastasis-by-myeloid-cells
#11
Masahisa Jinushi, Tomoko Morita, Zhihang Xu, Ichiro Kinoshita, Hirotoshi Dosaka-Akita, Hideo Yagita, Yutaka Kawakami
Autophagy is a vital process controlling the lysosomal degradation of cellular organelles and thereby regulating tissue homeostasis in an environment-dependent fashion. Recent studies have unveiled the critical role of tumor cell-derived autophagy in regulating pro-tumor and anti-tumor processes depending on different stages and tumor microenvironments. However, the precise mechanism whereby autophagy regulates tumor progression remains largely unclear. Since myeloid cells contribute to tumor progression and metastasis, we evaluated the role of myeloid cell-specific autophagy in the regulation of tumor progression...
2017: PloS One
https://www.readbyqxmd.com/read/28598529/association-of-a-reactive-intermediate-derived-from-1-6-dihydroxy-metabolite-with-benzbromarone-induced-hepatotoxicity
#12
Mina Yoshida, Naoki Cho, Hidetaka Akita, Kaoru Kobayashi
Treatment with benzbromarone can be associated with liver injury, but the detailed mechanism remains unknown. Our recent studies demonstrated that benzbromarone was metabolized to 1',6-dihydroxybenzbromarone and followed by formation of reactive intermediates that were trapped by glutathione, suggesting that the reactive intermediates may be responsible for the liver injury. The aim of this study was to clarify whether the reactive intermediates derived from 1',6-dihydroxybenzbromarone is a risk factor of liver injury in mice...
June 9, 2017: Journal of Biochemical and Molecular Toxicology
https://www.readbyqxmd.com/read/28535269/increased-retinal-oxygen-metabolism-precedes-microvascular-alterations-in-type-1-diabetic-mice
#13
Wenzhong Liu, Shoujian Wang, Brian Soetikno, Ji Yi, Kevin Zhang, Siyu Chen, Robert A Linsenmeier, Christine M Sorenson, Nader Sheibani, Hao F Zhang
Purpose: To investigate inner retinal oxygen metabolic rate (IRMRO2) during early stages of type 1 diabetes in a transgenic mouse model. Methods: In current study, we involved seven diabetic mice (Akita/+, TSP1-/-) and seven control mice (TSP1-/-), and applied visible-light optical coherence tomography (vis-OCT) to image functional parameters including retinal blood flow rate, oxygen saturation (sO2) and the IRMRO2 value longitudinally from 5 weeks of age to 13 weeks of age...
February 1, 2017: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/28522367/qrs-t-wave-and-calcium-alternans-in-a-type-i-diabetic-mouse-model-for-spontaneous-postmyocardial-infarction-ventricular-tachycardia-a-mechanism-for-the-antiarrhythmic-effect-of-statins
#14
Hongwei Jin, Charles M Welzig, Mark Aronovitz, Farzad Noubary, Robert Blanton, Bo Wang, Mohammad Rajab, Alfred Albano, Mark S Link, Sami F Noujaim, Ho-Jin Park, Jonas B Galper
BACKGROUND: The incidence of sudden arrhythmic death is markedly increased in diabetics. OBJECTIVE: The purpose of this study was to develop a mouse model for postmyocardial infarction (post-MI) ventricular tachycardia (VT) in the diabetic heart and determine the mechanism of an antiarrhythmic effect of statins. METHODS: ECG transmitters were implanted in wild-type (WT), placebo, and pravastatin-treated type I diabetic Akita mice. MIs were induced by coronary ligation, and Ca2+ transients were studied by optical mapping, and Ca2+ transients and sparks in left ventricular myocytes (VM) by the Ionoptix system and confocal microscopy...
September 2017: Heart Rhythm: the Official Journal of the Heart Rhythm Society
https://www.readbyqxmd.com/read/28508291/lobular-homology-in-cerebellar-hemispheres-of-humans-non-human-primates-and-rodents-a-structural-axonal-tracing-and-molecular-expression-analysis
#15
REVIEW
Yuanjun Luo, Hirofumi Fujita, Hermina Nedelescu, Mohammad Shahangir Biswas, Chika Sato, Sarah Ying, Mayu Takahashi, Keiichi Akita, Tatsuya Higashi, Ichio Aoki, Izumi Sugihara
Comparative neuroanatomy provides insights into the evolutionary functional adaptation of specific mammalian cerebellar lobules, in which the lobulation pattern and functional localization are conserved. However, accurate identification of homologous lobules among mammalian species is challenging. In this review, we discuss the inter-species homology of crus I and II lobules which occupy a large volume in the posterior cerebellar hemisphere, particularly in humans. Both crus I/II in humans are homologous to crus I/II in non-human primates, according to Paxinos and colleagues; however, this area has been defined as crus I alone in non-human primates, according to Larsell and Brodal...
May 15, 2017: Brain Structure & Function
https://www.readbyqxmd.com/read/28493939/inhibition-of-nitric-oxide-production-reverses-diabetes-induced-kupffer-cell-activation-and-klebsiella-pneumonia-liver-translocation
#16
Shu-Han Lin, Pei-Hsuan Chung, Ying-Ying Wu, Chang-Phone Fung, Ching-Mei Hsu, Lee-Wei Chen
Klebsiella pneumoniae (KP) is the most common pathogen of pyogenic liver abscess in East and Southeast Asia and diabetes mellitus (DM) is a major risk factor. The effect and mechanism of diabetes on KP liver abscess was examined in streptozotocin-induced diabetic mice and Akita mice (C57BL/6J-Ins2Akita). KP translocation to liver and plasma alaine transaminase levels were increased and liver clearance of KP was decreased in DM mice. Diabetic mice exhibited overgrowth of Enterococcus as well as E.coli and decreased lactobacilli/bifidas growth in intestine, increased intestinal iNOS protein and nitrite levels in portal vein, and increased IL-1β and TNF-α expression of Kupffer cells...
2017: PloS One
https://www.readbyqxmd.com/read/28490532/podocyte-specific-knockout-of-cyclooxygenase-2-exacerbates-diabetic-kidney-disease
#17
Liming Wang, Yonggang Sha, Jingyi Bai, William Eisner, Matthew A Sparks, Anne F Buckley, Robert F Spurney
Enhanced expression of cyclooxygenase 2 (COX2) in podocytes contributes to glomerular injury in diabetic kidney disease, but some basal level of podocyte COX2 expression might be required to promote podocyte attachment and/or survival. To investigate the role of podocyte COX2 expression in diabetic kidney disease, we deleted COX2 specifically in podocytes in a mouse model of Type 1 diabetes mellitus (Akita mice). Podocyte-specific knockout (KO) of COX2 did not affect renal morphology or albuminuria in nondiabetic mice...
August 1, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28432078/effect-of-4-5-6-7-8-tetrahydro-5-5-8-8-tetramethyl-2-naphthalenyl-carbamoyl-benzoic-acid-am80-on-alveolar-regeneration-in-adiponectin-deficient-mice-showing-a-chronic-obstructive-pulmonary-disease-like-pathophysiology
#18
Hitomi Sakai, Michiko Horiguchi, Tomomi Akita, Chihiro Ozawa, Mai Hirokawa, Yuki Oiso, Harumi Kumagai, Yoshito Takeda, Isao Tachibana, Norikazu Maeda, Chikamasa Yamashita
Chronic obstructive pulmonary disease (COPD) is an intractable pulmonary disease that causes widespread and irreversible alveolar collapse. Although COPD occurs worldwide, only symptomatic therapy is currently available. Our objective is the development of therapeutic agents to eradicate COPD. Therefore, we focused on 4-[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl) carbamoyl] benzoic acid (Am80), which is a derivative of all-trans retinoic acid. We evaluated the effects of Am80 on alveolar repair in a novel COPD model of adiponectin-deficient mice...
June 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28353063/the-microrna-7-mediated-reduction-in-epac-1-contributes-to-vascular-endothelial-permeability-and-enos-uncoupling-in-murine-experimental-retinopathy
#19
Veronica Garcia-Morales, Julian Friedrich, Lysanne M Jorna, Manuel Campos-Toimil, Hans-Peter Hammes, Martina Schmidt, Guido Krenning
AIMS: To investigate the consequences of oxidative stress and hypoxia on EPAC-1 expression during retinopathy. METHODS: Oxygen-induced retinopathy was induced in mice and EPAC-1 expression investigated by immunofluorescence. In silico analyses were used to identify a link between EPAC-1 expression and microRNA-7-5p in endothelial cells and confirmed by western blot analyses on cells expressing microRNA-7-5p. In vitro, endothelial cells were either incubated at 2% oxygen or transfected with microRNA-7-5p, and the effects of these treatments on EPAC-1 expression, endothelial hyperpermeability and NO production were assessed...
June 2017: Acta Diabetologica
https://www.readbyqxmd.com/read/28324005/insulin-inhibits-nrf2-gene-expression-via-heterogeneous-nuclear-ribonucleoprotein-f-k-in-diabetic-mice
#20
Anindya Ghosh, Shaaban Abdo, Shuiling Zhao, Chin-Han Wu, Yixuan Shi, Chao-Sheng Lo, Isabelle Chenier, Thierry Alquier, Janos G Filep, Julie R Ingelfinger, Shao-Ling Zhang, John S D Chan
Oxidative stress induces endogenous antioxidants via nuclear factor erythroid 2-related factor 2 (Nrf2), potentially preventing tissue injury. We investigated whether insulin affects renal Nrf2 expression in type 1 diabetes (T1D) and studied its underlying mechanism. Insulin normalized hyperglycemia, hypertension, oxidative stress, and renal injury; inhibited renal Nrf2 and angiotensinogen (Agt) gene expression; and upregulated heterogeneous nuclear ribonucleoprotein F and K (hnRNP F and hnRNP K) expression in Akita mice with T1D...
April 1, 2017: Endocrinology
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