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Artykuły w czasopismach na temat „Nestin-Cre mice”

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Data publikacji: 2 czerwca 2025
Data aktualizacji: 31 lipca 2025

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1

Swilley, Cody, Yu Lin, Yuze Zheng, et al. "Sex-Linked Growth Disorder and Aberrant Pituitary Gene Expression in Nestin-Cre-Mediated Egr1 Conditional Knockout Mice." Biology 12, no. 7 (2023): 966. http://dx.doi.org/10.3390/biology12070966.

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Genes that regulate hormone release are essential for maintaining metabolism and energy balance. Egr1 encodes a transcription factor that regulates hormone production and release, and a decreased in growth hormones has been reported in Egr1 knockout mice. A reduction in growth hormones has also been observed in Nestin-Cre mice, a model frequently used to study the nervous system. Currently, it is unknown how Egr1 loss or the Nestin-Cre driver disrupt pituitary gene expression. Here, we compared the growth curves and pituitary gene expression profiles of Nestin-Cre-mediated Egr1 conditional kno
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2

do Carmo, Jussara M., Alexandre A. da Silva, Fabio N. Gava, Sydney P. Moak, Xuemei Dai, and John E. Hall. "Impact of leptin deficiency compared with neuronal-specific leptin receptor deletion on cardiometabolic regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 317, no. 4 (2019): R552—R562. http://dx.doi.org/10.1152/ajpregu.00077.2019.

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The main goal of this study was to compare the impact of total body leptin deficiency with neuronal-specific leptin receptor (LR) deletion on metabolic and cardiovascular regulation. Liver fat, diacylglycerol acyltransferase-2 (DGTA2), and CD36 protein content were measured in wild-type (WT), nervous system LR-deficient (LR/Nestin-Cre), and leptin deficient ( ob/ob) mice. Blood pressure (BP) and heart rate (HR) were recorded by telemetry, and motor activity (MA) and oxygen consumption (V̇o2) were monitored at 24 wk of age. Female and male LR/Nestin-Cre and ob/ob mice were heavier than WT mice
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3

Kajitani, Yusuke, Takashi Miyazawa, Tomoaki Inoue, et al. "High frequency of germline recombination in Nestin-Cre transgenic mice crossed with Glucagon-like peptide 1 receptor floxed mice." PLOS ONE 18, no. 12 (2023): e0296006. http://dx.doi.org/10.1371/journal.pone.0296006.

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The Cre-loxP strategy for tissue-specific gene inactivation has become a widely employed tool in several research studies. Conversely, inadequate breeding and genotyping without considering the potential for non-specific Cre-recombinase expression may lead to misinterpretations of results. Nestin-Cre transgenic mice, widely used for the selective deletion of genes in neurons, have been observed to have an incidence of Cre-line germline recombination. In this study, we attempted to generate neuron-specific Glucagon-like peptide 1 receptor (Glp1r) knock-out mice by crossing mice harboring the Ne
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4

do Carmo, Jussara M., Alexandre A. da Silva, Zhen Wang, et al. "Regulation of Blood Pressure, Appetite, and Glucose by Leptin After Inactivation of Insulin Receptor Substrate 2 Signaling in the Entire Brain or in Proopiomelanocortin Neurons." Hypertension 67, no. 2 (2016): 378–86. http://dx.doi.org/10.1161/hypertensionaha.115.06153.

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Insulin receptor substrate 2 (IRS2) is one of the 3 major leptin receptor signaling pathways, but its role in mediating the chronic effects of leptin on blood pressure, food intake, and glucose regulation is unclear. We tested whether genetic inactivation of IRS2 in the entire brain (IRS2/Nestin-cre mice) or specifically in proopiomelanocortin (POMC) neurons (IRS2/POMC-cre mice) attenuates the chronic cardiovascular, metabolic, and antidiabetic effects of leptin. Mice were instrumented with telemetry probes for measurement of blood pressure and heart rate and with venous catheters for intraven
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5

Singh, Pratibha, Hongge Li, and Louis M. Pelus. "Engraftment and Reconstitution of Hematopoiesis Is Dependent on Endothelial Cell Expressed Prostaglandin EP4 Receptor Signaling Mediated Regeneration of Vascular Niche." Blood 132, Supplement 1 (2018): 1293. http://dx.doi.org/10.1182/blood-2018-99-119723.

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Abstract Defining the cellular and molecular components of the bone marrow (BM) niche that regulate the homeostasis and regeneration of hematopoietic stem and progenitor cells (HSPCs) can facilitate targeted interventions to improve hematopoietic recovery after injury and enhance stem cell engraftment after transplantation. We have recently shown that BM niche prostaglandin E2 (PGE2) signaling via the EP4 receptor is crucial for hematopoietic reconstitution, as transplantation of wild-type donor cells into EP4 receptor deficient recipient mice shows reduced stem cell engraftment. However, the
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6

Xue, Baojian, Zhongming Zhang, Terry G. Beltz, Fang Guo, Meredith Hay, and Alan Kim Johnson. "Genetic knockdown of estrogen receptor-alpha in the subfornical organ augments ANG II-induced hypertension in female mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 6 (2015): R507—R516. http://dx.doi.org/10.1152/ajpregu.00406.2014.

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The present study tested the hypotheses that 1) ERα in the brain plays a key role in the estrogen-protective effects against ANG II-induced hypertension, and 2) that the subfornical organ (SFO) is a key site where ERα mediates these protective actions. In this study, a “floxed” ERα transgenic mouse line (ERαflox) was used to create models in which ERα was knocked down in the brain or just in the SFO. Female mice with ERα ablated in the nervous system (Nestin-ERα− mice) showed greater increases in blood pressure (BP) in response to ANG II. Furthermore, females with ERα knockdown specifically in
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7

Wang, Xueqiao, Xiaoqing Zheng, Juanlian Zhang, et al. "Physiological functions of ferroportin in the regulation of renal iron recycling and ischemic acute kidney injury." American Journal of Physiology-Renal Physiology 315, no. 4 (2018): F1042—F1057. http://dx.doi.org/10.1152/ajprenal.00072.2018.

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Renal iron recycling preserves filtered iron from urinary excretion. However, it remains debated whether ferroportin (FPN), the only known iron exporter, is functionally involved in renal iron recycling and whether renal iron recycling is required for systemic iron homeostasis. We deleted FPN in whole nephrons by use of a Nestin-Cre and in the distal nephrons and collecting ducts, using a Ksp-Cre, and investigated its impacts on renal iron recycling and systemic iron homeostasis. FPN deletion by Nestin-Cre, but not by Ksp-Cre, caused excess iron retention and increased ferritin heavy chain (FT
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8

Jia, Junshuang, Xiaolin Lin, Xia Lin, et al. "R/L, a double reporter mouse line that expresses luciferase gene upon Cre-mediated excision, followed by inactivation of mRFP expression." Genome 59, no. 10 (2016): 816–26. http://dx.doi.org/10.1139/gen-2016-0090.

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The Cre/loxP system has become an important tool for the conditional gene knockout and conditional gene expression in genetically engineered mice. The applications of this system depend on transgenic reporter mouse lines that provide Cre recombinase activity with a defined cell type-, tissue-, or developmental stage-specificity. To develop a sensitive assay for monitoring Cre-mediated DNA excisions in mice, we generated Cre-mediated excision reporter mice, designated R/L mice (R/L: mRFP(monomeric red fluorescent protein)/luciferase), express mRFP throughout embryonic development and adult stag
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9

Aamir, Zoya, Melissa Galati, Emma Gattoni, et al. "BIOL-18. NEWLY DEVELOPED REPLICATION REPAIR DEFICIENT (RRD) MOUSE MODELS PROVIDE INSIGHTS INTO MEDULLOBLASTOMA/GLIOMAGENESIS AND RESPONSE TO IMMUNOTHERAPY." Neuro-Oncology 25, Supplement_1 (2023): i9—i10. http://dx.doi.org/10.1093/neuonc/noad073.037.

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Abstract Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-resistant, but respond favorably to immune checkpoint inhibition (ICI). Representative immunocompetent animal models are urgently needed for 3 recently identified subgroups based on specific somatically-acquired mutations, survival, and immunotherapy response (RRD1: MMRD with POLE mutations, RRD2: M
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10

Galati, Melissa, Li Li, Sumedha Sudhaman, et al. "MODL-25. REPLICATION REPAIR DEFICIENT MOUSE MODELS PROVIDE INSIGHT ON HYPERMUTANT BRAIN TUMOURS, MECHANISMS OF IMMUNE EVASION, AND COMBINATORIAL IMMUNOTHERAPY." Neuro-Oncology 22, Supplement_3 (2020): iii416. http://dx.doi.org/10.1093/neuonc/noaa222.598.

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Abstract Replication repair deficiency (RRD) is the leading cause of hypermutant brain tumours in children. RRD is caused by defects in one of four mismatch repair (MMR) genes and mutations in POLE or POLD1. Such tumours are resistant to common therapeutic agents and animal models are needed to study RRD in vivo and test novel therapies like immune checkpoint inhibitors (ICIs). To model RRD brain tumours specifically, we engineered a Pole mutant mouse model harbouring the S459F mutation (PoleS459F). We combined PoleS459F mice with conditional Msh2 knockout (Msh2LoxP) and Nestin-cre mice. All N
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11

Aamir, Zoya, Melissa Galati, Emma Gattoni, et al. "Abstract 1451: Replication repair deficient mouse models provide insights into gliomagenesis and response to immunotherapy." Cancer Research 84, no. 6_Supplement (2024): 1451. http://dx.doi.org/10.1158/1538-7445.am2024-1451.

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Abstract Background: Replication Repair Deficiency (RRD), caused by germline monoallelic (Lynch Syndrome) or biallelic (Constitutional Mismatch Repair Deficiency, CMMRD) mutations in MMR genes, is present in 5-10% of glioblastomas in children, adolescents, and young adults. RRD glioblastomas are chemoradiation-resistant, but respond favorably to immune checkpoint inhibition (ICI). Representative immunocompetent animal models are urgently needed for 3 recently identified subgroups based on specific somatically-acquired mutations, survival, and immunotherapy response (RRD1: MMRD with POLE mutati
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12

Aelvoet, Sarah-Ann, Brazo Jesus Pascual-, Sarah Libbrecht, et al. "Long-Term Fate Mapping Using Conditional Lentiviral Vectors Reveals a Continuous Contribution of Radial Glia-Like Cells to Adult Hippocampal Neurogenesis in Mice." PLoS One 10, no. 11 (2015): e0143772. https://doi.org/10.1371/journal.pone.0143772.

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Newborn neurons are generated throughout life in two neurogenic regions, the subventricular zone and the hippocampal dentate gyrus. Stimulation of adult neurogenesis is considered as an attractive endogenous repair mechanism to treat different neurological disorders. Although tremendous progress has been made in our understanding of adult hippocampal neurogenesis, important questions remain unanswered, regarding the identity and the behavior of neural stem cells in the dentate gyrus. We previously showed that conditional Cre-Flex lentiviral vectors can be used to label neural stem cells in the
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13

Zhang, Zhongming, Yijing Zhang, Yan Wang, et al. "Genetic knockdown of brain-derived neurotrophic factor in the nervous system attenuates angiotensin II-induced hypertension in mice." Journal of the Renin-Angiotensin-Aldosterone System 20, no. 1 (2019): 147032031983440. http://dx.doi.org/10.1177/1470320319834406.

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Introduction: Brain-derived neurotropic factor (BDNF) is expressed throughout the central nervous system and peripheral organs involved in the regulation of blood pressure, but the systemic effects of BDNF in the control of blood pressure are not well elucidated. Materials and methods: We utilized loxP flanked BDNF male mice to cross with nestin-Cre female mice to generate nerve system BDNF knockdown mice, nestin-BDNF (+/–), or injected Cre adenovirus into the subfornical organ to create subfornical organ BDNF knockdown mice. Histochemistry was used to verify injection location. Radiotelemetry
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14

Lucas, Daniel, Christoph Scheiermann, Andrew Chow, et al. "Bone Marrow Neuropathy Prevents Hematopoietic Regeneration." Blood 118, no. 21 (2011): 139. http://dx.doi.org/10.1182/blood.v118.21.139.139.

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Abstract Abstract 139 Chemotherapy regimens commonly produce long-term hematopoietic injury, possibly through a lesion to the hematopoietic stem cell (HSC) and/or its niche but the mechanisms have yet to be elucidated. Nestin-expressing mesenchymal stem cells, under regulation of the sympathetic nervous system (SNS), are a critical component of the HSC niche (Nature. 2010; 466:829). Since peripheral neuropathy is a common complication of chemotherapy, we hypothesized that chemotherapy-induced sympathetic bone marrow (BM) neuropathy could impair BM regeneration. To test this issue, we sympathec
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15

Kumar, Sachin, Jeff Vassallo, Kalpana Nattamai, Jose A. Cancelas, and Hartmut Geiger. "EGFR Signaling in Osteoblasts Regulates Circadian Rhythm of HSPC in Circulation." Blood 126, no. 23 (2015): 665. http://dx.doi.org/10.1182/blood.v126.23.665.665.

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Abstract EGFR signaling regulates growth, differentiation, proliferation and migration in multiple organ systems. We previously demonstrated that inhibition of EGFR signaling on hematopoietic stem and progenitor cells (HSPCs) enhances G-CSF induced stem cell mobilization, while preliminary data suggested that inhibition of EGFR signaling in the stem cell niche actually had the opposite effect of inhibiting mobilization (Ryan et al., Nat Med, 2010). We thus tested the novel hypothesis that there is a role for EGFR signaling in the bone marrow (BM) niche with respect to regulating hematopoiesis.
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16

Torrelli-Diljohn, Alex B., Svetlana Komarova, Vipul Sheth, et al. "Abstract 15: Investigating the spectrum of brain tumors associated with Adgrb3 and Tp53 loss in a mouse model of Li-Fraumeni syndrome." Cancer Research 83, no. 7_Supplement (2023): 15. http://dx.doi.org/10.1158/1538-7445.am2023-15.

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Abstract Adhesion G protein-coupled receptor 3 (ADGRB3), also known as brain specific angiogenesis inhibitor (BAI3) is a member of the ADGRB1-3 subfamily of adhesion transmembrane proteins, which are highly expressed in the brain specifically in cerebellum and hippocampal neurons. ADGRB3 has been shown to play diverse roles under physiological and pathological conditions which include dendritic morphogenesis, synaptic plasticity, synaptogenesis, and myogenesis. Loss of ADGRB3 expression and point mutations in the gene have been observed in sporadic tumors, including brain tumors, but the signi
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17

Singh, Pratibha, and Louis M. Pelus. "CXCR4-SDF-1 Signaling in Nestin+ Mesenchymal Stem Cell Is Required for HSC Maintenance during Homeostasis and Regeneration after Irradiation." Blood 128, no. 22 (2016): 3883. http://dx.doi.org/10.1182/blood.v128.22.3883.3883.

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Hematopoietic stem cells (HSC) reside in a complex microenvironment (niche) within the bone marrow (BM), where multiple populations of microenvironmental stromal cells regulate and finely tune their proliferation, differentiation and trafficking. Recent studies have shown that mesenchymal stem cells (MSC) are an essential component of the HSC niche. Intrinsic HSC CXCR4-SDF-1 signaling has been implicated in self-renewal and quiescence; however, the role of microenvironment CXCR4-SDF-1 signaling in supporting HSC function remains unclear. We previously demonstrated that microenvironmental strom
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18

Ahmed, Jalal, Yuya Kunisaki, Miriam Merad, and Paul S. Frenette. "Nestin+ Pericytes In The Fetal Liver Are Necessary To Maintain HSCs." Blood 122, no. 21 (2013): 583. http://dx.doi.org/10.1182/blood.v122.21.583.583.

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Abstract Although most hematopoietic stem cells (HSCs) are quiescent under homeostasis in the adult bone marrow, they are actively proliferating during development. Definitive HSCs, marked by the ability to repopulate a lethally irradiated adult mouse, are first detectable in the aorta-gonad-mesonephros region around E10.5, and then colonize the fetal liver (FL) to expand in this organ until E15 when hematopoietic activity shifts to the fetal bone marrow. The role of the microenvironment, or niche, in the regulation of HSCs in the FL, a site of physiological expansion, is unclear. Fetal liver
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Lin, Sen, Wei Liu, Chun-Lin Chen, et al. "Neogenin-loss in neural crest cells results in persistent hyperplastic primary vitreous formation." Journal of Molecular Cell Biology 12, no. 1 (2019): 17–31. http://dx.doi.org/10.1093/jmcb/mjz076.

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Abstract Neogenin is a transmembrane receptor critical for multiple cellular processes, including neurogenesis, astrogliogenesis, endochondral bone formation, and iron homeostasis. Here we present evidence that loss of neogenin contributes to pathogenesis of persistent hyperplastic primary vitreous (PHPV) formation, a genetic disorder accounting for ~ 5% of blindness in the USA. Selective loss of neogenin in neural crest cells (as observed in Wnt1-Cre; Neof/f mice), but not neural stem cells (as observed in GFAP-Cre and Nestin-Cre; Neof/f mice), resulted in a dysregulation of neural crest cell
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Méndez-Ferrer, Simón, Tatyana V. Michurina, Francesca Ferraro, et al. "Coordinated Regulation of Hematopoietic and Mesenchymal Stem Cells in a Bone Marrow Niche." Blood 114, no. 22 (2009): 2. http://dx.doi.org/10.1182/blood.v114.22.2.2.

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Abstract Abstract 2 Despite their therapeutic potential, mesenchymal stem cells (MSCs) remain poorly defined owing to their heterogeneity, the inability to assess in vivo self-renewal and the scarcity of markers allowing their identification, isolation and genetic manipulation. In the bone marrow (BM) of Nestin (Nes)-Gfp transgenic mice, CD31− CD45− GFP+ peri-vascular cells expressing endogenous nestin are associated with hematopoietic stem cells (HSCs) and innervated by fibers from the sympathetic nervous system (SNS). Flow cytometry sorting of BM CD45− Nes:GFP+ and CD45− Nes:GFP− cells has r
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Boettcher, Steffen, Rahel Gerosa, Ramin Radpour, and Markus G. Manz. "Endothelial Cells Are Essential to Sense Lipopolysaccharide in a MYD88-Dependent Manner and to Subsequently Induce Emergency Myelopoiesis." Blood 120, no. 21 (2012): 641. http://dx.doi.org/10.1182/blood.v120.21.641.641.

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Abstract Abstract 641 Severe systemic infections evoke a number of characteristic clinical signs such as fever, neutrophilia and the appearance of immature myeloid precursors in the circulation (left-shift). This reflects a well-regulated hematopoietic response program to enhance myeloid cell output during times of increased hematopoietic demand, a condition which is referred to as 'emergency myelopoiesis'. Important molecular components of the emergency myelopoiesis cascade, such as cytokines and transcription factors involved, have been elucidated. However, the initial steps of emergency mye
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22

Lee, Dong-won, Xiaohong Zhao, Yang-In Yim, Evan Eisenberg, and Lois E. Greene. "Essential Role of Cyclin-G–associated Kinase (Auxilin-2) in Developing and Mature Mice." Molecular Biology of the Cell 19, no. 7 (2008): 2766–76. http://dx.doi.org/10.1091/mbc.e07-11-1115.

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Hsc70 with its cochaperone, either auxilin or GAK, not only uncoats clathrin-coated vesicles but also acts as a chaperone during clathrin-mediated endocytosis. However, because synaptojanin is also involved in uncoating, it is not clear whether GAK is an essential gene. To answer this question, GAK conditional knockout mice were generated and then mated to mice expressing Cre recombinase under the control of the nestin, albumin, or keratin-14 promoters, all of which turn on during embryonic development. Deletion of GAK from brain, liver, or skin dramatically altered the histology of these tiss
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Renault-Mihara, Francois, Masahiko Mukaino, Munehisa Shinozaki, et al. "Regulation of RhoA by STAT3 coordinates glial scar formation." Journal of Cell Biology 216, no. 8 (2017): 2533–50. http://dx.doi.org/10.1083/jcb.201610102.

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Understanding how the transcription factor signal transducer and activator of transcription–3 (STAT3) controls glial scar formation may have important clinical implications. We show that astrocytic STAT3 is associated with greater amounts of secreted MMP2, a crucial protease in scar formation. Moreover, we report that STAT3 inhibits the small GTPase RhoA and thereby controls actomyosin tonus, adhesion turnover, and migration of reactive astrocytes, as well as corralling of leukocytes in vitro. The inhibition of RhoA by STAT3 involves ezrin, the phosphorylation of which is reduced in STAT3-CKO
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Giusti, Sebastian A., Claudia A. Vercelli, Annette M. Vogl, et al. "Behavioral phenotyping of Nestin-Cre mice: Implications for genetic mouse models of psychiatric disorders." Journal of Psychiatric Research 55 (August 2014): 87–95. http://dx.doi.org/10.1016/j.jpsychires.2014.04.002.

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Tomita, Shuhei, Masaki Ueno, Masami Sakamoto та ін. "Defective Brain Development in Mice Lacking the Hif-1α Gene in Neural Cells". Molecular and Cellular Biology 23, № 19 (2003): 6739–49. http://dx.doi.org/10.1128/mcb.23.19.6739-6749.2003.

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ABSTRACT Hypoxia-inducible factor 1α (HIF-1α) is essential for vascular development during embryogenesis and pathogenesis. However, little is known about its role in brain development. To investigate the function of HIF-1α in the central nervous system, a conditional knockout mouse was made with the Cre/LoxP system with a nestin promoter-driven Cre. Neural cell-specific HIF-1α-deficient mice exhibit hydrocephalus accompanied by a reduction in neural cells and an impairment of spatial memory. Apoptosis of neural cells coincided with vascular regression in the telencephalon of mutant embryos, an
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Asada, Noboru, Yuya Kunisaki, Takashi Nagasawa, and Paul S. Frenette. "Distinct Contributions By Perivascular Niche Cells in Hematopoietic Stem Cell Maintenance." Blood 126, no. 23 (2015): 661. http://dx.doi.org/10.1182/blood.v126.23.661.661.

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Abstract Hematopoietic stem cells (HSCs) self-renew and differentiate into all blood types in response to various demands through life. HSC functions are tightly and finely tuned by a specialized microenvironment called "niche" in the bone marrow (BM). Using Nestin-GFP transgenic mice, we have identified Nestin-GFP+ perivascular stromal cells exhibiting a mesenchymal stem/progenitor cell activity as niche cells. Furthermore, we found two types of Nestin-GFP+ cells expressing different surface markers, Nerve/glial antigen 2 (NG2) and Leptin receptor (Lepr) that are associated with arterioles an
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Vandeputte, Caroline, Veerle Reumers, Sarah-Ann Aelvoet, et al. "Bioluminescence Imaging of Stroke-Induced Neural Stem Cell Response." Neurobiol Dis. 69 (May 27, 2014): 144–55. https://doi.org/10.1016/j.nbd.2014.05.014.

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Brain injury following stroke affects neurogenesis in the adult mammalian brain. However, a complete understanding of the origin and fate of the endogenous neural stem cells (eNSCs) in vivo is missing. Tools and technology that allow non-invasive imaging and tracking of eNSCs in living animals will help to overcome this hurdle. In this study, we aimed to monitor eNSCs in a photothrombotic (PT) stroke model using in vivo bioluminescence imaging (BLI). In a first strategy, inducible transgenic mice expressing firefly luciferase (Fluc) in the eNSCs were generated. In animals that received stroke,
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Maeda, Yuki, Nami Nakagomi, Akiko Nakano-Doi, et al. "Potential of Adult Endogenous Neural Stem/Progenitor Cells in the Spinal Cord to Contribute to Remyelination in Experimental Autoimmune Encephalomyelitis." Cells 8, no. 9 (2019): 1025. http://dx.doi.org/10.3390/cells8091025.

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Demyelination and remyelination play pivotal roles in the pathological process of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), a well-established animal model of MS. Although increasing evidence shows that various stimuli can promote the activation/induction of endogenous neural stem/progenitor cells (NSPCs) in the central nervous system, the potential contributions of these cells to remyelination following inflammatory injury remain to be fully investigated. In the present study, using an adult mouse model of EAE induced by myelin oligodendrocyte glycoprotein (
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Chen, Chieh V., Jennifer L. Brummet, Cynthia L. Jordan, and S. Marc Breedlove. "Down, But Not Out: Partial Elimination of Androgen Receptors in the Male Mouse Brain Does Not Affect Androgenic Regulation of Anxiety or HPA Activity." Endocrinology 157, no. 2 (2015): 764–73. http://dx.doi.org/10.1210/en.2015-1417.

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Abstract We previously found that androgen receptor (AR) activity mediates two effects of T in adult male mice: reduction of anxiety-like behaviors and dampening of the hypothalamic-pituitary-adrenal response to stress. To determine whether brain ARs mediate these effects, we used the Cre/loxP technology seeking to disable AR throughout the central nervous system (CNS). Female mice carrying the floxed AR allele (ARlox) were crossed with males carrying cre recombinase transgene controlled by the nestin promoter (NesCre), producing cre in developing neurons and glia. Among male offspring, four g
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Tomita, Yuichi, Keisuke Matsumura, Yoshio Wakamatsu, et al. "Cardiac neural crest cells contribute to the dormant multipotent stem cell in the mammalian heart." Journal of Cell Biology 170, no. 7 (2005): 1135–46. http://dx.doi.org/10.1083/jcb.200504061.

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Arodent cardiac side population cell fraction formed clonal spheroids in serum-free medium, which expressed nestin, Musashi-1, and multi-drug resistance transporter gene 1, markers of undifferentiated neural precursor cells. These markers were lost following differentiation, and were replaced by the expression of neuron-, glial-, smooth muscle cell–, or cardiomyocyte-specific proteins. Cardiosphere-derived cells transplanted into chick embryos migrated to the truncus arteriosus and cardiac outflow tract and contributed to dorsal root ganglia, spinal nerves, and aortic smooth muscle cells. Line
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Pai, Christopher, Rajarshi Sengupta, and Robert O. Heuckeroth. "Sequencing Reveals miRNAs Enriched in the Developing Mouse Enteric Nervous System." Non-Coding RNA 10, no. 1 (2023): 1. http://dx.doi.org/10.3390/ncrna10010001.

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The enteric nervous system (ENS) is an essential network of neurons and glia in the bowel wall. Defects in ENS development can result in Hirschsprung disease (HSCR), a life-threatening condition characterized by severe constipation, abdominal distention, bilious vomiting, and failure to thrive. A growing body of literature connects HSCR to alterations in miRNA expression, but there are limited data on the normal miRNA landscape in the developing ENS. We sequenced small RNAs (smRNA-seq) and messenger RNAs (mRNA-seq) from ENS precursor cells of mid-gestation Ednrb-EGFP mice and compared them to
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32

Wu, Sophie R., Harrison Q. Liu, Joshua Tolliver, et al. "Abstract 1437: Generating primary mouse models of diffuse midline glioma through a combination of the RCAS/tv-a retrovirus system and CRISPR/Cas9 gene editing." Cancer Research 84, no. 6_Supplement (2024): 1437. http://dx.doi.org/10.1158/1538-7445.am2024-1437.

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Abstract Diffuse midline gliomas (DMGs) are deadly brain tumors that arise in the brainstem of children and young adults, resulting in a median survival of less than two years. Genetically engineered mouse models (GEMMs) are critical to studying tumorigenesis and tumor-immune interactions in DMG, which may inform the design of new urgently-needed treatment approaches. One approach to generate DMG GEMMs uses RCAS/tv-a, an avian retrovirus gene delivery system to express transgenes in specific brain cell lineages in the mouse brain. However, this approach often requires resource-intensive breedi
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33

Ko, Hyo Rim, Inwoo Hwang, Eun-Ju Jin, et al. "Roles of ErbB3-binding protein 1 (EBP1) in embryonic development and gene-silencing control." Proceedings of the National Academy of Sciences 116, no. 49 (2019): 24852–60. http://dx.doi.org/10.1073/pnas.1916306116.

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ErbB3-binding protein 1 (EBP1) is implicated in diverse cellular functions, including apoptosis, cell proliferation, and differentiation. Here, by generating genetic inactivation of Ebp1 mice, we identified the physiological roles of EBP1 in vivo. Loss of Ebp1 in mice caused aberrant organogenesis, including brain malformation, and death between E13.5 and 15.5 owing to severe hemorrhages, with massive apoptosis and cessation of cell proliferation. Specific ablation of Ebp1 in neurons caused structural abnormalities of brain with neuron loss in [Nestin-Cre; Ebp1flox/flox] mice. Notably, global
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34

Swift-Gallant, Ashlyn, Lindsay A. Coome, Firyal Ramzan, and D. Ashley Monks. "Nonneural Androgen Receptors Affect Sexual Differentiation of Brain and Behavior." Endocrinology 157, no. 2 (2015): 788–98. http://dx.doi.org/10.1210/en.2015-1355.

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Abstract Testosterone, acting via estrogenic and androgenic pathways, is the major endocrine mechanism promoting sexual differentiation of the mammalian nervous system and behavior, but we have an incomplete knowledge of which cells and tissues mediate these effects. To distinguish between neural and nonneural actions of androgens in sexual differentiation of brain and behavior, we generated a loxP-based transgenic mouse, which overexpresses androgen receptors (ARs) when activated by Cre. We used this transgene to overexpress AR globally in all tissues using a cytomegalovirus (CMV)-Cre driver
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35

Hanner, Fiona, Julia von Maltzahn, Stephan Maxeiner, et al. "Connexin45 is expressed in the juxtaglomerular apparatus and is involved in the regulation of renin secretion and blood pressure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 2 (2008): R371—R380. http://dx.doi.org/10.1152/ajpregu.00468.2007.

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Connexin (Cx) proteins are known to play a role in cell-to-cell communication via intercellular gap junction channels or transiently open hemichannels. Previous studies have identified several connexin isoforms in the juxtaglomerular apparatus (JGA), but the vascular connexin isoform Cx45 has not yet been studied in this region. The present work aimed to identify in detail the localization of Cx45 in the JGA and to suggest a functional role for Cx45 in the kidney using conditions where Cx45 expression or function was altered. Using mice that express lacZ coding DNA under the control of the Cx4
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Kajitani, Yusuke, Takashi Miyazawa, Tomoaki Inoue, et al. "Correction: High frequency of germline recombination in Nestin-Cre transgenic mice crossed with Glucagon-like peptide 1 receptor floxed mice." PLOS ONE 19, no. 5 (2024): e0303862. http://dx.doi.org/10.1371/journal.pone.0303862.

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Martin, Brice, Craig Thomas, Tyler Garman, Daisy Lin, Nadia Dahmane, and Mark Souweidane. "RARE-17. HIGH-THROUGHPUT SCREEN IDENTIFIES POTENTIAL CHEMOTHERAPIES FOR CHOROID PLEXUS CARCINOMA TREATMENT USING INTRAARTERIAL STRATEGY." Neuro-Oncology 23, Supplement_1 (2021): i44. http://dx.doi.org/10.1093/neuonc/noab090.178.

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Abstract Choroid plexus carcinoma is a rare infantile brain tumor with an aggressive clinical course.1 There is no optimal treatment and survival is poor. Gross total surgical removal is the single most important predictor of survival.1 Gross total surgical removal rates are inconsistent and associated with significant morbidity owing to the hemorrhagic nature of these tumors compounded by a small circulating blood volume. Neoadjuvant systemic chemotherapy with “second look surgery” helps to achieve gross total surgical removal2 but has an inefficient pharmacokinetic profile and exposes childr
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38

Mendez-Ferrer, Simon, Grigori N. Enikolopov, Sergio Lira, and Paul S. Frenette. "Mesenchymal Stem Cells, Regulated by the Sympathetic Nervous System, Form the Hematopoietic Stem Cell Niche." Blood 112, no. 11 (2008): 4. http://dx.doi.org/10.1182/blood.v112.11.4.4.

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Abstract The identity of mesenchymal stem cells (MSCs) and their relationship to hematopoietic stem cells (HSCs) remain poorly defined. In addition, there are discrepancies regarding the cellular constituents of the HSC niche, with studies suggesting a role for bone-lining osteoblasts, and other data implicating sinusoidal endothelial and adventitial reticular cells. Previous work from our group has demonstrated that the sympathetic nervous system (SNS) is critical for both physiological and enforced egress of HSCs from the bone marrow (BM). HSC mobilization induced by G-CSF requires signals f
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39

Declercq, Jeroen, Bas Brouwers, Vincent P. E. G. Pruniau, et al. "Metabolic and Behavioural Phenotypes in Nestin-Cre Mice Are Caused by Hypothalamic Expression of Human Growth Hormone." PLOS ONE 10, no. 8 (2015): e0135502. http://dx.doi.org/10.1371/journal.pone.0135502.

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Hossain, Anwar, Irtiza Hasan, Satoshi Adachi, et al. "TMIC-37. INTERCELLULAR COMMUNICATION BETWEEN NORMAL AND TUMOR CELLS IN GLIOMA MICROENVIRONMENT." Neuro-Oncology 21, Supplement_6 (2019): vi255—vi256. http://dx.doi.org/10.1093/neuonc/noz175.1071.

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Abstract The interactions between tumors cells and their microenvironment are increasingly recognized as contributors to tumor growth and therapeutic resistance in glioblastoma (GBM). Mesenchymal Stem Cells (MSCs) have been implicated as components of the microenvironment of several cancers, but their contribution to GBM remains obscure. Recently we reported that GBMs contain cells resembling human mesenchymal stem cells, called Glioma-associated-MSCs (GA-hMSCs), based on our ability to isolate these cells from patient tumors (Figueroa, et al. Can Res 2017. 77, 5808–5819). In order to characte
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41

Zhou, Yun, Leonie F. Waanders, Silvia Holmseth, et al. "Proteome Analysis and Conditional Deletion of the EAAT2 Glutamate Transporter Provide Evidence against a Role of EAAT2 in Pancreatic Insulin Secretion in Mice." Journal of Biological Chemistry 289, no. 3 (2013): 1329–44. http://dx.doi.org/10.1074/jbc.m113.529065.

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Islet function is incompletely understood in part because key steps in glutamate handling remain undetermined. The glutamate (excitatory amino acid) transporter 2 (EAAT2; Slc1a2) has been hypothesized to (a) provide islet cells with glutamate, (b) protect islet cells against high extracellular glutamate concentrations, (c) mediate glutamate release, or (d) control the pH inside insulin secretory granules. Here we floxed the EAAT2 gene to produce the first conditional EAAT2 knock-out mice. Crossing with Nestin-cyclization recombinase (Cre) eliminated EAAT2 from the brain, resulting in epilepsy
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42

Li, Lingli, En Yin Lai, Yuning Huang, et al. "Renal afferent arteriolar and tubuloglomerular feedback reactivity in mice with conditional deletions of adenosine 1 receptors." American Journal of Physiology-Renal Physiology 303, no. 8 (2012): F1166—F1175. http://dx.doi.org/10.1152/ajprenal.00222.2012.

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Adenosine 1 receptors (A1AR) have been shown in previous experiments to play a major role in the tubuloglomerular feedback (TGF) constrictor response of afferent arterioles (AA) to increased loop of Henle flow. Overexpression studies have pointed to a critical role of vascular A1AR, but it has remained unclear whether selective deletion of A1AR from smooth muscle cells is sufficient to abolish TGF responsiveness. To address this question, we have determined TGF response magnitude in mice in which vascular A1AR deletion was achieved using the loxP recombination approach with cre recombinase bei
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43

Bell, Sigourney, Claire King, Katherine Wickham Rahrmann, Amir Jassim, Jessica Taylor, and Richard Gilbertson. "EPEN-25. A novel spontaneous model of ZFTA-RELA fusion ependymoma." Neuro-Oncology 24, Supplement_1 (2022): i44. http://dx.doi.org/10.1093/neuonc/noac079.161.

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Abstract Ependymomas driven by the ZFTA-RELA fusion account for >70% of all supratentorial ependymomas. These tumours are now recognised in the WHO classification of CNS tumours and have been associated with a poor prognosis. Seven ZFTA-RELA fusion variants have been described: around two thirds of cases are fusion 1. No spontaneous genetically modified mouse models (GEMMS) have been described and current models require invasive intracranial injection (of transduced cells or RCAS-TVA system). Here we describe the first spontaneous GEMM of ZFTA-RELA fusion-driven ependymoma. Nestin-Flx-S
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44

Bonner, Sigourney, Claire King, Katherine Wickham Rarhmann, Elizabeth Cooper, Gunjan Katyal, and Richard Gilbertson. "EPEN-06. CHARACTERISING THE DEVELOPMENTAL ORIGINS AND TRAJECTORIES OF ZFTA-RELA FUSION EPENDYMOMA IN A NOVEL MOUSE MODEL." Neuro-Oncology 25, Supplement_1 (2023): i27—i28. http://dx.doi.org/10.1093/neuonc/noad073.110.

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Abstract Ependymomas driven by the ZFTA-RELA fusion account for >70% of all supratentorial ependymomas. These tumours are now recognised in the WHO classification of CNS tumours and have been associated with a poor prognosis. Seven ZFTA-RELA fusion variants have been described: around two thirds of cases are fusion 1. No spontaneous genetically modified mouse models (GEMMS) have been described and current models require invasive intracranial injection (of transduced cells or RCAS-TVA system). Here we describe the first spontaneous GEMM of ZFTA-RELA fusion-driven ependymoma. Nestin-Flx-S
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45

Dhar, Swati, Samantha Gadd, Daniel Brat, and Oren Becher. "DIPG-44. A GAIN OF FUNCTION Ezh2 MUTATION DELAYS DIFFUSE INTRINSIC PONTINE GLIOMA PROGRESSION." Neuro-Oncology 22, Supplement_3 (2020): iii295. http://dx.doi.org/10.1093/neuonc/noaa222.091.

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Abstract BACKGROUND Diffuse Intrinsic Pontine Glioma (DIPG) remains an incurable pediatric brain cancer. The oncohistone H3K27M implicated in 80% of the cases, is also predicted to target Enhancer of Zeste Homolog 2 (Ezh2), the catalytic component of the Polycomb Repressor Complex 2 (PRC2). There are no reported mutations of Ezh2 and its function in DIPG is not fully determined. This work aims to address the role of Ezh2 in DIPG. METHODS Brainstem tumors were established by intracranial injections of Nestin;Tv-a; Ezh2Y641F/+ (NTv-a; Ezh2Y641F/+) neonatal pups using Replication Competent Avian
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Wu, Sophie R., María E. Guerra Garcia, Harrison Liu, et al. "Abstract 2817: Combining the RCAS/TVA retrovirus system and a conditional oncohistone H3.3K27M allele to investigate radiosensitization strategies in primary mouse models of diffuse midline glioma." Cancer Research 83, no. 7_Supplement (2023): 2817. http://dx.doi.org/10.1158/1538-7445.am2023-2817.

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Abstract Diffuse midline gliomas (DMGs) are deadly brain tumors characterized by inactivating TP53 mutations and oncohistone H3.3K27M mutations. One potential strategy to improve outcomes for DMG patients is to inhibit Ataxia-telangiectasia mutated kinase (ATM), an orchestrator of the cellular response to the DNA double-strand breaks. Previous research showed that Atm inactivation strongly enhanced the efficacy of radiation therapy for primary mouse models of p53-inactivated DMG. However, it remained unclear whether Atm inactivation would also radiosensitize DMGs driven by both p53 loss and by
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47

Tang, Lie-Qi, Johnathan Fraebel, Shi Jin, et al. "Calcium/calcimimetic via calcium-sensing receptor ameliorates cholera toxin-induced secretory diarrhea in mice." World Journal of Gastroenterology 30, no. 3 (2024): 268–79. http://dx.doi.org/10.3748/wjg.v30.i3.268.

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BACKGROUND Enterotoxins produce diarrhea through direct epithelial action and indirectly by activating the enteric nervous system. Calcium-sensing receptor (CaSR) inhibits both actions. The latter has been well documented in vitro but not in vivo . The hypothesis to be tested was that activating CaSR inhibits diarrhea in vivo . AIM To determine whether CaSR agonists ameliorate secretory diarrhea evoked by cholera toxin (CTX) in mice. METHODS CTX was given orally to C57BL/6 mice to induce diarrhea. Calcium and calcimimetic R568 were used to activate CaSR. To maximize their local intestinal acti
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48

Das, Anirban, Owen Crump, Olha Kos, et al. "IMMU-07. COMBINED PD1 AND LAG3 INHIBITION IN PRECLINICAL MODELS AND PATIENTS WITH DNA REPLICATION REPAIR DEFICIENT GLIOBLASTOMA (RRD-GBM): AN IRRDC STUDY." Neuro-Oncology 26, Supplement_4 (2024): 0. http://dx.doi.org/10.1093/neuonc/noae064.378.

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Abstract BACKGROUND RRD-GBM harbour high tumor mutation burden (TMB) and respond to anti-PD1 immune checkpoint inhibition (ICI). However, the majority ultimately progress, highlighting the need for combinatorial therapies for sustained immune-surveillance. METHODS We performed transcriptomic analyses of human RRD-GBM specimens for immune checkpoint expression, and accordingly, tested combined ICI in immunocompetent murine models. Based on these preclinical data, we treated refractory patients using a combination of anti-PD1 and anti-LAG3 through single-patient trials/ compassionate access. Com
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Abdallah, Aalaa, Herminio J. Cardona, David J. Picketts, Daniel J. Brat, Xiao-Nan Li, and Oren J. Becher. "Abstract 912: A novel genetically engineered H3.3G34R model reveals cooperation with ATRX loss in upregulation of PRC2 target genes." Cancer Research 82, no. 12_Supplement (2022): 912. http://dx.doi.org/10.1158/1538-7445.am2022-912.

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Abstract Pediatric High Grade Glioma (pHGG) is a collection of molecularly distinct subtypes with different prognoses depending on the genetic drivers. One particularly aggressive subtype is H3.3G34R mutant gliomas, which are currently incurable and in need of improved therapies. Interestingly, H3.3G34R mutant gliomas commonly harbor TP53mutations, ATRX mutations, and alterations in PDGFRA signaling. The mechanism by which H3.3G34R promotes gliomagenesis is still somewhat unclear and additional models are needed to dissect its role in tumorigenesis. We used the RCAS Tv-a system to model H3.3G3
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Galichet, Christophe, Robin Lovell-Badge, and Karine Rizzoti. "Nestin-Cre Mice Are Affected by Hypopituitarism, Which Is Not Due to Significant Activity of the Transgene in the Pituitary Gland." PLoS ONE 5, no. 7 (2010): e11443. http://dx.doi.org/10.1371/journal.pone.0011443.

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