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Article ; Online: Rod phototransduction and light signal transmission during type 2 diabetes.

Becker, Silke / Carroll, Lara S / Vinberg, Frans

2020 Volume 8, Issue 1

Abstract: Introduction: Diabetic retinopathy is a major complication of diabetes recently associated with compromised photoreceptor function. Multiple stressors in diabetes, such as hyperglycemia, oxidative stress and inflammatory factors, have been identified, ... ...

Abstract	Introduction: Diabetic retinopathy is a major complication of diabetes recently associated with compromised photoreceptor function. Multiple stressors in diabetes, such as hyperglycemia, oxidative stress and inflammatory factors, have been identified, but systemic effects of diabetes on outer retina function are incompletely understood. We assessed photoreceptor physiology in vivo and in isolated retinas to better understand how alterations in the cellular environment compared with intrinsic cellular/molecular properties of the photoreceptors, affect light signal transduction and transmission in the retina in chronic type 2 diabetes. Research design and methods: Photoreceptor function was assessed in BKS.Cs-Dock7 Results: We found that both transduction and transmission of light signals by rod photoreceptors were compromised in 6-month-old (n=9-10 eyes from 5 animals, *p<0.001) but not in 3-month-old diabetic mice in vivo (n=4-8 eyes from 2 to 4 animals). In contrast, rod signaling was similar in isolated retinas from 6-month-old control and diabetic mice under normoglycemic conditions (n=11). Acutely elevated glucose ex vivo increased light-evoked rod photoreceptor responses in control mice (n=11, p<0.001), but did not affect light responses in diabetic mice (n=11). Conclusions:* Our data suggest that long-term diabetes does not irreversibly change the ability of rod photoreceptors to transduce and mediate light signals. However, type 2 diabetes appears to induce adaptational changes in the rods that render them less sensitive to increased availability of glucose.
MeSH term(s)	Animals ; Diabetes Mellitus, Experimental ; Diabetes Mellitus, Type 2 ; Light Signal Transduction ; Mice ; Mice, Inbred C57BL ; Retinal Rod Photoreceptor Cells
Language	English
Publishing date	2020-08-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2732918-5
ISSN	2052-4897 ; 2052-4897
ISSN (online)	2052-4897
ISSN	2052-4897
DOI	10.1136/bmjdrc-2020-001571
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Article ; Online: Diabetic photoreceptors: Mechanisms underlying changes in structure and function.

Becker, Silke / Carroll, Lara S / Vinberg, Frans

Visual neuroscience

2020 Volume 37, Page(s) E008

Abstract: Based on clinical findings, diabetic retinopathy (DR) has traditionally been defined as a retinal microvasculopathy. Retinal neuronal dysfunction is now recognized as an early event in the diabetic retina before development of overt DR. While detrimental ...

Abstract	Based on clinical findings, diabetic retinopathy (DR) has traditionally been defined as a retinal microvasculopathy. Retinal neuronal dysfunction is now recognized as an early event in the diabetic retina before development of overt DR. While detrimental effects of diabetes on the survival and function of inner retinal cells, such as retinal ganglion cells and amacrine cells, are widely recognized, evidence that photoreceptors in the outer retina undergo early alterations in diabetes has emerged more recently. We review data from preclinical and clinical studies demonstrating a conserved reduction of electrophysiological function in diabetic retinas, as well as evidence for photoreceptor loss. Complementing in vivo studies, we discuss the ex vivo electroretinography technique as a useful method to investigate photoreceptor function in isolated retinas from diabetic animal models. Finally, we consider the possibility that early photoreceptor pathology contributes to the progression of DR, and discuss possible mechanisms of photoreceptor damage in the diabetic retina, such as enhanced production of reactive oxygen species and other inflammatory factors whose detrimental effects may be augmented by phototransduction.
MeSH term(s)	Animals ; Diabetes Mellitus ; Diabetic Retinopathy ; Electroretinography ; Retina ; Retinal Ganglion Cells
Language	English
Publishing date	2020-10-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639436-x
ISSN	1469-8714 ; 0952-5238
ISSN (online)	1469-8714
ISSN	0952-5238
DOI	10.1017/S0952523820000097
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Article ; Online: Hoxc8 initiates an ectopic mammary program by regulating Fgf10 and Tbx3 expression and Wnt/β-catenin signaling.

Carroll, Lara S / Capecchi, Mario R

Development (Cambridge, England)

2015 Volume 142, Issue 23, Page(s) 4056–4067

Abstract: The role of Hox genes in the formation of cutaneous accessory organs such as hair follicles and mammary glands has proved elusive, a likely consequence of overlapping function and expression among various homeobox factors. Lineage and immunohistochemical ...

Abstract	The role of Hox genes in the formation of cutaneous accessory organs such as hair follicles and mammary glands has proved elusive, a likely consequence of overlapping function and expression among various homeobox factors. Lineage and immunohistochemical analysis of Hoxc8 in mice revealed that this midthoracic Hox gene has transient but strong regional expression in ventrolateral surface ectoderm at E10.5, much earlier than previously reported. Targeted mice were generated to conditionally misexpress Hoxc8 from the Rosa locus using select Cre drivers, which significantly expanded the domain of thoracic identity in mutant embryos. Accompanying this expansion was the induction of paired zones of ectopic mammary development in the cervical region, which generated between three and five pairs of mammary placodes anterior to the first wild-type mammary rudiment. These rudiments expressed the mammary placode markers Wnt10b and Tbx3 and were labeled by antibodies to the mammary mesenchyme markers ERα and androgen receptor. Somitic Fgf10 expression, which is required for normal mammary line formation, was upregulated in mutant cervical somites, and conditional ablation of ectodermal Tbx3 expression eliminated all normally positioned and ectopic mammary placodes. We present evidence that Hoxc8 participates in regulating the initiation stages of mammary placode morphogenesis, and suggest that this and other Hox genes are likely to have important roles during regional specification and initiation of these and other cutaneous accessory organs.
MeSH term(s)	Animals ; Body Patterning ; Cell Lineage ; Ectoderm/metabolism ; Female ; Fibroblast Growth Factor 10/genetics ; Fibroblast Growth Factor 10/metabolism ; Gene Expression Regulation, Developmental ; Genotype ; Green Fluorescent Proteins/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Immunohistochemistry ; In Situ Hybridization ; Lac Operon ; Male ; Mesoderm/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Time Factors ; Up-Regulation ; Wnt Signaling Pathway
Chemical Substances	Fgf10 protein, mouse ; Fibroblast Growth Factor 10 ; Homeodomain Proteins ; Hoxc8 protein, mouse ; T-Box Domain Proteins ; Tbx3 protein, mouse ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2015-12-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.128298
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Article ; Online: Systemic AAV10.COMP-Ang1 rescues renal glomeruli and pancreatic islets in type 2 diabetic mice.

Tian, Mi / Carroll, Lara S / Tang, Li / Uehara, Hironori / Westenfelder, Christof / Ambati, Balamurali K / Huang, Yufeng

BMJ open diabetes research & care

2020 Volume 8, Issue 1

Abstract: Introduction: Diabetic hyperglycemia causes progressive and generalized damage to the microvasculature. In renal glomeruli, this results in the loss of podocytes with consequent loss of constitutive angiopoietin-1 (Ang1) signaling, which is required for ...

Abstract	Introduction: Diabetic hyperglycemia causes progressive and generalized damage to the microvasculature. In renal glomeruli, this results in the loss of podocytes with consequent loss of constitutive angiopoietin-1 (Ang1) signaling, which is required for stability of the glomerular endothelium. Repeated tail vein injection of adenovirus expressing COMP-Ang1 (a stable bioengineered form of Ang1) was previously reported to improve diabetic glomerular damage despite the liver and lungs being primary targets of adenoviral infection. We thus hypothesized that localizing delivery of sustained COMP-Ang1 to the kidney could increase its therapeutic efficacy and safety for the treatment of diabetes. Research design and methods: Using AAVrh10 adeno-associated viral capsid with enhanced kidney tropism, we treated 10-week-old uninephrectomized db/db mice (a model of type 2 diabetes) with a single dose of AAVrh10.COMP-Ang1 delivered via the intracarotid artery, compared with untreated diabetic db/db control and non-diabetic db/m mice. Results: Surprisingly, both glomerular and pancreatic capillaries expressed COMP-Ang1, compensating for diabetes-induced loss of tissue Ang1. Importantly, treatment with AAVrh10.COMP-Ang1 yielded a significant reduction of glycemia (blood glucose, 241±193 mg/dL vs 576±31 mg/dL; glycosylated hemoglobin, 7.2±1.5% vs 11.3±1.3%) and slowed the progression of albuminuria and glomerulosclerosis in db/db mice by 70% and 61%, respectively, compared with untreated diabetic db/db mice. Furthermore, COMP-Ang1 ameliorated diabetes-induced increases of NF-kBp65, nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase-2 (Nox2), p47phox and productions of myeloperoxidase, the inflammatory markers in both renal and pancreatic tissues, and improved beta-cell density in pancreatic islets. Conclusions: These results highlight the potential of localized Ang1 therapy for treatment of diabetic visceropathies and provide a mechanistic explanation for reported improvements in glucose control via Ang1/Tie2 signaling in the pancreas.
MeSH term(s)	Angiopoietin-1/genetics ; Animals ; Diabetes Mellitus, Experimental/therapy ; Diabetes Mellitus, Type 2/therapy ; Islets of Langerhans ; Kidney ; Mice
Chemical Substances	Angiopoietin-1
Language	English
Publishing date	2020-10-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2732918-5
ISSN	2052-4897 ; 2052-4897
ISSN (online)	2052-4897
ISSN	2052-4897
DOI	10.1136/bmjdrc-2019-000882
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Article ; Online: COMP-Ang1 Stabilizes Hyperglycemic Disruption of Blood-Retinal Barrier Phenotype in Human Retinal Microvascular Endothelial Cells.

Rochfort, Keith D / Carroll, Lara S / Barabas, Peter / Curtis, Timothy M / Ambati, Balamurali K / Barron, Niall / Cummins, Philip M

Investigative ophthalmology & visual science

2019 Volume 60, Issue 10, Page(s) 3547–3555

Abstract: Purpose: Current treatments for diabetic retinopathy (DR) have considerable limitations, underpinning the need for new therapeutic options. In this article, the ability of an engineered angiopoietin-1 variant (COMP-Ang1) to ameliorate the injurious ... ...

Abstract	Purpose: Current treatments for diabetic retinopathy (DR) have considerable limitations, underpinning the need for new therapeutic options. In this article, the ability of an engineered angiopoietin-1 variant (COMP-Ang1) to ameliorate the injurious effects of hyperglycemia on barrier integrity in a human retinal microvascular endothelial cell (HRMvEC) model is comprehensively investigated. Methods: Confluent HRMvECs were treated (0-72 hours) with d-glucose (5 or 30 mM) in the absence and presence of COMP-Ang1 (10-200 ng/mL). l-glucose (30 mM) was used as osmotic control. Posttreatment, intact cell monolayers were monitored for permeability to FITC-dextran 40 kDa. Cells were also harvested for analysis of interendothelial junction targets by RT-qPCR and Western blotting. The impact of receptor tyrosine kinase Tie2 gene silencing on COMP-Ang1 efficacy was also evaluated. Results: Treatment with 30 mM d-glucose (but not l-glucose) demonstrated a time-dependent elevation in the mean rate of FITC-dextran diffusion across intact HRMvEC monolayers, in parallel with significant reductions in mRNA/protein levels of occludin, claudin-5, ZO-1, and VE-Cadherin. These effects were all attenuated by COMP-Ang1 in a concentration-dependent fashion, with 200 ng/mL recovering barrier function by ∼88%, and recovering reduced interendothelial junction protein levels by more than 50%. Finally, Tie2 knockdown by small interfering RNA silencing blocked the ability of COMP-Ang1 to mitigate against hyperglycemia-induced permeabilization of HRMvECs and depletion of junctional expression levels. Conclusions: In summary, this article presents a reproducible in vitro cell study that quantifies the concentration-dependent efficacy of COMP-Ang1 to mitigate the injurious effects of hyperglycemic challenge on HRMvEC barrier properties via Tie2-mediated signaling.
MeSH term(s)	Antigens, CD/genetics ; Blood-Retinal Barrier/physiology ; Blotting, Western ; Cadherins/genetics ; Capillary Permeability/drug effects ; Cells, Cultured ; Claudin-5/genetics ; Dextrans/metabolism ; Dose-Response Relationship, Drug ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Fluorescein-5-isothiocyanate/analogs & derivatives ; Fluorescein-5-isothiocyanate/metabolism ; Gene Silencing/physiology ; Glucose/pharmacology ; Humans ; Hyperglycemia/metabolism ; Hyperglycemia/prevention & control ; Occludin/genetics ; Phenotype ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptor, TIE-2/genetics ; Recombinant Fusion Proteins/pharmacology ; Retinal Vessels/drug effects ; Retinal Vessels/metabolism
Chemical Substances	Antigens, CD ; CLDN5 protein, human ; COMP-Ang1 fusion protein ; Cadherins ; Claudin-5 ; Dextrans ; OCLN protein, human ; Occludin ; RNA, Messenger ; Recombinant Fusion Proteins ; cadherin 5 ; fluorescein isothiocyanate dextran ; Receptor, TIE-2 (EC 2.7.10.1) ; TEK protein, human (EC 2.7.10.1) ; Fluorescein-5-isothiocyanate (I223NX31W9) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.19-27644
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Article ; Online: ASPSCR1-TFE3 reprograms transcription by organizing enhancer loops around hexameric VCP/p97.

Pozner, Amir / Li, Li / Verma, Shiv Prakash / Wang, Shuxin / Barrott, Jared J / Nelson, Mary L / Yu, Jamie S E / Negri, Gian Luca / Colborne, Shane / Hughes, Christopher S / Zhu, Ju-Fen / Lambert, Sydney L / Carroll, Lara S / Smith-Fry, Kyllie / Stewart, Michael G / Kannan, Sarmishta / Jensen, Bodrie / John, Cini M / Sikdar, Saif /

Liu, Hongrui / Dang, Ngoc Ha / Bourdage, Jennifer / Li, Jinxiu / Vahrenkamp, Jeffery M / Mortenson, Katelyn L / Groundland, John S / Wustrack, Rosanna / Senger, Donna L / Zemp, Franz J / Mahoney, Douglas J / Gertz, Jason / Zhang, Xiaoyang / Lazar, Alexander J / Hirst, Martin / Morin, Gregg B / Nielsen, Torsten O / Shen, Peter S / Jones, Kevin B

Nature communications

2024 Volume 15, Issue 1, Page(s) 1165

Abstract: The t(X,17) chromosomal translocation, generating the ASPSCR1::TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCCs), frustrating efforts to identify therapeutic ...

Abstract	The t(X,17) chromosomal translocation, generating the ASPSCR1::TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCCs), frustrating efforts to identify therapeutic targets for these rare cancers. Here, proteomic analysis identifies VCP/p97, an AAA+ ATPase with known segregase function, as strongly enriched in co-immunoprecipitated nuclear complexes with ASPSCR1::TFE3. We demonstrate that VCP is a likely obligate co-factor of ASPSCR1::TFE3, one of the only such fusion oncoprotein co-factors identified in cancer biology. Specifically, VCP co-distributes with ASPSCR1::TFE3 across chromatin in association with enhancers genome-wide. VCP presence, its hexameric assembly, and its enzymatic function orchestrate the oncogenic transcriptional signature of ASPSCR1::TFE3, by facilitating assembly of higher-order chromatin conformation structures demonstrated by HiChIP. Finally, ASPSCR1::TFE3 and VCP demonstrate co-dependence for cancer cell proliferation and tumorigenesis in vitro and in ASPS and RCC mouse models, underscoring VCP's potential as a novel therapeutic target.
MeSH term(s)	Animals ; Mice ; Humans ; Proteomics ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/pathology ; Translocation, Genetic ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Kidney Neoplasms/genetics ; Chromatin/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Chromosomes, Human, X/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Valosin Containing Protein/genetics
Chemical Substances	Oncogene Proteins, Fusion ; Chromatin ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; TFE3 protein, human ; ASPSCR1 protein, human ; Intracellular Signaling Peptides and Proteins ; VCP protein, human (EC 3.6.4.6) ; Valosin Containing Protein (EC 3.6.4.6)
Language	English
Publishing date	2024-02-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45280-5
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Article ; Online: Intravitreal AAV2.COMP-Ang1 Attenuates Deep Capillary Plexus Expansion in the Aged Diabetic Mouse Retina.

Carroll, Lara S / Uehara, Hironori / Fang, Daniel / Choi, Susie / Zhang, Xiaohui / Singh, Malkit / Sandhu, Zoya / Cummins, Philip M / Curtis, Tim M / Stitt, Alan W / Archer, Bonnie J / Ambati, Balamurali K

Investigative ophthalmology & visual science

2019 Volume 60, Issue 7, Page(s) 2494–2502

Abstract: Purpose: We determine whether intravitreal angiopoietin-1 combined with the short coiled-coil domain of cartilage oligomeric matrix protein by adeno-associated viral serotype 2 (AAV2.COMP-Ang1) delivery following the onset of vascular damage could ... ...

Abstract	Purpose: We determine whether intravitreal angiopoietin-1 combined with the short coiled-coil domain of cartilage oligomeric matrix protein by adeno-associated viral serotype 2 (AAV2.COMP-Ang1) delivery following the onset of vascular damage could rescue or repair damaged vascular beds and attenuate neuronal atrophy and dysfunction in the retinas of aged diabetic mice. Methods: AAV2.COMP-Ang1 was bilaterally injected into the vitreous of 6-month-old male Ins2Akita mice. Age-matched controls consisted of uninjected C57BL/6J and Ins2Akita males, and of Ins2Akita males injected with PBS or AAV2.REPORTER (AcGFP or LacZ). Retinal thickness and visual acuity were measured in vivo at baseline and at the 10.5-month endpoint. Ex vivo vascular parameters were measured from retinal flat mounts, and Western blot was used to detect protein expression. Results: All three Ins2Akita control groups showed significantly increased deep vascular density at 10.5 months compared to uninjected C57BL/6J retinas (as measured by vessel area, length, lacunarity, and number of junctions). In contrast, deep microvascular density of Ins2Akita retinas treated with AAV2.COMP-Ang1 was more similar to uninjected C57BL/6J retinas for all parameters. However, no significant improvement in retinal thinning or diabetic retinopathy-associated visual loss was found in treated diabetic retinas. Conclusions: Deep retinal microvasculature of diabetic Ins2Akita eyes shows late stage changes consistent with disorganized vascular proliferation. We show that intravitreally injected AAV2.COMP-Ang1 blocks this increase in deep microvascularity, even when administered subsequent to development of the first detectable vascular defects. However, improving vascular normalization did not attenuate neuroretinal degeneration or loss of visual acuity. Therefore, additional interventions are required to address neurodegenerative changes that are already underway.
MeSH term(s)	Angiopoietin-1/administration & dosage ; Animals ; Blood Glucose/metabolism ; Blotting, Western ; Capillaries/drug effects ; Cartilage Oligomeric Matrix Protein/administration & dosage ; Diabetes Mellitus, Type 1/complications ; Diabetic Retinopathy/physiopathology ; Diabetic Retinopathy/prevention & control ; Drug Carriers ; Drug Combinations ; Female ; Genetic Therapy ; Genetic Vectors ; Insulin/genetics ; Intravitreal Injections ; Male ; Mice ; Mice, Inbred C57BL ; Parvovirinae/genetics ; Retina/pathology ; Retinal Neovascularization/physiopathology ; Retinal Neovascularization/prevention & control ; Retinal Vessels/drug effects ; Retinal Vessels/pathology ; Visual Acuity/physiology
Chemical Substances	Angiopoietin-1 ; Blood Glucose ; Cartilage Oligomeric Matrix Protein ; Drug Carriers ; Drug Combinations ; Ins2 protein, mouse ; Insulin
Language	English
Publishing date	2019-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.18-26182
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Article: Targeted Delivery of FLT-Morpholino Using Cyclic RGD Peptide.

Uehara, Hironori / Muddana, Santosh Kumar / Zhang, Xiaohui / Das, Subrata Kumar / Bhuvanagiri, Sai / Liu, Jinlu / Wu, Yuanyuan / Choi, Susie / Carroll, Lara S / Archer, Bonnie / Ambati, Balamurali K

Translational vision science & technology

2017 Volume 6, Issue 3, Page(s) 9

Abstract: Purpose: We previously showed that intravitreal injection of the sFLT morpholino-oligomer (FLT-MO) suppresses laser-induced choroidal neovascularization (CNV) in mice by decreasing the membrane bound form of Flt-1 while increasing the soluble form of ... ...

Abstract	Purpose: We previously showed that intravitreal injection of the sFLT morpholino-oligomer (FLT-MO) suppresses laser-induced choroidal neovascularization (CNV) in mice by decreasing the membrane bound form of Flt-1 while increasing the soluble form of Flt-1 via alternative splicing shift. In this study, we examined whether cyclic RGD peptide (cRGD) can promote morpholino-oligomer accumulation in CNV following tail vein injection, and whether systemic cRGD conjugated FLT-MO (cRGD-FLT-MO) suppresses CNV growth. Methods: cRGD conjugated fluorescent morpholino-oligomer (cRGD-F-MO) was injected via tail vein into mice with previous retinal laser photocoagulation and examined for cRGD-F-MO accumulation in CNV. To examine whether cRGD-FLT-MO suppresses CNV growth, mice were tail-vein injected with cRGD-FLT-MO, cRGD conjugated standard morpholino-oligomer (cRGD-STD-MO), or Dulbecco's Phosphate-Buffered Saline (DPBS) 1 and 4 days postlaser photocoagulation. Seven days postlaser photocoagulation, eyes were harvested and laser CNV was stained with isolectin GS-IB4, allowing quantification of CNV size by confocal microscopy. Results: cRGD-F-MO accumulation in CNV commenced immediately after tail vein injection and could be observed even 1 day after injection. cRGD-FLT-MO tail vein injection significantly suppressed CNV size (2.7 × 10 Conclusions: cRGD peptide facilitates morpholino-oligomer accumulation in CNV following systemic delivery. cRGD-FLT-MO suppressed CNV growth after tail-vein injection, demonstrating the potential utility of cRGD peptide for morpholino-oligomer delivery to CNV. Translational relevance: Current therapy for neovascular age-related macular degeneration involves intravitreal injection of anti-vascular endothelial growth factor drugs. Our results indicate that CNV can be treated systemically, thus eliminating risks and hazards associated with intravitreal injection.
Language	English
Publishing date	2017-05-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674602-5
ISSN	2164-2591
ISSN	2164-2591
DOI	10.1167/tvst.6.3.9
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Article: (with research data) Sexual selection constrains the body mass of male but not female mice.

Ruff, James S / Cornwall, Douglas H / Morrison, Linda C / Cauceglia, Joseph W / Nelson, Adam C / Gaukler, Shannon M / Meagher, Shawn / Carroll, Lara S / Potts, Wayne K

Ecology and evolution

2017 Volume 7, Issue 4, Page(s) 1271–1275

Abstract: Sexual size dimorphism results when female and male body size is influenced differently by natural and sexual selection. Typically, in polygynous species larger male body size is thought to be favored in competition for mates and constraints on maximal ... ...

Abstract	Sexual size dimorphism results when female and male body size is influenced differently by natural and sexual selection. Typically, in polygynous species larger male body size is thought to be favored in competition for mates and constraints on maximal body size are due to countervailing natural selection on either sex; however, it has been postulated that sexual selection itself may result in stabilizing selection at an optimal mass. Here we test this hypothesis by retrospectively assessing the influence of body mass, one metric of body size, on the fitness of 113 wild-derived house mice
Language	English
Publishing date	2017-01-27
Publishing country	England
Document type	Journal Article
ISSN	2045-7758
ISSN	2045-7758
DOI	10.1002/ece3.2753
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Article: ASPSCR1-TFE3 reprograms transcription by organizing enhancer loops around hexameric VCP/p97.

Pozner, Amir / Verma, Shiv Prakash / Li, Li / Wang, Shuxin / Barrott, Jared J / Nelson, Mary L / Yu, Jamie S E / Negri, Gian Luca / Colborne, Shane / Hughes, Christopher S / Zhu, Ju-Fen / Lambert, Sydney L / Carroll, Lara S / Smith-Fry, Kyllie / Stewart, Michael G / Kannan, Sarmishta / Jensen, Bodrie / Mortenson, Katelyn L / John, Cini /

Sikdar, Saif / Liu, Hongrui / Dang, Ngoc Ha / Bourdage, Jennifer / Li, Jinxiu / Vahrenkamp, Jeffery M / Groundland, John S / Wustrack, Rosanna / Senger, Donna L / Zemp, Franz J / Mahoney, Douglas J / Gertz, Jason / Zhang, Xiaoyang / Lazar, Alexander J / Hirst, Martin / Morin, Gregg B / Nielsen, Torsten O / Shen, Peter S / Jones, Kevin B

bioRxiv : the preprint server for biology

2023

Abstract: The t(X,17) chromosomal translocation, generating the ASPSCR1-TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCC), frustrating efforts to identify therapeutic ... ...

Abstract	The t(X,17) chromosomal translocation, generating the ASPSCR1-TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCC), frustrating efforts to identify therapeutic targets for these rare cancers. Proteomic analysis showed that VCP/p97, an AAA+ ATPase with known segregase function, was strongly enriched in co-immunoprecipitated nuclear complexes with ASPSCR1-TFE3. We demonstrate that VCP is a likely obligate co-factor of ASPSCR1-TFE3, one of the only such fusion oncoprotein co-factors identified in cancer biology. Specifically, VCP co-distributed with ASPSCR1-TFE3 across chromatin in association with enhancers genome-wide. VCP presence, its hexameric assembly, and its enzymatic function orchestrated the oncogenic transcriptional signature of ASPSCR1-TFE3, by facilitating assembly of higher-order chromatin conformation structures as demonstrated by HiChIP. Finally, ASPSCR1-TFE3 and VCP demonstrated co-dependence for cancer cell proliferation and tumorigenesis
Language	English
Publishing date	2023-10-02
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.29.560242
Database	MEDical Literature Analysis and Retrieval System OnLINE

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