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Quantification of MRI signal of transgenic grafts overexpressing ferritin in murine myocardial infarcts.

ABSTRACT: The noninvasive detection of transplanted cells in damaged organs and the longitudinal follow-up of cell fate and graft size are important for the evaluation of cell therapy. We have shown previously that the overexpression of the natural iron storage protein, ferritin, permits the detection of engrafted cells in mouse heart by MRI, but further imaging optimization is required. Here, we report a systematic evaluation of ferritin-based stem cell imaging in infarcted mouse hearts in vivo using three cardiac-gated pulse sequences in a 3-T scanner: black-blood proton-density-weighted turbo spin echo (PD TSE BB), bright-blood T(2) -weighted gradient echo (GRE) and black-blood T(2) -weighted GRE with improved motion-sensitized-driven equilibrium (iMSDE) preparation. Transgenic C2C12 myoblast grafts overexpressing ferritin did not change MRI contrast in the PD TSE BB images, but showed a 20% reduction in signal intensity ratio in black-blood T(2) -weighted iMSDE (p < 0.05) and a 30% reduction in bright-blood T(2) -weighted GRE (p < 0.0001). Graft size measurements by T(2) iMSDE and T(2) GRE were highly correlated with histological assessments (r = 0.79 and r = 0.89, respectively). Unlabeled wild-type C2C12 cells transplanted to mouse heart did not change the MRI signal intensity, although endogenous hemosiderin was seen in some infarcts. These data support the use of ferritin to track the survival, growth and migration of stem cells transplanted into the injured heart.

SUBMITTER: Naumova AV

PROVIDER: S-EPMC3389131 | biostudies-other | 2012 Oct

REPOSITORIES: biostudies-other

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Transgenic mice overexpressing desmocollin-2 (DSC2) develop cardiomyopathy associated with myocardial inflammation and fibrotic remodeling.

Project description:BackgroundArrhythmogenic cardiomyopathy is an inherited heart muscle disorder leading to ventricular arrhythmias and heart failure, mainly as a result of mutations in cardiac desmosomal genes. Desmosomes are cell-cell junctions mediating adhesion of cardiomyocytes; however, the molecular and cellular mechanisms underlying the disease remain widely unknown. Desmocollin-2 is a desmosomal cadherin serving as an anchor molecule required to reconstitute homeostatic intercellular adhesion with desmoglein-2. Cardiac specific lack of desmoglein-2 leads to severe cardiomyopathy, whereas overexpression does not. In contrast, the corresponding data for desmocollin-2 are incomplete, in particular from the view of protein overexpression. Therefore, we developed a mouse model overexpressing desmocollin-2 to determine its potential contribution to cardiomyopathy and intercellular adhesion pathology.Methods and resultsWe generated transgenic mice overexpressing DSC2 in cardiac myocytes. Transgenic mice developed a severe cardiac dysfunction over 5 to 13 weeks as indicated by 2D-echocardiography measurements. Corresponding histology and immunohistochemistry demonstrated fibrosis, necrosis and calcification which were mainly localized in patches near the epi- and endocardium of both ventricles. Expressions of endogenous desmosomal proteins were markedly reduced in fibrotic areas but appear to be unchanged in non-fibrotic areas. Furthermore, gene expression data indicate an early up-regulation of inflammatory and fibrotic remodeling pathways between 2 to 3.5 weeks of age.ConclusionCardiac specific overexpression of desmocollin-2 induces necrosis, acute inflammation and patchy cardiac fibrotic remodeling leading to fulminant biventricular cardiomyopathy.

| S-EPMC5365111 | biostudies-literature

Quantification of image contrast of infarcts on computed tomography scans.

Project description:Introduction Accurate identification of infarcts in non-contrast computed tomography (NC-CT) scans of the brain is fundamental in the diagnosis and management of patients with stroke. Quantification of image contrast properties at the boundaries of ischemic infarct regions in NC-CT can contribute to a more precise manual or automatic delineation of these regions. Here we explore these properties quantitatively. Methods We retrospectively investigated 519 NC-CT studies of 425 patients with clinically confirmed ischemic strokes. The average and standard deviation (SD) of patients' age was 67.5?±?12.4 years and the average(median)±SD time from symptoms onset to NC-CT examination was 27.4(12)±35.7?h. For every scan with an ischemic lesion identified by experts, the image contrast of the lesion vs. normal surrounding parenchyma was calculated as a difference of mean Hounsfield Unit (HU) of 1-5 consecutive voxels (the contrast window width) belonging to the lesion and to the parenchyma. This contrast was calculated at each single voxel of ischemic lesion boundaries (previously delineated by the experts) in horizontal and vertical directions in each image. The distributions of obtained horizontal, vertical and both contrasts combined were calculated among all 519 NC-CTs. Results The highest applicative contrast window width was identified as 5 voxels. The ischemic infarcts were found to be characterized by 6.60?HU, 8.28?HU and 7.55?HU mean values for distributions of horizontal, vertical and combined contrasts. Approximately 40-50% of the infarct boundary voxels were found to refer to the image contrast below 5?HU. Conclusion Low image contrast of ischemic lesions prevents accurate delineation of the infarcts in NC-CT.

| S-EPMC5564335 | biostudies-literature

MRI characteristics of globus pallidus infarcts in isolated methylmalonic acidemia.

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| S-EPMC7965933 | biostudies-literature

Microarray dataset of transgenic rice overexpressing Abp57.

Project description:The dataset presented in this article describes microarray experiment of Auxin-binding protein 57, Abp57-overexpressing transgenic rice. The gene expression profiles were generated using Affymetrix GeneChip® Rice (Cn) Gene 1.0 ST Arrays. Total RNA from seedlings tissue of transgenic rice and wildtype, which serve as control were used as starting materials for microarray experiment. Detailed experimental methods and data analysis were described here. The raw and normalized microarray data were deposited into Gene Expression Omnibus (GEO) under accession number GSE99055.

| S-EPMC5540701 | biostudies-literature

Quantification of myocardial blood flow using non-electrocardiogram-triggered MRI with three-slice coverage.

Project description:Accurate quantification of myocardial perfusion is dependent on reliable electrocardiogram (ECG) triggering. Measuring myocardial blood flow (MBF) in patients with arrhythmias or poor ECGs is currently infeasible with MR. The purpose of this study was to demonstrate the feasibility of a non-ECG-triggered method with clinically useful three-slice ventricular coverage for measurement of MBF in healthy volunteers.A saturation recovery magnetization-prepared gradient recalled echo acquisition was continuously repeated during first-pass imaging. A slice-interleaved radial trajectory was employed to enable image-based retrospective triggering. The arterial input function was generated using a beat-by-beat T1 estimation method. The proposed technique was validated against a conventional ECG-triggered dual-bolus technique in 10 healthy volunteers. The technique was further demonstrated under adenosine stress in 12 healthy volunteers.The proposed method produced MBF with no significant difference compared with the ECG-triggered technique. The proposed method yielded mean myocardial perfusion reserve comparable to published literature.We have developed a non-ECG-triggered quantitative perfusion imaging method. In this preliminary study, our results demonstrate that our method yields comparable MBF compared with the conventional ECG-triggered method and that it is feasible for stress imaging.

| S-EPMC4766039 | biostudies-literature

Longitudinal MRI dynamics of recent small subcortical infarcts and possible predictors.

Project description:We aimed to explore the morphological evolution of recent small subcortical infarcts (RSSIs) over 15 months. Moreover, we hypothesized that quantitative lesion apparent diffusion coefficient (ADC) values and serum neurofilament light (NfL) levels predict subsequent lacunar cavitation. We prospectively studied 78 RSSI patients, who underwent pre-defined follow-up investigations three and 15 months poststroke using 3 T MRI including high-resolution T1 sequences. To identify potential predictors of cavitation, we determined RSSI size and quantitative ADC values, and serum NfL using the SIMOA technique. The majority of RSSIs showed cavitation at three months (n = 61, 78%) with only minimal changes regarding cavitation status thereafter. The maximum axial lacunar diameter decreased from 8 mm at three to 7 mm at 15 months (p < 0.05). RSSIs which cavitated had lower lesional ADC values and were associated with higher baseline NfL levels compared to those without cavitation, but did not differ regarding lesion size. In logistic regression analysis, only baseline NfL levels predicted cavitation (p = 0.017). In this prospective study using predefined high-resolution MRI protocols, the majority of RSSIs evolved into lacunes during the first three months poststroke with not much change thereafter. Serum NfL seems to be a promising biomarker for more advanced subsequent tissue destruction in RSSIs.

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MRI Characteristics of the Evolution of Supratentorial Recent Small Subcortical Infarcts.

Project description:ObjectiveMorphological changes of recent small subcortical infarcts are not well defined. The purpose of the present study was to describe the MRI characteristics of the evolution for this stroke subtype.MethodsWe conducted a retrospective review of patients diagnosed with definite supratentorial recent small subcortical infarcts according to the ASCO classification with baseline and follow-up MRI (≥90 days of stroke onset). We investigated the incidence of cavity formation, the infarct volume change, and the positional relationship between infarct lesions and preexisting white matter hyperintensities (WMHs) of presumed vascular origin.ResultsWe identified 62 patients with a median age of 71 years (range: 30-87). Median follow-up period was 26 months (range: 3-99). Cavity formation was observed in 38 infarct lesions (61%). Eighteen lesions (29%) were partially adjacent to WMHs and 7 (11%) were fused into WMHs. In a multiple logistic regression analysis, age [odds ratio per 5-year increase: 1.34; 95% confidence interval (CI): 1.03-1.80; p = 0.03] and baseline infarct volume (odds ratio per 1-ml increase: 4.7; 95% CI: 1.6-19.7; p = 0.003) were independent predictors of cavity formation. There was a significant volume reduction between baseline and follow-up infarct lesions (median volume reduction rate: 44%).ConclusionMore than one-third of recent small subcortical infarcts do not lead to cavity formation and 40% of infarct lesions overlap with WMHs. Our data indicate the continuity between recent small subcortical infarcts and WMHs.

| S-EPMC4443727 | biostudies-literature

Phenotypic characterization of transgenic mice overexpressing neuregulin-1.

Project description:BackgroundNeuregulin-1 (NRG1) is one of the susceptibility genes for schizophrenia and implicated in the neurotrophic regulation of GABAergic and dopaminergic neurons, myelination, and NMDA receptor function. Postmortem studies often indicate a pathologic association of increased NRG1 expression or signaling with this illness. However, the psychobehavioral implication of NRG1 signaling has mainly been investigated using hypomorphic mutant mice for individual NRG1 splice variants.Methodology/principal findingsTo assess the behavioral impact of hyper NRG1 signaling, we generated and analyzed two independent mouse transgenic (Tg) lines carrying the transgene of green fluorescent protein (GFP)-tagged type-1 NRG1 cDNA. The promoter of elongation-factor 1? gene drove ubiquitous expression of GFP-tagged NRG1 in the whole brain. As compared to control littermates, both heterozygous NRG1-Tg lines showed increased locomotor activity, a nonsignificant trend toward decreasing prepulse inhibition, and decreased context-dependent fear learning but exhibited normal levels of tone-dependent learning. In addition, social interaction scores in both Tg lines were reduced in an isolation-induced resident-intruder test. There were also phenotypic increases in a GABAergic marker (parvalbumin) as well as in myelination markers (myelin basic protein and 2',3'-cyclic nucleotide 3'-phosphodiesterase) in their frontal cortex, indicating the authenticity of NRG1 hyper-signaling, although there were marked decreases in tyrosine hydroxylase levels and dopamine content in the hippocampus.ConclusionsThese findings suggest that aberrant hyper-signals of NRG1 also disrupt various cognitive and behavioral processes. Thus, neuropathological implication of hyper NRG1 signaling in psychiatric diseases should be evaluated with further experimentation.

| S-EPMC3000321 | biostudies-literature

Transgenic mice overexpressing reticulon 3 develop neuritic abnormalities.

Project description:Dystrophic neurites are swollen dendrites or axons recognizable near amyloid plaques as a part of important pathological feature of Alzheimer's disease (AD). We report herein that reticulon 3 (RTN3) is accumulated in a distinct population of dystrophic neurites named as RTN3 immunoreactive dystrophic neurites (RIDNs). The occurrence of RIDNs is concomitant with the formation of high-molecular-weight RTN3 aggregates in brains of AD cases and mice expressing mutant APP. Ultrastructural analysis confirms accumulation of RTN3-containing aggregates in RIDNs. It appears that the protein level of RTN3 governs the formation of RIDNs because transgenic mice expressing RTN3 will develop RIDNs, initially in the hippocampal CA1 region, and later in other hippocampal and cortical regions. Importantly, we show that the presence of dystrophic neurites in Tg-RTN3 mice causes impairments in spatial learning and memory, as well as synaptic plasticity, implying that RIDNs potentially contribute to AD cognitive dysfunction. Together, we demonstrate that aggregation of RTN3 contributes to AD pathogenesis by inducing neuritic dystrophy. Inhibition of RTN3 aggregation is likely a therapeutic approach for reducing neuritic dystrophy.

| S-EPMC1888669 | biostudies-literature

No association of ALOX5AP polymorphisms with risk of MRI-defined brain infarcts.

Project description:The arachidonate 5-lipoxygenase-activating protein (ALOX5AP) gene has been associated with stroke. The majority of the reported ALOX5AP associations have considered non-radiologically confirmed infarcts as the stroke phenotype. We assessed the association of genetic variants in ALOX5AP with stroke defined by the presence of infarcts on brain magnetic resonance imaging (MRI). We studied 202 persons with MRI-defined brain infarcts and 487 healthy individuals of Caribbean Hispanic ancestry. Another sample of European ancestry comprised 1823 persons with MRI-defined brain infarct and 7578 control subjects. Subjects were genotyped for the 4 single nucleotide polymorphisms (SNPs) that define ALOX5AP HapA haplotype. No association was found between SNPs and MRI-defined brain infarcts. Our data do not support the hypothesis that variants in ALOX5AP are associated with risk of MRI-defined brain infarcts.

| S-EPMC3259245 | biostudies-literature

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