Mones Abu-Asab

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Papers by Mones Abu-Asab

Differential effect of vasopressin on open-field activity and passive avoidance behaviour following intracerebroventricular versus intracisternal administration in rats

Acta physiologica Hungarica, 1988

The effects of lysine8-vasopressin (LVP) on the open-field activity and passive avoidance behavio... more The effects of lysine8-vasopressin (LVP) on the open-field activity and passive avoidance behaviour in rats were studied following intracerebroventricular (i.c.v.) and intracisternal (c.m.) administration. Following i.c.v. administration, LVP caused a long-lasting facilitation of the passive avoidance behaviour and did not influence open-field activity. When injected into the cisterna magna, on the other hand, the same amount of LVP was without effect on the passive avoidance behaviour, while decreasing open-field activity. It is concluded that the site of injection in the cerebrospinal space might be of importance in determining the behavioural effects of neuropeptides.

Genomic deletions at 1p and 14q are associated with an abnormal cDNA microarray gene expression pattern in meningiomas but not in schwannomas 1 Victor Martínez-Glez, Luis Alvarez, Carmen Franco-Hernández, Miguel Torres-Martin, Jose M. de Campos, Alberto Isla, Jesús Vaquero, Luis Lassaletta, Javie...

Pde8b haploinsufficiency in mice is associated with modest adrenal defects, impaired steroidogenesis, and male infertility, unaltered by concurrent PKA or Wnt activation

Molecular and Cellular Endocrinology

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Author response: CSF1R blockade induces macrophage ablation and results in mouse choroidal vascular atrophy and RPE disorganization

Adult human RPE has greater susceptibility to IL17A-induced degeneration than fetal human RPE

Investigative Ophthalmology & Visual Science, 2013

Choriocapillaris Loss of Endothelial Polarity and Fenestration May Be Contributing Factors in AMD

Investigative Ophthalmology & Visual Science, 2016

IJMS-93795-SUPPLEMENTY-PROOF Done

Myocilin affects differentiation of oligodendrocytes and regulates myelination of the optic nerve via Lingo-1/RhoA signaling

Investigative Ophthalmology & Visual Science, 2013

Inflammasomes in human eyes with AMD and mouse retinas with focal retinal degeneration

Investigative Ophthalmology & Visual Science, 2013

Ultrastructural Characterization and Autoantibodies of Melanoma Associated Autoimmune Retinopathy

Investigative Ophthalmology & Visual Science, 2012

PEDF deficiency increases the susceptibility of rd10 mice to retinal degeneration

Experimental Eye Research, 2020

The SERPINF1 gene encodes pigment epithelium-derived factor (PEDF), a member of the serpin superf... more The SERPINF1 gene encodes pigment epithelium-derived factor (PEDF), a member of the serpin superfamily with neurotrophic and antiangiogenic properties in the retina. We hypothesized that absence of PEDF would lead to increased stress-associated retinal degeneration in Serpinf1 null mice. Accordingly, using a Serpinf1 null mouse model, we investigated the impact of PEDF absence on retinal morphology, and susceptibility to induced and inherited retinal degeneration. We studied the pattern of Serpinf1 expression in the mouse retina layers. PEDF protein was detected by western blotting. Transmission electron microscopy was performed on mouse retina. Serpinf1 null mice and wild type littermates were injected with NaIO 3 (30 mg/kg body weight) intraperitonially. At post-injection day 1, 3, 4, 6 and 8 mice were euthanized, and eyes were enucleated. Serpinf1 null and rd10 double mutant mice were generated and their eyes enucleated at different time points from post-natal day 15 to post-natal day 28. Enucleated eyes were processed for hematoxylin and eosin staining and histopathological evaluations. We found that Serpinf1 was expressed in the retinal pigment epithelium, in the inner nuclear layer and in the ganglion cell layer, but undetectable in the outer nuclear layer of wild type mice. Plasma PEDF protein levels were undetectable in Serpinf1 null animals. RPE atrophy and retinal thinning were Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

format_quoteSerpinf1 null mice had undetectable plasma PEDF, leading to greater retinal degeneration compared to wild type, especially in rd10 models.format_quote

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Phylogenetic Implications of Leaf Anatomy in Subtribe Melittidinae (Labiatae) and Related Taxa

Journal of the Arnold Arboretum., 1987

Go to AGRIS search. Journal of the Arnold Arboretum (Jan 1987). Phylogenetic implications of leaf... more

Degradation of Photoreceptor Outer Segments by the Retinal Pigment Epithelium Requires Pigment Epithelium-derived Factor Receptor (PEDF-R)

PurposeTo examine the contribution of PEDF-R to the phagocytosis process. Previously, we identifi... more PurposeTo examine the contribution of PEDF-R to the phagocytosis process. Previously, we identified PEDF-R, the protein encoded by thePNPLA2gene, as a phospholipase A2 in the retinal pigment epithelium (RPE). During phagocytosis, RPE cells ingest abundant phospholipids and protein in the form of photoreceptor outer segment (POS) tips, which are then hydrolyzed. The role of PEDF-R in RPE phagocytosis is not known.MethodsMice in whichPNPLA2was conditionally knocked out in the RPE were generated (cKO). Mouse RPE/choroid explants were cultured. Human ARPE-19 cells were transfected with siPNPLA2silencing duplexes. POS were isolated from bovine retinas. The phospholipase A2 inhibitor bromoenol lactone was used. Transmission electron microscopy, immunofluorescence, lipid labeling, pulse-chase experiments, western blots, and free fatty acid and β-hydroxybutyrate assays were performed.ResultsThe RPE of the cKO mice accumulated lipids as well as more abundant and larger rhodopsin particles co...

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Somatic Mutations in UBA1 and Severe Adult-Onset Autoinflammatory Disease

New England Journal of Medicine, 2020

BACKGROUND Adult-onset inflammatory syndromes often manifest with overlapping clinical features. ... more BACKGROUND Adult-onset inflammatory syndromes often manifest with overlapping clinical features. Variants in ubiquitin-related genes, previously implicated in autoinflammatory disease, may define new disorders. METHODS We analyzed peripheral-blood exome sequence data independent of clinical phenotype and inheritance pattern to identify deleterious mutations in ubiquitin-related genes. Sanger sequencing, immunoblotting, immunohistochemical testing, flow cytometry, and transcriptome and cytokine profiling were performed. CRISPR-Cas9edited zebrafish were used as an in vivo model to assess gene function. RESULTS We identified 25 men with somatic mutations affecting methionine-41 (p.Met41) in UBA1, the major E1 enzyme that initiates ubiquitylation. (The gene UBA1 lies on the X chromosome.) In such patients, an often fatal, treatment-refractory inflammatory syndrome develops in late adulthood, with fevers, cytopenias, characteristic vacuoles in myeloid and erythroid precursor cells, dysplastic bone marrow, neutrophilic cutaneous and pulmonary inflammation, chondritis, and vasculitis. Most of these 25 patients met clinical criteria for an inflammatory syndrome (relapsing polychondritis, Sweet's syndrome, polyarteritis nodosa, or giant-cell arteritis) or a hematologic condition (myelodysplastic syndrome or multiple myeloma) or both. Mutations were found in more than half the hematopoietic stem cells, including peripheral-blood myeloid cells but not lymphocytes or fibroblasts. Mutations affecting p.Met41 resulted in loss of the canonical cytoplasmic isoform of UBA1 and in expression of a novel, catalytically impaired isoform initiated at p.Met67. Mutant peripheral-blood cells showed decreased ubiquitylation and activated innate immune pathways. Knockout of the cytoplasmic UBA1 isoform homologue in zebrafish caused systemic inflammation. CONCLUSIONS Using a genotype-driven approach, we identified a disorder that connects seemingly unrelated adult-onset inflammatory syndromes. We named this disorder the VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome. (Funded by the NIH Intramural Research Programs and the EU Horizon 2020 Research and Innovation Program.

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Tyrosinase Nanoparticles: Understanding the Melanogenesis Pathway by Isolating the Products of Tyrosinase Enzymatic Reaction