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Article ; Online: Sex and the Brain: Novel ADNP Syndrome Mice Are Protected by NAP.

Amal, Haitham

2022 Volume 92, Issue 1, Page(s) 8–9

MeSH term(s)	Animals ; Autistic Disorder ; Brain/metabolism ; Homeodomain Proteins ; Mice ; Nerve Tissue Proteins/metabolism
Chemical Substances	Adnp protein, mouse ; Homeodomain Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2022-06-13
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2022.03.011
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Article ; Online: Editorial: Nitric oxide signaling from synapse to disease.

Amal, Haitham / Steinert, Joern R

Free radical biology & medicine

2023 Volume 196, Page(s) 9–10

MeSH term(s)	Nitric Oxide ; Signal Transduction ; Nitric Oxide Synthase Type I/metabolism ; Synapses
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type I (EC 1.14.13.39)
Language	English
Publishing date	2023-01-07
Publishing country	United States
Document type	Editorial
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2023.01.005
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Article ; Online: The contribution of an imbalanced redox signalling to neurological and neurodegenerative conditions.

Steinert, Joern R / Amal, Haitham

Free radical biology & medicine

2022 Volume 194, Page(s) 71–83

Abstract: Nitric oxide and other redox active molecules such as oxygen free radicals provide essential signalling in diverse neuronal functions, but their excess production and insufficient scavenging induces cytotoxic redox stress which is associated with ... ...

Abstract	Nitric oxide and other redox active molecules such as oxygen free radicals provide essential signalling in diverse neuronal functions, but their excess production and insufficient scavenging induces cytotoxic redox stress which is associated with numerous neurodegenerative and neurological conditions. A further component of redox signalling is mediated by a homeostatic regulation of divalent metal ions, the imbalance of which contributes to neuronal dysfunction. Additional antioxidant molecules such as glutathione and enzymes such as super oxide dismutase are involved in maintaining a physiological redox status within neurons. When cellular processes are perturbed and generation of free radicals overwhelms the antioxidants capacity of the neurons, a resulting redox damage leads to neuronal dysfunction and cell death. Cellular sources for production of redox-active molecules may include NADPH oxidases, mitochondria, cytochrome P450 and nitric oxide (NO)-generating enzymes, such as endothelial, neuronal and inducible NO synthases. Several neurodegenerative and developmental neurological conditions are associated with an imbalanced redox state as a result of neuroinflammatory processes leading to nitrosative and oxidative stress. Ongoing research aims at understanding the causes and consequences of such imbalanced redox homeostasis and its role in neuronal dysfunction.
Language	English
Publishing date	2022-11-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2022.11.035
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Article ; Online: Mutations associated with autism lead to similar synaptic and behavioral alterations in both sexes of male and female mouse brain.

Tripathi, Manish Kumar / Ojha, Shashank Kumar / Kartawy, Maryam / Khaliulin, Igor / Hamoudi, Wajeha / Amal, Haitham

Scientific reports

2024 Volume 14, Issue 1, Page(s) 10

Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental disorder based on synaptic abnormalities. The estimated prevalence rate of male individuals diagnosed with ASD prevails over females is in a proportion of 4:1. Consequently, males remain the main ... ...

Abstract	Autism spectrum disorder (ASD) is a neurodevelopmental disorder based on synaptic abnormalities. The estimated prevalence rate of male individuals diagnosed with ASD prevails over females is in a proportion of 4:1. Consequently, males remain the main focus in ASD studies in clinical and experimental settings. Meanwhile, some studies point to an underestimation of this disorder in females. In this work, we studied the sex differences of the synaptic and behavioral phenotypes of ASD mouse models. Juvenile male and female Shank3
MeSH term(s)	Mice ; Female ; Male ; Animals ; Autistic Disorder ; Autism Spectrum Disorder/genetics ; Mutation ; Behavior, Animal/physiology ; Cerebral Cortex ; Disease Models, Animal ; Microfilament Proteins/genetics ; Nerve Tissue Proteins/genetics
Chemical Substances	Shank3 protein, mouse ; Microfilament Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2024-01-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-50248-4
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Article ; Online: Arsenic alters nitric oxide signaling similar to autism spectrum disorder and Alzheimer's disease-associated mutations.

Tripathi, Manish Kumar / Kartawy, Maryam / Ginzburg, Shelly / Amal, Haitham

Translational psychiatry

2022 Volume 12, Issue 1, Page(s) 127

Abstract: Epidemiological studies have proven that exposure to Arsenic (AS) leads to the development of many neurological disorders. However, few studies have investigated its molecular mechanisms in the brain. Our previous work has revealed nitric oxide (NO)- ... ...

Abstract	Epidemiological studies have proven that exposure to Arsenic (AS) leads to the development of many neurological disorders. However, few studies have investigated its molecular mechanisms in the brain. Our previous work has revealed nitric oxide (NO)-mediated apoptosis and SNO reprogramming in the cortex following arsenic treatment, yet the role of NO and S-nitrosylation (SNO) in AS-mediated neurotoxicity has not been investigated. Therefore, we have conducted a multidisciplinary in-vivo study in mice with two different doses of Sodium Arsenite (SA) (0.1 ppm and 1 ppm) in drinking water. We used the novel SNOTRAP-based mass spectrometry method followed by the bioinformatics analysis, Western blot validation, and five different behavioral tests. Bioinformatics analysis of SA-treated mice showed significant SNO-enrichment of processes involved in mitochondrial respiratory function, endogenous antioxidant systems, transcriptional regulation, cytoskeleton maintenance, and regulation of apoptosis. Western blotting showed increased levels of cleaved PARP-1 and cleaved caspase-3 in SA-treated mice consistent with SA-induced apoptosis. Behavioral studies showed significant cognitive dysfunctions similar to those of Autism spectrum disorder (ASD) and Alzheimer's disease (AD). A comparative analysis of the SNO-proteome of SA-treated mice with two transgenic mouse strains, models of ASD and AD, showed molecular convergence of SA environmental neurotoxicity and the genetic mutations causing ASD and AD. This is the first study to show the effects of AS on SNO-signaling in the striatum and hippocampus and its effects on behavioral characteristics. Finally, further investigation of the NO-dependent mechanisms of AS-mediated neurotoxicity may reveal new drug targets for its prevention.
MeSH term(s)	Alzheimer Disease/genetics ; Animals ; Arsenic/toxicity ; Autism Spectrum Disorder/genetics ; Mice ; Mutation ; Nitric Oxide
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2022-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-022-01890-5
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Article ; Online: A cross-talk between nitric oxide and the glutamatergic system in a Shank3 mouse model of autism.

Hamoudi, Wajeha / Tripathi, Manish Kumar / Ojha, Shashank Kumar / Amal, Haitham

Free radical biology & medicine

2022 Volume 188, Page(s) 83–91

Abstract: Nitric oxide (NO) is a multifunctional signaling molecule that plays a crucial role in synaptic transmission and neuronal function. Pioneering studies show that nitric oxide (NO) and S-nitrosylation (SNO, the NO-mediated posttranslational modification) ... ...

Abstract	Nitric oxide (NO) is a multifunctional signaling molecule that plays a crucial role in synaptic transmission and neuronal function. Pioneering studies show that nitric oxide (NO) and S-nitrosylation (SNO, the NO-mediated posttranslational modification) can engender nitrosative stress in the brain, contributing to neurodegenerative diseases. Little is known, however, about the aberrant NO signaling in neurodevelopmental disorders including autism spectrum disorder (ASD). We have recently shown that the Shank3 mutation in mice representing a model of ASD causes excessive NO levels and aberrant protein SNO. The glutamatergic system is involved in ASD, specifically in SHANK3 pathology. We used SNOTRAP technology to identify the SNO-proteome in the brain of the Shank3 mutant mice to understand the role of SNO in the glutamatergic system during the development of these mice. We conducted a systems biology analysis of the SNO-proteome to investigate the biological processes and signaling pathways in the brain of juvenile and adult Shank3 mutant and wild-type mice. The Shank3 mutation caused significant SNO-enrichment of a glutamate signaling pathway in the juvenile and adult mutant mice, although different protein subsets were S-nitrosylated in both ages. Cellular compartments analysis showed that "glutamatergic Synapse" is SNO-enriched significantly in the mutant mice of both ages. We also found eight S-nitrosylated proteins involved in glutamate transmission in both ages. 38 SNO-proteins found in the mutant mice are among the high-risk SFARI gene list. Biochemical examination shows a reduction in the levels of NMDA Receptor (NR1) in the cortex and striatum of the mutant mice of both ages. Neuronal NOS knockdown in SHSY-5Y rescued NR1 levels. In conclusion, this study reveals novel SNO of key glutamatergic proteins in Shank3 mutant mice and a cross-talk between nitric oxide and the glutamatergic system.
MeSH term(s)	Animals ; Autism Spectrum Disorder/genetics ; Autistic Disorder/genetics ; Disease Models, Animal ; Glutamic Acid ; Mice ; Microfilament Proteins ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Nitric Oxide/metabolism ; Proteome/metabolism
Chemical Substances	Microfilament Proteins ; Nerve Tissue Proteins ; Proteome ; Shank3 protein, mouse ; Nitric Oxide (31C4KY9ESH) ; Glutamic Acid (3KX376GY7L)
Language	English
Publishing date	2022-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2022.06.007
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Article: Systems Biology Reveals S-Nitrosylation-Dependent Regulation of Mitochondrial Functions in Mice with

Kartawy, Maryam / Khaliulin, Igor / Amal, Haitham

Brain sciences

2021 Volume 11, Issue 6

Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental disorder manifested in repetitive behavior, abnormalities in social interactions, and communication. The pathogenesis of this disorder is not clear, and no effective treatment is currently available. ...

Abstract	Autism spectrum disorder (ASD) is a neurodevelopmental disorder manifested in repetitive behavior, abnormalities in social interactions, and communication. The pathogenesis of this disorder is not clear, and no effective treatment is currently available. Protein S-nitrosylation (SNO), the nitric oxide (NO)-mediated posttranslational modification, targets key proteins implicated in synaptic and neuronal functions. Previously, we have shown that NO and SNO are involved in the ASD mouse model based on the
Language	English
Publishing date	2021-05-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci11060677
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Article ; Online: Systems biology reveals reprogramming of the S-nitroso-proteome in the cortical and striatal regions of mice during aging process.

Kartawy, Maryam / Khaliulin, Igor / Amal, Haitham

Scientific reports

2020 Volume 10, Issue 1, Page(s) 13913

Abstract: Cell aging depends on the rate of cumulative oxidative and nitrosative damage to DNA and proteins. Accumulated data indicate the involvement of protein S-nitrosylation (SNO), the nitric oxide (NO)-mediated posttranslational modification (PTM) of cysteine ...

Abstract	Cell aging depends on the rate of cumulative oxidative and nitrosative damage to DNA and proteins. Accumulated data indicate the involvement of protein S-nitrosylation (SNO), the nitric oxide (NO)-mediated posttranslational modification (PTM) of cysteine thiols, in different brain disorders. However, the changes and involvement of SNO in aging including the development of the organism from juvenile to adult state is still unknown. In this study, using the state-of-the-art mass spectrometry technology to identify S-nitrosylated proteins combined with large-scale computational biology, we tested the S-nitroso-proteome in juvenile and adult mice in both cortical and striatal regions. We found reprogramming of the S-nitroso-proteome in adult mice of both cortex and striatum regions. Significant biological processes and protein-protein clusters associated with synaptic and neuronal terms were enriched in adult mice. Extensive quantitative analysis revealed a large set of potentially pathological proteins that were significantly upregulated in adult mice. Our approach, combined with large scale computational biology allowed us to perform a system-level characterization and identification of the key proteins and biological processes that can serve as drug targets for aging and brain disorders in future studies.
MeSH term(s)	Aging/metabolism ; Animals ; Cerebral Cortex/metabolism ; Cluster Analysis ; Mice ; Neostriatum/metabolism ; Nitrosation ; Protein Interaction Maps ; Proteome/metabolism ; Systems Biology
Chemical Substances	Proteome
Language	English
Publishing date	2020-08-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-70383-6
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Article: Sex Differences in Biological Processes and Nitrergic Signaling in Mouse Brain.

Khaliulin, Igor / Kartawy, Maryam / Amal, Haitham

Biomedicines

2020 Volume 8, Issue 5

Abstract: Nitric oxide (NO) represents an important signaling molecule which modulates the functions of different organs, including the brain. S-nitrosylation (SNO), a post-translational modification that involves the binding of the NO group to a cysteine residue, ...

Abstract	Nitric oxide (NO) represents an important signaling molecule which modulates the functions of different organs, including the brain. S-nitrosylation (SNO), a post-translational modification that involves the binding of the NO group to a cysteine residue, is a key mechanism of nitrergic signaling. Most of the experimental studies are carried out on male animals. However, significant differences exist between males and females in the signaling mechanisms. To investigate the sex differences in the SNO-based regulation of biological functions and signaling pathways in the cortices of 6-8-weeks-old mice, we used the mass spectrometry technique, to identify S-nitrosylated proteins, followed by large-scale computational biology. This work revealed significant sex differences in the NO and SNO-related biological functions in the cortices of mice for the first-time. The study showed significant SNO-induced enrichment of the synaptic processes in female mice, but enhanced SNO-related cytoskeletal processes in the male mice. Proteins, which were S-nitrosylated in the cortices of mice of both groups, were more abundant in the female brain. Finally, we investigated the shared molecular processes that were found in both sexes. This study presents a mechanistic insight into the role of S-nitrosylation in both sexes and provides strong evidence of sex difference in many biological processes and signalling pathways, which will open future research directions on sex differences in neurological disorders.
Language	English
Publishing date	2020-05-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines8050124
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Article ; Online: The role of nitric oxide in brain disorders: Autism spectrum disorder and other psychiatric, neurological, and neurodegenerative disorders.

Tripathi, Manish Kumar / Kartawy, Maryam / Amal, Haitham

Redox biology

2020 Volume 34, Page(s) 101567

Abstract: Nitric oxide (NO) is a multifunctional signalling molecule and a neurotransmitter that plays an important role in physiological and pathophysiological processes. In physiological conditions, NO regulates cell survival, differentiation and proliferation ... ...

Abstract	Nitric oxide (NO) is a multifunctional signalling molecule and a neurotransmitter that plays an important role in physiological and pathophysiological processes. In physiological conditions, NO regulates cell survival, differentiation and proliferation of neurons. It also regulates synaptic activity, plasticity and vesicle trafficking. NO affects cellular signalling through protein S-nitrosylation, the NO-mediated posttranslational modification of cysteine thiols (SNO). SNO can affect protein activity, protein-protein interaction and protein localization. Numerous studies have shown that excessive NO and SNO can lead to nitrosative stress in the nervous system, contributing to neuropathology. In this review, we summarize the role of NO and SNO in the progression of neurodevelopmental, psychiatric and neurodegenerative disorders, with special attention to autism spectrum disorder (ASD). We provide mechanistic insights into the contribution of NO in diverse brain disorders. Finally, we suggest that pharmacological agents that can inhibit or augment the production of NO as well as new approaches to modulate the formation of SNO-proteins can serve as a promising approach for the treatment of diverse brain disorders.
MeSH term(s)	Autism Spectrum Disorder/drug therapy ; Brain Diseases ; Humans ; Neurodegenerative Diseases/drug therapy ; Nitric Oxide/metabolism ; Protein Processing, Post-Translational
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2020-05-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101567
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