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Article ; Online: Carotid stenosis and cryptogenic stroke.

Saba, Luca / Cau, Riccardo / Spinato, Giacomo / Suri, Jasjit S / Melis, Marta / De Rubeis, Gianluca / Antignani, Pierluigi / Gupta, Ajay

Journal of vascular surgery

2024 Volume 79, Issue 5, Page(s) 1119–1131

Abstract: Objectives: Cryptogenic stroke represents a type of ischemic stroke with an unknown origin, presenting a significant challenge in both stroke management and prevention. According to the Trial of Org 10,172 in Acute Stroke Treatment criteria, a stroke is ...

Abstract	Objectives: Cryptogenic stroke represents a type of ischemic stroke with an unknown origin, presenting a significant challenge in both stroke management and prevention. According to the Trial of Org 10,172 in Acute Stroke Treatment criteria, a stroke is categorized as being caused by large artery atherosclerosis only when there is >50% luminal narrowing of the ipsilateral internal carotid artery. However, nonstenosing carotid artery plaques can be an underlying cause of ischemic stroke. Indeed, emerging evidence documents that some features of plaque vulnerability may act as an independent risk factor, regardless of the degree of stenosis, in precipitating cerebrovascular events. This review, drawing from an array of imaging-based studies, explores the predictive values of carotid imaging modalities in the detection of nonstenosing carotid plaque (<50%), that could be the cause of a cerebrovascular event when some features of vulnerability are present. Methods: Google Scholar, Scopus, and PubMed were searched for articles on cryptogenic stroke and those reporting the association between cryptogenic stroke and imaging features of carotid plaque vulnerability. Results: Despite extensive diagnostic evaluations, the etiology of a considerable proportion of strokes remains undetermined, contributing to the recurrence rate and persistent morbidity in affected individuals. Advances in imaging modalities, such as magnetic resonance imaging, computed tomography scans, and ultrasound examination, facilitate more accurate detection of nonstenosing carotid artery plaque and allow better stratification of stroke risk, leading to a more tailored treatment strategy. Conclusions: Early detection of nonstenosing carotid plaque with features of vulnerability through carotid imaging techniques impacts the clinical management of cryptogenic stroke, resulting in refined stroke subtype classification and improved patient management. Additional research is required to validate these findings and recommend the integration of these state-of-the-art imaging methodologies into standard diagnostic protocols to improve stroke management and prevention.
MeSH term(s)	Humans ; Carotid Stenosis/complications ; Carotid Stenosis/diagnostic imaging ; Carotid Stenosis/therapy ; Stroke/diagnostic imaging ; Stroke/etiology ; Stroke/therapy ; Carotid Arteries/pathology ; Ischemic Stroke ; Plaque, Atherosclerotic/complications
Language	English
Publishing date	2024-01-07
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	605700-7
ISSN	1097-6809 ; 0741-5214
ISSN (online)	1097-6809
ISSN	0741-5214
DOI	10.1016/j.jvs.2024.01.004
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Article ; Online: Retinoids in the Pathogenesis and Treatment of Liver Diseases.

Melis, Marta / Tang, Xiao-Han / Trasino, Steven E / Gudas, Lorraine J

Nutrients

2022 Volume 14, Issue 7

Abstract: Vitamin A (VA), all-trans-retinol (ROL), and its analogs are collectively called retinoids. Acting through the retinoic acid receptors RARα, RARβ, and RARγ, all-trans-retinoic acid, an active metabolite of VA, is a potent regulator of numerous biological ...

Abstract	Vitamin A (VA), all-trans-retinol (ROL), and its analogs are collectively called retinoids. Acting through the retinoic acid receptors RARα, RARβ, and RARγ, all-trans-retinoic acid, an active metabolite of VA, is a potent regulator of numerous biological pathways, including embryonic and somatic cellular differentiation, immune functions, and energy metabolism. The liver is the primary organ for retinoid storage and metabolism in humans. For reasons that remain incompletely understood, a body of evidence shows that reductions in liver retinoids, aberrant retinoid metabolism, and reductions in RAR signaling are implicated in numerous diseases of the liver, including hepatocellular carcinoma, non-alcohol-associated fatty liver diseases, and alcohol-associated liver diseases. Conversely, restoration of retinoid signaling, pharmacological treatments with natural and synthetic retinoids, and newer agonists for specific RARs show promising benefits for treatment of a number of these liver diseases. Here we provide a comprehensive review of the literature demonstrating a role for retinoids in limiting the pathogenesis of these diseases and in the treatment of liver diseases.
MeSH term(s)	Humans ; Liver Diseases/drug therapy ; Liver Diseases/etiology ; Receptors, Retinoic Acid/metabolism ; Retinoids/metabolism ; Tretinoin/therapeutic use ; Vitamin A/therapeutic use
Chemical Substances	Receptors, Retinoic Acid ; Retinoids ; Vitamin A (11103-57-4) ; Tretinoin (5688UTC01R)
Language	English
Publishing date	2022-03-31
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14071456
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Article ; Online: Acute Stereotypic Behavior: Expanding the Spectrum of Movement Disorders Attributed to Vitamin B12 Deficiency.

Oppo, Valentina / Melis, Marta / Melis, Maurizio / Cossu, Giovanni

Movement disorders clinical practice

2020 Volume 7, Issue Suppl 3, Page(s) S63–S64

Language	English
Publishing date	2020-09-29
Publishing country	United States
Document type	Case Reports
ISSN	2330-1619
ISSN (online)	2330-1619
DOI	10.1002/mdc3.13060
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Article ; Online: Early juvenile reading epilepsy and later frontotemporal dementia (FTD): expanding the clinical phenotype of C9ORF72 mutation?

Melis, Marta / Defazio, Giovanni / Casaglia, Elisa / Melas, Valerio / Floris, Gianluca

Amyotrophic lateral sclerosis & frontotemporal degeneration

2021 Volume 23, Issue 1-2, Page(s) 139–142

Abstract: C9orf72 mutation ( ... ...

Abstract	C9orf72 mutation (C9
MeSH term(s)	Amyotrophic Lateral Sclerosis/genetics ; C9orf72 Protein/genetics ; DNA Repeat Expansion ; Epilepsy, Reflex/genetics ; Frontotemporal Dementia/complications ; Frontotemporal Dementia/genetics ; Humans ; Mutation/genetics ; Phenotype
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human
Language	English
Publishing date	2021-04-05
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	2705049-X
ISSN	2167-9223 ; 2167-8421
ISSN (online)	2167-9223
ISSN	2167-8421
DOI	10.1080/21678421.2021.1903505
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Article ; Online: Fenretinide Reduces Intestinal Mucin-2-Positive Goblet Cells in Chronic Alcohol Abuse.

Melis, Marta / Tang, Xiao-Han / Mai, Karen / Gudas, Lorraine J / Trasino, Steven E

Pharmacology

2022 Volume 107, Issue 7-8, Page(s) 406–416

Abstract: Introduction: Alcohol-induced thickening of the gut mucosal layer and increased expression of goblet cell gel-forming mucins, such as mucin-2 (MUC2) are associated with disruptions to the gut barrier in alcoholic liver disease (ALD). Interest in drugs ... ...

Abstract	Introduction: Alcohol-induced thickening of the gut mucosal layer and increased expression of goblet cell gel-forming mucins, such as mucin-2 (MUC2) are associated with disruptions to the gut barrier in alcoholic liver disease (ALD). Interest in drugs that can target gut mucins in ALD has grown; however to date, no studies have examined the properties of drugs on expression of gut mucins in models of ALD. We previously demonstrated that at 10 mg/kg/day, the drug fenretinide (N-[4-hydroxyphenyl] retinamide [Fen]), a synthetic retinoid, mitigates alcohol-associated damage to the gut barrier and liver injury in a murine model of ALD. Methods: In this study, we specifically sought to examine the effects of Fen on gut goblet cells, and expression of mucins, including MUC2 using a 25-day Lieber-DeCarli model of chronic alcohol intake. Results: Our results show that chronic alcohol intake increased gut-mucosal thickening, goblet cell numbers, and mRNA and protein expression of MUC2 in both the ileum and colon. Alcohol intake was associated with marked decreases in ileal and colonic Notch signaling, levels of Notch ligands Dll1 and Dll4, and increases in the expression of Notch-associated genes indispensable for goblet cell specification, including Math1 and Spdef. Interestingly, ileal and colonic expression of KLF4, which is involved in terminal differentiation of goblet cells, was reduced in mice chronically fed alcohol. Coadministration of alcohol with Fen at 10 mg/kg/day significantly reduced alcohol-associated increases in ileal and colonic mucosal thickening, ileal Muc2, colonic Muc2, Muc5ac and Muc6 mRNAs, and goblet cell numbers. We also found that Fen strongly prevented alcohol-mediated suppression of the Notch ligand Dll1, Notch signaling, and alcohol-induced increases in expression of Notch-associated goblet cell specification genes in both the ileum and colon. In the absence of alcohol, Fen treatments alone at 10 mg/kg/day had no effects on any of the goblet cell-related endpoints. Conclusion: These data show for the first time that the drug Fen possesses mucosal layer-modulating properties in response to chronic alcohol abuse. These data warrant further preclinical examination of Fen given the need for anti-ALD drugs and emerging evidence of a role for intestinal goblet cell mucins in the progression of ALD.
MeSH term(s)	Alcoholism/metabolism ; Animals ; Colon/metabolism ; Fenretinide/metabolism ; Goblet Cells/metabolism ; Intestinal Mucosa/metabolism ; Mice ; Mucin-2/genetics ; Mucin-2/metabolism
Chemical Substances	Mucin-2 ; Fenretinide (187EJ7QEXL)
Language	English
Publishing date	2022-05-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	206671-3
ISSN	1423-0313 ; 0031-7012
ISSN (online)	1423-0313
ISSN	0031-7012
DOI	10.1159/000524386
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Article ; Online: Retinoic Acid Receptor β Loss in Hepatocytes Increases Steatosis and Elevates the Integrated Stress Response in Alcohol-Associated Liver Disease.

Melis, Marta / Trasino, Steven E / Tang, Xiao-Han / Rappa, Andrew / Zhang, Tuo / Qin, Lihui / Gudas, Lorraine J

International journal of molecular sciences

2023 Volume 24, Issue 15

Abstract: In alcohol-associated liver disease (ALD), hepatic reductions in vitamin A and perturbations in vitamin A metabolism are common. However, the roles that the vitamin A receptors, termed retinoic acid receptors (RARs), may have in preventing the ... ...

Abstract	In alcohol-associated liver disease (ALD), hepatic reductions in vitamin A and perturbations in vitamin A metabolism are common. However, the roles that the vitamin A receptors, termed retinoic acid receptors (RARs), may have in preventing the pathophysiology of ALD remains unclear. Our prior data indicate that a RARβ agonist limits the pathology of alcohol-related liver disease. Thus, we generated liver-specific AlbCre-RARβ knockout (BKO) mice and compared them to wild type (WT) mice in an early ALD model. Both strains showed similar blood ethanol concentrations and ETOH-metabolizing enzymes. However, the livers of pair-fed-BKO and ETOH-BKO mice developed higher levels of steatosis and triglycerides than pair-fed-WT and ETOH-WT mice. The increased hepatic steatosis observed in the pair-fed-BKO and ETOH-BKO mice was associated with higher lipid synthesis/trafficking transcripts and lower beta-oxidation transcripts. ETOH-BKO mice also exhibited a higher integrated stress response (ISR) signature, including higher transcript and protein levels of ATF4 and its target, 4-EBP1. In human hepatocytes (HepG2) that lack RARβ (RARβ-KO), ETOH treatments resulted in greater reactive oxygen species compared to their parental cells. Notably, even without ETOH, ATF4 and 4-EBP1 protein levels were higher in the RARβ-KO cells than in their parental cells. These 4-EBP1 increases were greatly attenuated in cultured ATF4-deficient and RARβ/ATF4-deficient HepG2, suggesting that RARβ is a crucial negative regulator of 4-EBP1 through ATF4 in cultured hepatocytes. Here, we identify RARβ as a negative regulator of lipid metabolism and cellular stress in ALD.
MeSH term(s)	Mice ; Humans ; Animals ; Ethanol/toxicity ; Ethanol/metabolism ; Vitamin A/metabolism ; Mice, Knockout ; Liver Diseases, Alcoholic/metabolism ; Fatty Liver/metabolism ; Hepatocytes/metabolism ; Liver/metabolism ; Receptors, Retinoic Acid/genetics ; Receptors, Retinoic Acid/metabolism
Chemical Substances	retinoic acid receptor beta ; Ethanol (3K9958V90M) ; Vitamin A (11103-57-4) ; Receptors, Retinoic Acid
Language	English
Publishing date	2023-07-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241512035
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Article ; Online: Mechanism and Effect of HNF4α Decrease in a Rat Model of Cirrhosis and Liver Failure.

Melis, Marta / Marino, Rebecca / Tian, Jianmin / Johnson, Carla / Sethi, Rahil / Oertel, Michael / Fox, Ira J / Locker, Joseph

Cellular and molecular gastroenterology and hepatology

2023 Volume 17, Issue 3, Page(s) 453–479

Abstract: Background & aims: HNF4α, a master regulator of liver development and the mature hepatocyte phenotype, is down-regulated in chronic and inflammatory liver disease. We used contemporary transcriptomics and epigenomics to study the cause and effects of ... ...

Abstract	Background & aims: HNF4α, a master regulator of liver development and the mature hepatocyte phenotype, is down-regulated in chronic and inflammatory liver disease. We used contemporary transcriptomics and epigenomics to study the cause and effects of this down-regulation and characterized a multicellular etiology. Methods: Progressive changes in the rat carbon tetrachloride model were studied by deep RNA sequencing and genome-wide chromatin immunoprecipitation sequencing analysis of transcription factor (TF) binding and chromatin modification. Studies compared decompensated cirrhosis with liver failure after 26 weeks of treatment with earlier compensated cirrhosis and with additional rat models of chronic fibrosis. Finally, to resolve cell-specific responses and intercellular signaling, we compared transcriptomes of liver, nonparenchymal, and inflammatory cells. Results: HNF4α was significantly lower in 26-week cirrhosis, part of a general reduction of TFs that regulate metabolism. Nevertheless, increased binding of HNF4α contributed to strong activation of major phenotypic genes, whereas reduced binding to other genes had a moderate phenotypic effect. Decreased Hnf4a expression was the combined effect of STAT3 and nuclear factor kappa B (NFκB) activation, which similarly reduced expression of other metabolic TFs. STAT/NFκB also induced de novo expression of Osmr by hepatocytes to complement induced expression of Osm by nonparenchymal cells. Conclusions: Liver decompensation by inflammatory STAT3 and NFκB signaling was not a direct consequence of progressive cirrhosis. Despite significant reduction of Hnf4a expression, residual levels of this abundant TF still stimulated strong new gene expression. Reduction of HNF4α was part of a broad hepatocyte transcriptional response to inflammation.
MeSH term(s)	Animals ; Rats ; Hepatocyte Nuclear Factor 4/genetics ; Hepatocyte Nuclear Factor 4/metabolism ; Hepatocytes/metabolism ; Liver Cirrhosis/pathology ; Liver Failure/metabolism
Chemical Substances	Hepatocyte Nuclear Factor 4 ; Hnf4a protein, rat
Language	English
Publishing date	2023-11-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2023.11.009
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Article ; Online: Mutations in long-lived epithelial stem cells and their clonal progeny in pre-malignant lesions and in oral squamous cell carcinoma.

Melis, Marta / Zhang, Tuo / Scognamiglio, Theresa / Gudas, Lorraine J

Carcinogenesis

2020 Volume 41, Issue 11, Page(s) 1553–1564

Abstract: Oral squamous cell carcinomas (OSCCs) are the most common cancers of the oral cavity, but the molecular mechanisms driving OSCC carcinogenesis remain unclear. Our group previously established a murine OSCC model based on a 10-week carcinogen [4- ... ...

Abstract	Oral squamous cell carcinomas (OSCCs) are the most common cancers of the oral cavity, but the molecular mechanisms driving OSCC carcinogenesis remain unclear. Our group previously established a murine OSCC model based on a 10-week carcinogen [4-nitroquinoline 1-oxide (4-NQO)] treatment. Here we used K14CreERTAM;Rosa26LacZ mice to perform lineage tracing to delineate the mutational profiles in clonal cell populations resulting from single, long-lived epithelial stem cells, here called LacZ+ stem cell clones (LSCCs). Using laser-capture microdissection, we examined mutational changes in LSCCs immediately after the 10-week 4-NQO treatment and >17 weeks after 4-NQO treatment. We found a 1.8-fold ±0.4 (P = 0.009) increase in single-nucleotide variants and insertions/deletions (indels) in tumor compared with pre-neoplastic LSCCs. The percentages of indels and of loss of heterozygosity events were 1.3-fold±0.3 (P = 0.02) and 2.2-fold±0.7 (P = 0.08) higher in pre-neoplastic compared with tumor LSCCs. Mutations in cell adhesion- and development-associated genes occurred in 83% of the tumor LSCCs. Frequently mutated genes in tumor LSCCs were involved in planar cell polarity (Celsr1, Fat4) or development (Notch1). Chromosomal amplifications in 50% of the tumor LSCCs occurred in epidermal growth factor receptor, phosphoinositide 3-kinase and cell adhesion pathways. All pre-neoplastic and tumor LSCCs were characterized by key smoking-associated changes also observed in human OSCC, C>A and G>T. DeconstructSigs analysis identified smoking and head and neck cancer as the most frequent mutational signatures in pre-neoplastic and tumor LSCCs. Thus, this model recapitulates a smoking-associated mutational profile also observed in humans and illustrates the role of LSCCs in early carcinogenesis and OSCCs.
MeSH term(s)	4-Nitroquinoline-1-oxide/toxicity ; Animals ; Carcinogens/toxicity ; Carcinoma, Squamous Cell/chemically induced ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Cell Lineage ; Clone Cells/drug effects ; Clone Cells/metabolism ; Clone Cells/pathology ; Disease Models, Animal ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Expression Regulation, Neoplastic ; Mice ; Mice, Transgenic ; Mouth Neoplasms/chemically induced ; Mouth Neoplasms/genetics ; Mouth Neoplasms/metabolism ; Mouth Neoplasms/pathology ; Mutation ; Precancerous Conditions/chemically induced ; Precancerous Conditions/genetics ; Precancerous Conditions/metabolism ; Precancerous Conditions/pathology ; Stem Cells/drug effects ; Stem Cells/metabolism ; Stem Cells/pathology
Chemical Substances	Carcinogens ; 4-Nitroquinoline-1-oxide (56-57-5)
Language	English
Publishing date	2020-02-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgaa019
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Article: Fenretinide Improves Intestinal Barrier Function and Mitigates Alcohol Liver Disease.

Tang, Xiao-Han / Melis, Marta / Mai, Karen / Gudas, Lorraine J / Trasino, Steven E

Frontiers in pharmacology

2021 Volume 12, Page(s) 630557

Abstract: Alcohol liver disease (ALD) is a major cause of liver-related mortality globally, yet there remains an unmet demand for approved ALD drugs. The pathogenesis of ALD involves perturbations to the intestinal barrier and subsequent translocation of bacterial ...

Abstract	Alcohol liver disease (ALD) is a major cause of liver-related mortality globally, yet there remains an unmet demand for approved ALD drugs. The pathogenesis of ALD involves perturbations to the intestinal barrier and subsequent translocation of bacterial endotoxin that, acting through toll-like receptor 4 (TLR4), promotes hepatic inflammation and progression of ALD. In the present study we investigated the ability of fenretinide (Fen) [N-(4-hydroxyphenyl) retinamide], a synthetic retinoid with known anti-cancer and anti-inflammatory properties, to modulate intestinal permeability and clinical hallmarks of ALD in a mouse model of chronic ethanol (EtOH) exposure. Our results show that EtOH-treated mice had reductions in mRNA and protein expression of intestinal tight junction proteins, including claudin one and occludin, and increases in intestinal permeability and endotoxemia compared to pair-fed mice. Also, EtOH-treated mice had marked increases in hepatic steatosis, liver injury, and expression of pro-inflammatory mediators, including TNF-α, and TLR4-positive macrophages, Kupffer cells, and hepatocytes in the intestines and liver, respectively. In contrast, EtOH + Fen-treated mice were resistant to the effects of EtOH on promoting intestinal permeability and had higher intestinal protein levels of claudin one and occludin. Also, EtOH + Fen-treated mice had significantly lower plasma levels of endotoxin, and reductions in expression of TNF-α and TLR4 positive macrophages, Kupffer cells, and hepatocytes in the intestine and liver. Lastly, we found that EtOH + Fen-treated mice exhibited major reductions in hepatic triglycerides, steatosis, and liver injury compared to EtOH-treated mice. Our findings are the first to demonstrate that Fen possesses anti-ALD properties, potentially through modulation of the intestinal barrier function, endotoxemia, and TLR4-mediated inflammation. These data warrant further pre-clinical investigations of Fen as a potential anti-ALD drug.
Language	English
Publishing date	2021-03-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2021.630557
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Article: "Smelling and Tasting" Parkinson's Disease: Using Senses to Improve the Knowledge of the Disease.

Oppo, Valentina / Melis, Marta / Melis, Melania / Tomassini Barbarossa, Iole / Cossu, Giovanni

Frontiers in aging neuroscience

2020 Volume 12, Page(s) 43

Abstract: Among non-motor manifestations of Parkinson's Disease (PD), peripheral, sensory symptoms are particularly relevant. Smell dysfunction starts very early and frequently precedes the PD motor symptoms by years (being often a cue to the diagnosis). Moreover, ...

Abstract	Among non-motor manifestations of Parkinson's Disease (PD), peripheral, sensory symptoms are particularly relevant. Smell dysfunction starts very early and frequently precedes the PD motor symptoms by years (being often a cue to the diagnosis). Moreover, olfactory system could be, together with gut, one of those peripheral sites where PD pathology first develops. Unlike smell loss, the relationship between PD and taste impairment is far less established. It can start early in the course of the disease but more frequently appears in advanced stages, in parallel with the advent of MCI, likely reflecting cortical involvement. Among PD patients has been demonstrated an increase in the frequency of the non-tasters for PROP (prototypical gustatory stimulus, 6- n-propylthiouracil), a genetically determined bitter taste which is mediated by TAS2RS38 receptor, and a significant increase of the recessive non-testing variant of this receptor. TAS2R38 receptors are expressed also in other tissues, such as in the epithelia of the gut and nasal cavities, where they can influence epithelial immunity ad its interaction with microbiota. Those pieces of evidence suggest that not only systematic assessment of taste and smell can be of a remarkable help for clinicians in the early diagnosis, but also that understanding the mechanisms of sensory involvement in PD could increase the knowledge of the pathophysiology of the disease.
Language	English
Publishing date	2020-02-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2020.00043
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