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Article ; Online: Comprehensive meta-analysis reveals distinct gene expression signatures of MASLD progression.

Piras, Ignazio S / DiStefano, Johanna K

Life science alliance

2024 Volume 7, Issue 6

Abstract: Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), pose significant risks of severe fibrosis, cirrhosis, and hepatocellular carcinoma. Despite their ... ...

Abstract	Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), pose significant risks of severe fibrosis, cirrhosis, and hepatocellular carcinoma. Despite their widespread prevalence, the molecular mechanisms underlying the development and progression of these common chronic hepatic conditions are not fully understood. Here, we conducted the most extensive meta-analysis of hepatic gene expression datasets from liver biopsy samples to date, integrating 10 RNA-sequencing and microarray datasets (1,058 samples). Using a random-effects meta-analysis model, we compared over 12,000 shared genes across datasets. We identified 685 genes differentially expressed in MASLD versus normal liver, 1,870 in MASH versus normal liver, and 3,284 in MASLD versus MASH. Integrating these results with genome-wide association studies and coexpression networks, we identified two functionally relevant, validated coexpression modules mainly driven by SMOC2, ITGBL1, LOXL1, MGP, SOD3, and TAT, HGD, SLC25A15, respectively, the latter not previously associated with MASLD and MASH. Our findings provide a comprehensive and robust analysis of hepatic gene expression alterations associated with MASLD and MASH and identify novel key drivers of MASLD progression.
MeSH term(s)	Humans ; Genome-Wide Association Study ; Transcriptome/genetics ; Fatty Liver ; Carcinoma, Hepatocellular/genetics ; Liver Neoplasms/genetics ; Integrin beta1
Chemical Substances	ITGBL1 protein, human ; Integrin beta1
Language	English
Publishing date	2024-04-02
Publishing country	United States
Document type	Meta-Analysis ; Journal Article
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202302517
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Article: Editorial: Omics of Human Aging and Longevity in the Post Genome Era: From Single Biomarkers to Systems Biology Approaches.

Dato, Serena / Piras, Ignazio S

Frontiers in genetics

2022 Volume 13, Page(s) 913531

Language	English
Publishing date	2022-05-02
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2022.913531
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Article ; Online: Correction: Glyphosate infiltrates the brain and increases pro-inflammatory cytokine TNFα: implications for neurodegenerative disorders.

Winstone, Joanna K / Pathak, Khyatiben V / Winslow, Wendy / Piras, Ignazio S / White, Jennifer / Sharma, Ritin / Huentelman, Matthew J / Pirrotte, Patrick / Velazquez, Ramon

Journal of neuroinflammation

2024 Volume 21, Issue 1, Page(s) 20

Language	English
Publishing date	2024-01-17
Publishing country	England
Document type	Published Erratum
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02990-9
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Article ; Online: A preliminary transcriptomic analysis of the orbitofrontal cortex of antisocial individuals.

Piras, Ignazio S / Braccagni, Giulia / Huentelman, Matthew J / Bortolato, Marco

CNS neuroscience & therapeutics

2023 Volume 29, Issue 11, Page(s) 3173–3182

Abstract: Aims: Antisocial personality disorder (ASPD) and conduct disorder (CD) are characterized by a persistent pattern of violations of societal norms and others' rights. Ample evidence shows that the pathophysiology of these disorders is contributed by ... ...

Abstract	Aims: Antisocial personality disorder (ASPD) and conduct disorder (CD) are characterized by a persistent pattern of violations of societal norms and others' rights. Ample evidence shows that the pathophysiology of these disorders is contributed by orbitofrontal cortex (OFC) alterations, yet the underlying molecular mechanisms remain elusive. To address this knowledge gap, we performed the first-ever RNA sequencing study of postmortem OFC samples from subjects with a lifetime diagnosis of ASPD and/or CD. Methods: The transcriptomic profiles of OFC samples from subjects with ASPD and/or CD were compared to those of unaffected age-matched controls (n = 9/group). Results: The OFC of ASPD/CD-affected subjects displayed significant differences in the expression of 328 genes. Further gene-ontology analyses revealed an extensive downregulation of excitatory neuron transcripts and upregulation of astrocyte transcripts. These alterations were paralleled by significant modifications in synaptic regulation and glutamatergic neurotransmission pathways. Conclusion: These preliminary findings suggest that ASPD and CD feature a complex array of functional deficits in the pyramidal neurons and astrocytes of the OFC. In turn, these aberrances may contribute to the reduced OFC connectivity observed in antisocial subjects. Future analyses on larger cohorts are needed to validate these results.
MeSH term(s)	Humans ; Transcriptome ; Antisocial Personality Disorder/genetics ; Antisocial Personality Disorder/diagnosis ; Conduct Disorder ; Prefrontal Cortex
Chemical Substances	4-aminospiroperidol (114442-96-5)
Language	English
Publishing date	2023-06-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2423461-8
ISSN	1755-5949 ; 1755-5930
ISSN (online)	1755-5949
ISSN	1755-5930
DOI	10.1111/cns.14283
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Article ; Online: The sinking platform test: a novel paradigm to measure persistence in animal models.

Floris, Gabriele / Godar, Sean C / Braccagni, Giulia / Piras, Ignazio S / Ravens, Alicia / Zanda, Mary T / Huentelman, Matthew J / Bortolato, Marco

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2024

Abstract: Persistence is the propensity to maintain goal-directed actions despite adversities. While this temperamental trait is crucial to mitigate depression risk, its neurobiological foundations remain elusive. Developing behavioral tasks to capture persistence ...

Abstract	Persistence is the propensity to maintain goal-directed actions despite adversities. While this temperamental trait is crucial to mitigate depression risk, its neurobiological foundations remain elusive. Developing behavioral tasks to capture persistence in animal models is crucial for understanding its molecular underpinnings. Here, we introduce the Sinking Platform Test (SPT), a novel high-throughput paradigm to measure persistence. Mice were trained to exit a water-filled tank by ascending onto a platform above water level. Throughout the training, mice were also occasionally exposed to "failure trials," during which an operator would submerge a platform right after the mouse climbed onto it, requiring the mouse to reach and ascend a newly introduced platform. Following training, mice were subjected to a 5-min test exclusively consisting of failure trials. Male and female mice exhibited comparable persistence, measured by the number of climbed platforms during the test. Furthermore, this index was increased by chronic administration of fluoxetine or imipramine; conversely, it was reduced by acute and chronic haloperidol. Notably, six weeks of social isolation reduced SPT performance, and this effect was rescued by imipramine treatment over the last two weeks. A 4-week regimen of voluntary wheel running also improved persistence in socially isolated mice. Finally, comparing transcriptomic profiles of the prefrontal cortex of mice with high and low SPT performance revealed significant enrichment of immediate-early genes known to shape susceptibility for chronic stress. These findings highlight the potential of SPT as a promising method to uncover the biological mechanisms of persistence and evaluate novel interventions to enhance this response.
Language	English
Publishing date	2024-02-23
Publishing country	England
Document type	Journal Article
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-024-01827-0
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Article ; Online: Evaluating the Association Between Genetically Proxied Neurodevelopmental Language Phenotypes and the Risk of Primary Progressive Aphasia.

Nassan, Malik / Piras, Ignazio S / Rogalski, Emily / Geula, Changiz / Mesulam, M Marsel / Huentelman, Matt

Neurology

2023 Volume 100, Issue 18, Page(s) e1922–e1929

Abstract: Background and objectives: Primary progressive aphasia (PPA) is a neurodegenerative syndrome of progressive language decline. PPA has 3 main subtypes: logopenic, semantic, and agrammatic. Observational studies suggested an association between language- ... ...

Abstract	Background and objectives: Primary progressive aphasia (PPA) is a neurodegenerative syndrome of progressive language decline. PPA has 3 main subtypes: logopenic, semantic, and agrammatic. Observational studies suggested an association between language-related neurodevelopmental phenotypes and an increased risk of PPA. We sought to assess such relationships through Mendelian randomization (MR) approach, which can suggest potentially causal associations. Methods: Genome-wide significant single-nucleotide polymorphisms (SNPs) associated with dyslexia (42 SNPs), developmental speech disorders (29 SNPs), and left-handedness (41 SNPs) were used as genetic proxies for the exposures. Eighteen of 41 SNPs of left-handedness were associated with structural asymmetry of the cerebral cortex. Genome-wide association study summary statistics were obtained from publicly available databases for semantic (308 cases/616 controls) and agrammatic PPA (269 cases/538 controls). The logopenic PPA (324 cases/3,444 controls) was approximated by proxy through the rubric of clinically diagnosed Alzheimer disease with salient language impairment. Inverse-weighted variance MR was performed as the main analysis for testing the relationship between the exposures and outcomes. Sensitivity analyses were completed to test the robustness of the results. Results: Dyslexia, developmental speech disorders, and left-handedness were not associated with any PPA subtype ( Discussion: Our results do not support a causal association between dyslexia, developmental speech disorders, and handedness with any of the PPA subtypes. Our data suggest a complex association between cortical asymmetry genes and agrammatic PPA. Whether the additional association with left-handedness is necessary remains to be determined but is unlikely, given the absence of association between left-handedness and PPA. Genetic proxy of brain asymmetry (regardless of handedness) was not tested as an exposure due to lack of suitable genetic proxy. Furthermore, the genes related to cortical asymmetry associated with agrammatic PPA are implicated in microtubule-related proteins (
MeSH term(s)	Humans ; Aphasia, Primary Progressive/diagnosis ; Genome-Wide Association Study ; Brain ; Phenotype ; Dyslexia
Language	English
Publishing date	2023-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000207136
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Article ; Online: Dog-human translational genomics: state of the art and genomic resources.

Pallotti, Stefano / Piras, Ignazio S / Marchegiani, Andrea / Cerquetella, Matteo / Napolioni, Valerio

Journal of applied genetics

2022 Volume 63, Issue 4, Page(s) 703–716

Abstract: Innovative models for medical research are strongly required nowadays. Convincing evidence supports dog as the most suitable spontaneous model for several human genetic diseases. Decades of studies on dog genome allowed the identification of hundreds of ... ...

Abstract	Innovative models for medical research are strongly required nowadays. Convincing evidence supports dog as the most suitable spontaneous model for several human genetic diseases. Decades of studies on dog genome allowed the identification of hundreds of mutations causing genetic disorders, many of which are proposed as counterparts responsible for human diseases. Traditionally, the murine model is the most extensively used in human translational research. However, this species shows large physiological differences from humans, and it is kept under a controlled artificial environment. Conversely, canine genetic disorders often show pathophysiological and clinical features highly resembling the human counterpart. In addition, dogs share the same environment with humans; therefore, they are naturally exposed to many risk factors. Thus, different branches of translational medicine aim to study spontaneously occurring diseases in dogs to provide a more reliable model for human disorders. This review offers a comprehensive overview of the knowledge and resources available today for all the researchers involved in the field of dog-human translational medicine. Some of the main successful examples from dog-human translational genomics are reported, such as the canine association studies which helped to identify the causal mutation in the human counterpart. We also illustrated the ongoing projects aiming to create public canine big datasets. Finally, specific online databases are discussed along with several information resources that can speed up clinical translational research.
MeSH term(s)	Dogs ; Humans ; Animals ; Mice ; Disease Models, Animal ; Genomics ; Dog Diseases/genetics ; Mutation ; Genome, Human
Language	English
Publishing date	2022-09-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1235302-4
ISSN	2190-3883 ; 1234-1983
ISSN (online)	2190-3883
ISSN	1234-1983
DOI	10.1007/s13353-022-00721-z
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Article ; Online: Changes in proteomic cargo of circulating extracellular vesicles in response to lifestyle intervention in adolescents with hepatic steatosis.

DiStefano, Johanna K / Piras, Ignazio S / Wu, Xiumei / Sharma, Ritin / Garcia-Mansfield, Krystine / Willey, Maya / Lovell, Brooke / Pirrotte, Patrick / Olson, Micah L / Shaibi, Gabriel Q

Clinical nutrition ESPEN

2024 Volume 60, Page(s) 333–342

Abstract: Background: Recent studies suggest that proteomic cargo of extracellular vesicles (EVs) may play a role in metabolic improvements following lifestyle interventions. However, the relationship between changes in liver fat and circulating EV-derived ... ...

Abstract	Background: Recent studies suggest that proteomic cargo of extracellular vesicles (EVs) may play a role in metabolic improvements following lifestyle interventions. However, the relationship between changes in liver fat and circulating EV-derived protein cargo following intervention remains unexplored. Methods: The study cohort comprised 18 Latino adolescents with obesity and hepatic steatosis (12 males/6 females; average age 13.3 ± 1.2 y) who underwent a six-month lifestyle intervention. EV size distribution and concentration were determined by light scattering intensity; EV protein composition was characterized by liquid chromatography tandem-mass spectrometry. Results: Average hepatic fat fraction (HFF) decreased 23% by the end of the intervention (12.5% [5.5] to 9.6% [4.9]; P = 0.0077). Mean EV size was smaller post-intervention compared to baseline (120.2 ± 16.4 nm to 128.4 ± 16.5 nm; P = 0.031), although the difference in mean EV concentration (1.1E+09 ± 4.1E+08 particles/mL to 1.1E+09 ± 1.8E+08 particles/mL; P = 0.656)) remained unchanged. A total of 462 proteins were identified by proteomic analysis of plasma-derived EVs from participants pre- and post-intervention, with 113 proteins showing differential abundance (56 higher and 57 lower) between the two timepoints (adj-p <0.05). Pathway analysis revealed enrichment in complement cascade, initial triggering of complement, creation of C4 and C2 activators, and regulation of complement cascade. Hepatocyte-specific EV affinity purification identified 40 proteins with suggestive (p < 0.05) differential abundance between pre- and post-intervention samples. Conclusions: Circulating EV-derived proteins, particularly those associated with the complement cascade, may contribute to improvements in liver fat in response to lifestyle intervention.
MeSH term(s)	Male ; Female ; Humans ; Adolescent ; Child ; Proteomics/methods ; Extracellular Vesicles/chemistry ; Extracellular Vesicles/metabolism ; Chromatography, Liquid ; Proteins/metabolism ; Mass Spectrometry
Chemical Substances	Proteins
Language	English
Publishing date	2024-02-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2405-4577
ISSN (online)	2405-4577
DOI	10.1016/j.clnesp.2024.02.024
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Article ; Online: Palmitate and Fructose Interact to Induce Human Hepatocytes to Produce Pro-Fibrotic Transcriptional Responses in Hepatic Stellate Cells Exposed to Conditioned Media.

Piras, Ignazio S / Gerhard, Glenn S / DiStefano, Johanna K

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2020 Volume 54, Issue 5, Page(s) 1068–1082

Abstract: Background/aims: Excessive consumption of dietary fat and sugar is associated with an elevated risk of nonalcoholic fatty liver disease (NAFLD). Hepatocytes exposed to saturated fat or sugar exert effects on nearby hepatic stellate cells (HSCs); however, ...

Abstract	Background/aims: Excessive consumption of dietary fat and sugar is associated with an elevated risk of nonalcoholic fatty liver disease (NAFLD). Hepatocytes exposed to saturated fat or sugar exert effects on nearby hepatic stellate cells (HSCs); however, the mechanisms by which this occurs are poorly understood. We sought to determine whether paracrine effects of hepatocytes exposed to palmitate and fructose produced profibrotic transcriptional responses in HSCs. Methods: We performed expression profiling of mRNA and lncRNA from HSCs treated with conditioned media (CM) from human hepatocytes treated with palmitate (P), fructose (F), or both (PF). Results: In HSCs exposed to CM from palmitate-treated hepatocytes, we identified 374 mRNAs and 607 lncRNAs showing significant differential expression (log Conclusion: The results reported here have implications for dietary modifications in the prevention and treatment of NAFLD.
MeSH term(s)	Computational Biology ; Culture Media, Conditioned/pharmacology ; Fibrosis/genetics ; Fibrosis/metabolism ; Fibrosis/pathology ; Fructose/pharmacology ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/pathology ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Palmitates/pharmacology ; Sweetening Agents/pharmacology ; Transcriptome/drug effects
Chemical Substances	Culture Media, Conditioned ; Palmitates ; Sweetening Agents ; Fructose (30237-26-4)
Language	English
Publishing date	2020-10-23
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.33594/000000288
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Zs.A 3160: Show issues

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Article ; Online: RNA sequencing of olfactory bulb in Parkinson's disease reveals gene alterations associated with olfactory dysfunction.

Tremblay, Cécilia / Aslam, Sidra / Walker, Jessica E / Lorenzini, Ileana / Intorcia, Anthony J / Arce, Richard A / Choudhury, Parichita / Adler, Charles H / Shill, Holly A / Driver-Dunckley, Erika / Mehta, Shyamal / Piras, Ignazio S / Belden, Christine M / Atri, Alireza / Beach, Thomas G / Serrano, Geidy E

Neurobiology of disease

2024 Volume 196, Page(s) 106514

Abstract: The olfactory bulb is involved early in the pathophysiology of Parkinson's disease (PD), which is consistent with the early onset of olfactory dysfunction. Identifying the molecular mechanisms through which PD affects the olfactory bulb could lead to a ... ...

Abstract	The olfactory bulb is involved early in the pathophysiology of Parkinson's disease (PD), which is consistent with the early onset of olfactory dysfunction. Identifying the molecular mechanisms through which PD affects the olfactory bulb could lead to a better understanding of the pathophysiology and etiology of olfactory dysfunction in PD. We specifically aimed to assess gene expression changes, affected pathways and co-expression network by whole transcriptomic profiling of the olfactory bulb in subjects with clinicopathologically defined PD. Bulk RNA sequencing was performed on frozen human olfactory bulbs of 20 PD and 20 controls without dementia or any other neurodegenerative disorder, from the Arizona Study of Aging and Neurodegenerative disorders and the Brain and Body Donation Program. Differential expression analysis (19 PD vs 19 controls) revealed 2164 significantly differentially expressed genes (1090 upregulated and 1074 downregulated) in PD. Pathways enriched in downregulated genes included oxidative phosphorylation, olfactory transduction, metabolic pathways, and neurotransmitters synapses while immune and inflammatory responses as well as cellular death related pathways were enriched within upregulated genes. An overrepresentation of microglial and astrocyte-related genes was observed amongst upregulated genes, and excitatory neuron-related genes were overrepresented amongst downregulated genes. Co-expression network analysis revealed significant modules highly correlated with PD and olfactory dysfunction that were found to be involved in the MAPK signaling pathway, cytokine-cytokine receptor interaction, cholinergic synapse, and metabolic pathways. LAIR1 (leukocyte associated immunoglobulin like receptor 1) and PPARA (peroxisome proliferator activated receptor alpha) were identified as hub genes with a high discriminative power between PD and controls reinforcing an important role of neuroinflammation in the olfactory bulb of PD subjects. Olfactory identification test score positively correlated with expression of genes coding for G-coupled protein, glutamatergic, GABAergic, and cholinergic receptor proteins and negatively correlated with genes for proteins expressed in glial olfactory ensheathing cells. In conclusion, this study reveals gene alterations associated with neuroinflammation, neurotransmitter dysfunction, and disruptions of factors involved in the initiation of olfactory transduction signaling that may be involved in PD-related olfactory dysfunction.
Language	English
Publishing date	2024-04-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2024.106514
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