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Article ; Online: Transcriptomic study of anastasis for reversal of ethanol-induced apoptosis in mouse primary liver cells.

Tang, Ho Man / Talbot, C Conover / Fung, Ming Chiu / Tang, Ho Lam

2022 Volume 9, Issue 1, Page(s) 418

Abstract: Anastasis is a cell recovery mechanism that rescues dying cells from the brink of death. Reversal of apoptosis is the first example of anastasis. Here, we describe a comprehensive dataset containing time-course mRNA expression profiles for reversal of ... ...

Abstract	Anastasis is a cell recovery mechanism that rescues dying cells from the brink of death. Reversal of apoptosis is the first example of anastasis. Here, we describe a comprehensive dataset containing time-course mRNA expression profiles for reversal of ethanol-induced apoptosis in mouse primary liver cells in νitro. This transcriptome dataset includes the conditions of the untreated cells, cells undergoing apoptosis triggered by incubating with cell death inducer of 4.5% ethanol for 5 hours, and apoptosis reversal of ethanol-induced cells at the early (3
MeSH term(s)	Animals ; Apoptosis ; Cell Death Reversal ; Ethanol/pharmacology ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Mice ; Transcriptome
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2022-07-18
Publishing country	England
Document type	Dataset ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2775191-0
ISSN	2052-4463 ; 2052-4463
ISSN (online)	2052-4463
ISSN	2052-4463
DOI	10.1038/s41597-022-01470-8
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Article ; Online: Presence of Uterine Leiomyomas Has No Significant Impact on Gene Expression Profile in the Scalp of Patients with Central Centrifugal Cicatricial Alopecia.

Jamerson, Taylor A / Talbot, C Conover / Dina, Yemisi / Aguh, Crystal

JID innovations

2021 Volume 2, Issue 1, Page(s) 100060

Abstract: Central centrifugal cicatricial alopecia (CCCA) is associated with increased expression of genes implicated in fibroproliferative disorders and a higher prevalence of uterine leiomyomas (ULs) among affected individuals. We sought to examine the effect of ...

Abstract	Central centrifugal cicatricial alopecia (CCCA) is associated with increased expression of genes implicated in fibroproliferative disorders and a higher prevalence of uterine leiomyomas (ULs) among affected individuals. We sought to examine the effect of UL status on the gene expression profile of the lesional scalp in patients with CCCA. Scalp biopsy was obtained from 16 patients with a confirmed diagnosis of CCCA between 2017 and 2020. Microarray analysis was used to identify differential gene expression between patients with CCCA with a history of UL and those without the history. Of more than 20,000 genes analyzed, 23 of 25 genes with the highest expression in patients with CCCA with UL held no statistical significance. No genes previously implicated in fibroproliferative disorders were found among the upregulated transcripts. Of all genes analyzed, only eight upregulated genes and zero downregulated genes had a fold change in expression >2 in patients with CCCA with UL compared with those in patients with CCCA without UL. Our findings highlight similar gene expression patterns in the lesional scalp of patients with CCCA with and without a history of UL. This analysis is key in highlighting no evidence of causational or linked mechanobiology that accounts for the increased prevalence of UL seen in patients with CCCA that previous studies have not addressed.
Language	English
Publishing date	2021-10-06
Publishing country	United States
Document type	Journal Article
ISSN	2667-0267
ISSN (online)	2667-0267
DOI	10.1016/j.xjidi.2021.100060
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Article ; Online: Hypereosinophilia causes progressive cardiac pathologies in mice.

Diny, Nicola Laura / Wood, Megan Kay / Won, Taejoon / Talor, Monica Vladut / Lukban, Clarisse / Bedja, Djahida / Wang, Nadan / Kalinoski, Hannah / Daoud, Abdel / Talbot, C Conover / Leei Lin, Brian / Čiháková, Daniela

iScience

2023 Volume 26, Issue 10, Page(s) 107990

Abstract: Hypereosinophilic syndrome is a progressive disease with extensive eosinophilia that results in organ damage. Cardiac pathologies are the main reason for its high mortality rate. A better understanding of the mechanisms of eosinophil-mediated tissue ... ...

Abstract	Hypereosinophilic syndrome is a progressive disease with extensive eosinophilia that results in organ damage. Cardiac pathologies are the main reason for its high mortality rate. A better understanding of the mechanisms of eosinophil-mediated tissue damage would benefit therapeutic development. Here, we describe the cardiac pathologies that developed in a mouse model of hypereosinophilic syndrome. These IL-5 transgenic mice exhibited decreased left ventricular function at a young age which worsened with age. Mechanistically, we demonstrated infiltration of activated eosinophils into the heart tissue that led to an inflammatory environment. Gene expression signatures showed tissue damage as well as repair and remodeling processes. Cardiomyocytes from IL-5Tg mice exhibited significantly reduced contractility relative to wild type (WT) controls. This impairment may result from the inflammatory stress experienced by the cardiomyocytes and suggest that dysregulation of contractility and Ca
Language	English
Publishing date	2023-09-21
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.107990
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Article ; Online: Decoding Angiotensin Receptors: TOMAHAQ-Based Detection and Quantification of Angiotensin Type-1 and Type-2 Receptors.

Cosarderelioglu, Caglar / Kreimer, Simion / Plaza-Rodriguez, Alma I / Iglesias, Pablo A / Talbot, C Conover / Siragy, Helmy M / Carey, Robert M / Ubaida-Mohien, Ceereena / O'Rourke, Brian / Ferrucci, Luigi / Bennett, David A / Walston, Jeremy / Abadir, Peter

Journal of the American Heart Association

2023 Volume 12, Issue 18, Page(s) e030791

Abstract: Background The renin-angiotensin system plays a crucial role in human physiology, and its main hormone, angiotensin, activates 2 G-protein-coupled receptors, the angiotensin type-1 and type-2 receptors, in almost every organ. However, controversy exists ... ...

Abstract	Background The renin-angiotensin system plays a crucial role in human physiology, and its main hormone, angiotensin, activates 2 G-protein-coupled receptors, the angiotensin type-1 and type-2 receptors, in almost every organ. However, controversy exists about the location, distribution, and expression levels of these receptors. Concerns have been raised over the low sensitivity, low specificity, and large variability between lots of commercially available antibodies for angiotensin type-1 and type-2 receptors, which makes it difficult to reconciliate results of different studies. Here, we describe the first non-antibody-based sensitive and specific targeted quantitative mass spectrometry assay for angiotensin receptors. Methods and Results Using a technique that allows targeted analysis of multiple peptides across multiple samples in a single mass spectrometry analysis, known as TOMAHAQ (triggered by offset, multiplexed, accurate mass, high resolution, and absolute quantification), we have identified and validated specific human tryptic peptides that permit identification and quantification of angiotensin type-1 and type-2 receptors in biological samples. Several peptide sequences are conserved in rodents, making these mass spectrometry assays amenable to both preclinical and clinical studies. We have used this method to quantify angiotensin type-1 and type-2 receptors in postmortem frontal cortex samples of older adults (n=28) with Alzheimer dementia. We correlated levels of angiotensin receptors to biomarkers classically linked to renin-angiotensin system activation, including oxidative stress, inflammation, amyloid-β load, and paired helical filament-tau tangle burden. Conclusions These robust high-throughput assays will not only catalyze novel mechanistic studies in the angiotensin research field but may also help to identify patients with an unbalanced angiotensin receptor distribution who would benefit from angiotensin receptor blocker treatment.
MeSH term(s)	Humans ; Aged ; Angiotensins ; Receptors, Angiotensin ; Renin-Angiotensin System ; Angiotensin Receptor Antagonists ; Antibodies
Chemical Substances	Angiotensins ; Receptors, Angiotensin ; Angiotensin Receptor Antagonists ; Antibodies
Language	English
Publishing date	2023-09-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.123.030791
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Article ; Online: The Interaction of Borrelia burgdorferi with Human Dendritic Cells: Functional Implications.

Gutierrez-Hoffmann, Maria / Fan, Jinshui / O'Meally, Robert N / Cole, Robert N / Florea, Liliana / Antonescu, Corina / Talbot, C Conover / Tiniakou, Eleni / Darrah, Erika / Soloski, Mark J

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 211, Issue 4, Page(s) 612–625

Abstract: Dendritic cells bridge the innate and adaptive immune responses by serving as sensors of infection and as the primary APCs responsible for the initiation of the T cell response against invading pathogens. The naive T cell activation requires the ... ...

Abstract	Dendritic cells bridge the innate and adaptive immune responses by serving as sensors of infection and as the primary APCs responsible for the initiation of the T cell response against invading pathogens. The naive T cell activation requires the following three key signals to be delivered from dendritic cells: engagement of the TCR by peptide Ags bound to MHC molecules (signal 1), engagement of costimulatory molecules on both cell types (signal 2), and expression of polarizing cytokines (signal 3). Initial interactions between Borrelia burgdorferi, the causative agent of Lyme disease, and dendritic cells remain largely unexplored. To address this gap in knowledge, we cultured live B. burgdorferi with monocyte-derived dendritic cells (mo-DCs) from healthy donors to examine the bacterial immunopeptidome associated with HLA-DR. In parallel, we examined changes in the expression of key costimulatory and regulatory molecules as well as profiled the cytokines released by dendritic cells when exposed to live spirochetes. RNA-sequencing studies on B. burgdorferi-pulsed dendritic cells show a unique gene expression signature associated with B. burgdorferi stimulation that differs from stimulation with lipoteichoic acid, a TLR2 agonist. These studies revealed that exposure of mo-DCs to live B. burgdorferi drives the expression of both pro- and anti-inflammatory cytokines as well as immunoregulatory molecules (e.g., PD-L1, IDO1, Tim3). Collectively, these studies indicate that the interaction of live B. burgdorferi with mo-DCs promotes a unique mature DC phenotype that likely impacts the nature of the adaptive T cell response generated in human Lyme disease.
MeSH term(s)	Humans ; Borrelia burgdorferi ; Dendritic Cells ; Lyme Disease ; T-Lymphocytes/metabolism ; Cytokines/metabolism
Chemical Substances	Cytokines
Language	English
Publishing date	2023-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300235
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Article ; Online: Fibroproliferative genes are preferentially expressed in central centrifugal cicatricial alopecia.

Aguh, Crystal / Dina, Yemisi / Talbot, C Conover / Garza, Luis

Journal of the American Academy of Dermatology

2018 Volume 79, Issue 5, Page(s) 904–912.e1

Abstract: Background: Central centrifugal cicatricial alopecia (CCCA) is a primary cicatricial alopecia that most commonly affects women of African descent. Like CCCA, fibroproliferative disorders (FPDs) such as keloids, atherosclerosis, and fibroids are ... ...

Abstract	Background: Central centrifugal cicatricial alopecia (CCCA) is a primary cicatricial alopecia that most commonly affects women of African descent. Like CCCA, fibroproliferative disorders (FPDs) such as keloids, atherosclerosis, and fibroids are characterized by low-grade inflammation and irritation, resulting in end-stage fibrosis. Objective: We sought to determine whether fibroproliferative genes were up-regulated in patients with CCCA. Methods: A total of 5 patients with biopsy-proven CCCA were recruited for this study. Two scalp biopsy specimens were obtained from each patient; 1 from CCCA-affected vertex scalp and 1 from the unaffected occipital scalp. Microarray analysis was performed to determine the differential gene expression patterns. Results: There was an upregulation of genes implicated in FPDs in patients with CCCA. Specifically, we noted increased expression of platelet derived growth factor gene (PDGF), collagen I gene (COL I), collagen III gene (COL III), matrix metallopeptidase 1 gene (MMP1), matrix metallopeptidase 2 gene (MMP2), matrix metallopeptidase 7 gene (MMP7), and matrix metallopeptidase 9 gene (MMP9) in affected scalp compared with in unaffected scalp. Significant overlap in the canonic pathways was noted between patients with CCCA and patients with both atherosclerosis and hepatic fibrosis (P < .001). Limitations: Small sample size and the use of whole skin tissue for analysis. Conclusion: We have identified the upregulation of critical genes implicated in FPDs in the gene expression profile of patients with CCCA. These findings may help identify future therapeutic targets for this otherwise difficult-to-treat condition.
MeSH term(s)	Adult ; Aged ; Alopecia/genetics ; Alopecia/pathology ; Biopsy, Needle ; Cicatrix/genetics ; Cicatrix/pathology ; Female ; Genetic Predisposition to Disease ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Platelet-Derived Growth Factor/genetics ; Prognosis ; Risk Assessment ; Sampling Studies ; Up-Regulation
Chemical Substances	Platelet-Derived Growth Factor ; platelet-derived growth factor A
Language	English
Publishing date	2018-06-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	603641-7
ISSN	1097-6787 ; 0190-9622
ISSN (online)	1097-6787
ISSN	0190-9622
DOI	10.1016/j.jaad.2018.05.1257
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Article ; Online: Cigarette Smoke Triggers Loss of Corneal Endothelial Cells and Disruption of Descemet's Membrane Proteins in Mice.

Ali, Muhammad / Khan, Shahid Y / Jang, Yura / Na, Chan Hyun / Talbot, C Conover / Gottsch, John D / Handa, James T / Riazuddin, S Amer

Investigative ophthalmology & visual science

2021 Volume 62, Issue 3, Page(s) 3

Abstract: Purpose: To investigate changes at a molecular level in the mouse corneal endothelium (CE) exposed to chronic cigarette smoke (CS).: Methods: Pregnant mice (gestation days 18-20) were placed in a whole-body exposure smoking chamber, and a few days ... ...

Abstract	Purpose: To investigate changes at a molecular level in the mouse corneal endothelium (CE) exposed to chronic cigarette smoke (CS). Methods: Pregnant mice (gestation days 18-20) were placed in a whole-body exposure smoking chamber, and a few days later pups were born. After 3.5 months of CS exposure, a ConfoScan4 scanning microscope was used to examine the corneal endothelial cells (CECs) of CS-exposed and control (Ct) mice. The CE was peeled under a microscope and maintained as four biological replicates (two male and two female) for CS-exposed and Ct mice; each replicate consisted of 16 CEs. The proteome of the CE was investigated through mass spectrometry. Results: The CE images of CS-exposed and Ct mice revealed a difference in the shape of CECs accompanied by a nearly 10% decrease in CEC density (P < 0.00003) following CS exposure. Proteome profiling identified a total of 524 proteins exhibiting statistically significant changes in CE from CS-exposed mice. Importantly, proteins associated with Descemet's membrane (DM), including COL4α1, COL4α2, COL4α3, COL4α4, COL4α5, COL4α6, COL8α1, COL8α2, and FN1, among others, exhibited diminished protein levels in the CE of CS-exposed mice. Conclusions: Our data confirm that exposure to CS results in reduced CEC density accompanied by diminished levels of multiple collagen and extracellular matrix proteins associated with DM.
MeSH term(s)	Animals ; Atmosphere Exposure Chambers ; Cigarette Smoking/adverse effects ; Corneal Endothelial Cell Loss/etiology ; Corneal Endothelial Cell Loss/metabolism ; Corneal Endothelial Cell Loss/pathology ; Descemet Membrane/metabolism ; Eye Proteins/metabolism ; Female ; Male ; Mass Spectrometry ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Pregnancy ; Pregnancy, Animal ; Proteome/metabolism
Chemical Substances	Eye Proteins ; Proteome
Language	English
Publishing date	2021-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.62.3.3
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Article: Molecular signature of anastasis for reversal of apoptosis.

Tang, Ho Man / Talbot, C Conover / Fung, Ming Chiu / Tang, Ho Lam

F1000Research

2017 Volume 6, Page(s) 43

Abstract: Anastasis (Greek for "rising to life") is a cell recovery phenomenon that rescues dying cells from the brink of cell death. We recently discovered anastasis to occur after the execution-stage of ... ...

Abstract	Anastasis (Greek for "rising to life") is a cell recovery phenomenon that rescues dying cells from the brink of cell death. We recently discovered anastasis to occur after the execution-stage of apoptosis
Language	English
Publishing date	2017
Publishing country	England
Document type	Journal Article
ZDB-ID	2699932-8
ISSN	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.10568.2
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Article ; Online: The XIST lncRNA is a sex-specific reservoir of TLR7 ligands in SLE.

Crawford, Jonathan D / Wang, Hong / Trejo-Zambrano, Daniela / Cimbro, Raffaello / Talbot, C Conover / Thomas, Mekha A / Curran, Ashley M / Girgis, Alexander A / Schroeder, John T / Fava, Andrea / Goldman, Daniel W / Petri, Michelle / Rosen, Antony / Antiochos, Brendan / Darrah, Erika

JCI insight

2023 Volume 8, Issue 20

Abstract: Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a dramatic sex bias, affecting 9 times more women than men. Activation of Toll-like receptor 7 (TLR7) by self-RNA is a central pathogenic process leading to aberrant production of ... ...

Abstract	Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a dramatic sex bias, affecting 9 times more women than men. Activation of Toll-like receptor 7 (TLR7) by self-RNA is a central pathogenic process leading to aberrant production of type I interferon (IFN) in SLE, but the specific RNA molecules that serve as TLR7 ligands have not been defined. By leveraging gene expression data and the known sequence specificity of TLR7, we identified the female-specific X-inactive specific transcript (XIST) long noncoding RNA as a uniquely rich source of TLR7 ligands in SLE. XIST RNA stimulated IFN-α production by plasmacytoid DCs in a TLR7-dependent manner, and deletion of XIST diminished the ability of whole cellular RNA to activate TLR7. XIST levels were elevated in blood leukocytes from women with SLE compared with controls, correlated positively with disease activity and the IFN signature, and were enriched in extracellular vesicles released from dying cells in vitro. Importantly, XIST was not IFN inducible, suggesting that XIST is a driver, rather than a consequence, of IFN in SLE. Overall, our work elucidated a role for XIST RNA as a female sex-specific danger signal underlying the sex bias in SLE.
MeSH term(s)	Male ; Humans ; Female ; RNA, Long Noncoding/genetics ; Toll-Like Receptor 7 ; Lupus Erythematosus, Systemic ; Interferon Type I/genetics ; Gene Expression ; Ligands
Chemical Substances	RNA, Long Noncoding ; Toll-Like Receptor 7 ; Interferon Type I ; Ligands ; TLR7 protein, human
Language	English
Publishing date	2023-09-21
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.169344
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Article: Genome-wide expression analysis comparing hypertrophic changes in normal and dysferlinopathy mice.

Lee, Yun-Sil / Talbot, C Conover / Lee, Se-Jin

Genomics data

2015 Volume 6, Page(s) 253–257

Abstract: Because myostatin normally limits skeletal muscle growth, there are extensive efforts to develop myostatin inhibitors for clinical use. One potential concern is that in muscle degenerative diseases, inducing hypertrophy may increase stress on dystrophic ... ...

Abstract	Because myostatin normally limits skeletal muscle growth, there are extensive efforts to develop myostatin inhibitors for clinical use. One potential concern is that in muscle degenerative diseases, inducing hypertrophy may increase stress on dystrophic fibers. Our study shows that blocking this pathway in dysferlin deficient mice results in early improvement in histopathology but ultimately accelerates muscle degeneration. Hence, benefits of this approach should be weighed against these potential detrimental effects. Here, we present detailed experimental methods and analysis for the gene expression profiling described in our recently published study in Human Molecular Genetics (Lee et al., 2015). Our data sets have been deposited in the Gene Expression Omnibus (GEO) database (GSE62945) and are available at http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62945. Our data provide a resource for exploring molecular mechanisms that are related to hypertrophy-induced, accelerated muscular degeneration in dysferlinopathy.
Language	English
Publishing date	2015-10-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2751131-5
ISSN	2213-5960
ISSN	2213-5960
DOI	10.1016/j.gdata.2015.10.010
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