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Article: Reappraisal of oxidized HMGB1 as a mediator and biomarker.

Pirnie, Ross / P Gillespie, Kevin / Mesaros, Clementina / Blair, Ian A

Future science OA

2023 Volume 8, Issue 10, Page(s) FSO828

Abstract: HMGB1 is a dual-function protein that acts as a chromatin-binding protein and as a danger-associated molecular pattern (DAMP) when released from activated immune cells or injured tissue. In much of the HMGB1 literature, immunomodulatory effects of ... ...

Abstract	HMGB1 is a dual-function protein that acts as a chromatin-binding protein and as a danger-associated molecular pattern (DAMP) when released from activated immune cells or injured tissue. In much of the HMGB1 literature, immunomodulatory effects of extracellular HMGB1 are proposed to depend on its oxidation state. However, many of the foundational studies for this model have been retracted or flagged with expressions of concern. The literature on HMGB1 oxidation reveals a diversity of redox proteoforms of HMGB1 that are inconsistent with current models of redox modulation regulating HMGB1 secretion. A recent study of acetaminophen toxicity has identified previously unrecognized HMGB1 oxidized proteoforms. HMGB1 undergoes oxidative modifications that could serve as pathology-specific biomarkers and drug targets.
Language	English
Publishing date	2023-02-10
Publishing country	England
Document type	Journal Article ; Review
ISSN	2056-5623
ISSN	2056-5623
DOI	10.2144/fsoa-2022-0052
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Article ; Online: Cisplatin Dependent Secretion of Immunomodulatory High Mobility Group Box 1 (HMGB1) Protein from Lung Cancer Cells.

Gillespie, Kevin P / Pirnie, Ross / Mesaros, Clementina / Blair, Ian A

Biomolecules

2023 Volume 13, Issue 9

Abstract: High mobility group box 1 (HMGB1) is secreted from activated immune cells, necrotic cells, and certain cancers. Previous studies have reported that different patterns of post-translational modification, particularly acetylation and oxidation, mediate ... ...

Abstract	High mobility group box 1 (HMGB1) is secreted from activated immune cells, necrotic cells, and certain cancers. Previous studies have reported that different patterns of post-translational modification, particularly acetylation and oxidation, mediate HMGB1 release and confer distinct extracellular HMGB1 signaling activity. Here we report that cisplatin but not carboplatin induces secretion of HMGB1 from human A549 non-small cell lung cancer (NSCLC) cells. Cisplatin-mediated HMGB1 secretion was dose-dependent and was regulated by nuclear exportin 1 (XPO1) also known as chromosomal maintenance 1 (CRM1) rather than adenosine diphosphate (ADP)-ribosylation, acetylation, or oxidation. HMGB1, as well as lysine acetylation and cysteine disulfide oxidation of secreted HMGB1, were monitored by sensitive and specific assays using immunoprecipitation, stable isotope dilution, differential alkylation, and nano liquid chromatography parallel reaction monitoring/high-resolution mass spectrometry (nano-LC-PRM/HRMS). A major fraction of the HMGB1 secreted by low-dose cisplatin treatment of A549 NSCLC cells was found to be in the fully reduced form. In contrast, mainly oxidized forms of HMGB1 were secreted by dimethyl sulfoxide (DMSO)-mediated apoptosis. These findings suggest that inhibition of XPO1 could potentiate the anti-tumor activity of cisplatin by increasing the nuclear accumulation of HMGB1 protein, an inhibitor of cisplatin DNA-adduct repair. Furthermore, low-dose cisplatin therapy could modulate the immune response in NSCLC through the established chemokine activity of extracellular reduced HMGB1. This could potentially enhance the efficacy of subsequent immunotherapy treatment.
MeSH term(s)	Humans ; Cisplatin ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Carcinoma, Non-Small-Cell Lung/pathology ; HMGB1 Protein/metabolism ; Immunity
Chemical Substances	Cisplatin (Q20Q21Q62J) ; HMGB1 Protein
Language	English
Publishing date	2023-08-31
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13091335
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Article: A dynamic career in MS: applications to biomedical research.

Blair, Ian A

Future science OA

2015 Volume 1, Issue 4, Page(s) FSO52

Abstract: Ian A Blair speaks to Francesca Lake, Managing ... ...

Abstract	Ian A Blair speaks to Francesca Lake, Managing Editor
Language	English
Publishing date	2015-11-01
Publishing country	England
Document type	Journal Article
ISSN	2056-5623
ISSN	2056-5623
DOI	10.4155/fso.15.52
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Article ; Online: Liquid Chromatography–Mass Spectrometry Analysis of Frataxin Proteoforms in Whole Blood as Biomarkers of the Genetic Disease Friedreich’s Ataxia

Rojsajjakul, Teerapat / Wu, Linfeng / Grady, Connor B. / Hwang, Wei-Ting / Mesaros, Clementina / Lynch, David R. / Blair, Ian A.

Analytical Chemistry. 2023 Feb. 17, v. 95, no. 8 p.4251-4260

2023

Abstract: Friedreich’s ataxia (FRDA) is caused primarily by expanded GAA repeats in intron 1 of both alleles of the FXN gene, which causes transcriptional silencing and reduced expression of frataxin mRNA and protein. FRDA is characterized by slowly progressive ... ...

Abstract	Friedreich’s ataxia (FRDA) is caused primarily by expanded GAA repeats in intron 1 of both alleles of the FXN gene, which causes transcriptional silencing and reduced expression of frataxin mRNA and protein. FRDA is characterized by slowly progressive ataxia and cardiomyopathy. Symptoms generally appear during adolescence, and patients slowly progress to wheelchair dependency usually in the late teens or early twenties with death on average in the 4th decade. There are two known mature proteoforms of frataxin. Mitochondrial frataxin (frataxin-M) is a 130-amino acid protein with a molecular weight of 14,268 Da, and there is an alternatively spliced N-terminally acetylated 135-amino acid form (frataxin-E) with a molecular weight of 14,953 Da found in erythrocytes. There is reduced expression of frataxin in the heart and brain, but frataxin is not secreted into the systemic circulation, so it cannot be analyzed in serum or plasma. Blood is a readily accessible biofluid that contains numerous different cell types that express frataxin. We have found that pig blood can serve as an excellent surrogate matrix to validate an assay for frataxin proteoforms because pig frataxin is lost during the immunoprecipitation step used to isolate human frataxin. Frataxin-M is expressed in blood cells that contain mitochondria, whereas extra-mitochondrial frataxin-E is found in erythrocytes. This means that the analysis of frataxin in whole blood provides information on the concentration of both proteoforms without having to isolate the individual cell types. In the current study, we observed that the distributions of frataxin levels for a sample of 25 healthy controls and 50 FRDA patients were completely separated from each other, suggesting 100% specificity and 100% sensitivity for distinguishing healthy controls from FRDA cases, a very unusual finding for a biomarker assay. Additionally, frataxin levels were significantly correlated with the GAA repeat length and age of onset with higher correlations for extra-mitochondrial frataxin-E than those for mitochondrial frataxin-M. These findings auger well for using frataxin levels measured by the validated stable isotope dilution ultrahigh-performance liquid chromatography–multiple reaction monitoring/mass spectrometry assay to monitor therapeutic interventions and the natural history of FRDA. Our study also illustrates the utility of using whole blood for protein disease biomarker discovery and validation.
Keywords	adolescence ; analytical chemistry ; biomarkers ; blood serum ; brain ; cardiomyopathy ; death ; erythrocytes ; genetic disorders ; heart ; humans ; introns ; isotope dilution technique ; liquid chromatography ; mass spectrometry ; mitochondria ; molecular weight ; natural history ; precipitin tests ; stable isotopes ; swine ; therapeutics ; transcription (genetics)
Language	English
Dates of publication	2023-0217
Size	p. 4251-4260.
Publishing place	American Chemical Society
Document type	Article ; Online
ZDB-ID	1508-8
ISSN	1520-6882 ; 0003-2700
ISSN (online)	1520-6882
ISSN	0003-2700
DOI	10.1021/acs.analchem.3c00091
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Article ; Online: Characterization and Quantification of Oxidized High Mobility Group Box 1 Proteoforms Secreted from Hepatocytes by Toxic Levels of Acetaminophen.

Pirnie, Ross / Gillespie, Kevin P / Weng, Liwei / Mesaros, Clementina / Blair, Ian A

Chemical research in toxicology

2022 Volume 35, Issue 10, Page(s) 1893–1902

Abstract: The high mobility group box 1 (HMGB1), which is released during acute acetaminophen (APAP) overdose, is thought to mediate a subsequent immune response, particularly hepatic infiltration of macrophages. The redox behavior of HMGB1 and the proteoforms of ... ...

Abstract	The high mobility group box 1 (HMGB1), which is released during acute acetaminophen (APAP) overdose, is thought to mediate a subsequent immune response, particularly hepatic infiltration of macrophages. The redox behavior of HMGB1 and the proteoforms of HMGB1 present in oxidative environments has been the subject of a number of confusing and contradictory studies. Therefore, a stable isotope dilution two-dimensional nanoultrahigh-performance liquid chromatography parallel reaction monitoring/high-resolution mass spectrometry method was developed in order to characterize and quantify oxidative modifications to the cysteine (Cys) residues (Cys-23, Cys-45, and Cys-106) that are present in HMGB1. Disulfide linkages were determined using carbamidoethyl derivatization before and after reduction as well as by direct analysis of disulfide cross-linked peptides. A stable isotope labeled form of HMGB1 was used as an internal standard to correct for sample to sample differences in immunoaffinity precipitation, derivatization, and electrospray ionization. Four discrete HMGB1 proteoforms were found to be released from a hepatocarcinoma cell model of APAP overdose after 24 h. Fully reduced HMGB1 with all three Cys-residues in their free thiol state accounted for 18% of the secreted HMGB1. The proteoform with disulfide between Cys-23 and Cys-45 accounted for 24% of the HMGB1. No evidence was obtained for a disulfide cross-link between Cys-106 and the other two Cys-residues. However, 45% of the HMGB1 formed a cross-link with unidentified intracellular proteins via an intermolecular disulfide bond, and 12% was present as the terminally oxidized cysteic acid. Surprisingly, there was no evidence for the formation of HMGB1 disulfides with GSH or other low molecular weight thiols. Secreted plasma HMGB1 Cys-23/Cys45 disulfide proteoform together with the Cys-106/protein disulfide proteoforms could potentially serve as early biomarkers of hepatoxicity after APAP overdose as well as biomarkers of drug-induced liver injury.
MeSH term(s)	Acetaminophen/toxicity ; Biomarkers/metabolism ; Cysteic Acid/metabolism ; Cysteine/chemistry ; Disulfides/chemistry ; HMGB1 Protein/metabolism ; Hepatocytes/metabolism ; Oxidation-Reduction ; Peptides/metabolism ; Proteins/metabolism ; Sulfhydryl Compounds/metabolism
Chemical Substances	Biomarkers ; Disulfides ; HMGB1 Protein ; Peptides ; Proteins ; Sulfhydryl Compounds ; Acetaminophen (362O9ITL9D) ; Cysteic Acid (A3OGP4C37W) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2022-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/acs.chemrestox.2c00161
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Article ; Online: Quantification of human mature frataxin protein expression in nonhuman primate hearts after gene therapy.

Rojsajjakul, Teerapat / Hordeaux, Juliette J / Choudhury, Gourav R / Hinderer, Christian J / Mesaros, Clementina / Wilson, James M / Blair, Ian A

Communications biology

2023 Volume 6, Issue 1, Page(s) 1093

Abstract: Deficiency in human mature frataxin (hFXN-M) protein is responsible for the devastating neurodegenerative and cardiodegenerative disease of Friedreich's ataxia (FRDA). It results primarily through epigenetic silencing of the FXN gene by GAA triplet ... ...

Abstract	Deficiency in human mature frataxin (hFXN-M) protein is responsible for the devastating neurodegenerative and cardiodegenerative disease of Friedreich's ataxia (FRDA). It results primarily through epigenetic silencing of the FXN gene by GAA triplet repeats on intron 1 of both alleles. GAA repeat lengths are most commonly between 600 and 1200 but can reach 1700. A subset of approximately 3% of FRDA patients have GAA repeats on one allele and a mutation on the other. FRDA patients die most commonly in their 30s from heart disease. Therefore, increasing expression of heart hFXN-M using gene therapy offers a way to prevent early mortality in FRDA. We used rhesus macaque monkeys to test the pharmacology of an adeno-associated virus (AAV)hu68.CB7.hFXN therapy. The advantage of using non-human primates for hFXN-M gene therapy studies is that hFXN-M and monkey FXN-M (mFXN-M) are 98.5% identical, which limits potential immunologic side-effects. However, this presented a formidable bioanalytical challenge in quantification of proteins with almost identical sequences. This could be overcome by the development of a species-specific quantitative mass spectrometry-based method, which has revealed for the first time, robust transgene-specific human protein expression in monkey heart tissue. The dose response is non-linear resulting in a ten-fold increase in monkey heart hFXN-M protein expression with only a three-fold increase in dose of the vector.
MeSH term(s)	Animals ; Humans ; Macaca mulatta ; Iron-Binding Proteins/genetics ; Heart ; Friedreich Ataxia/genetics ; Friedreich Ataxia/therapy ; Friedreich Ataxia/metabolism ; Genetic Therapy ; Frataxin
Chemical Substances	Iron-Binding Proteins
Language	English
Publishing date	2023-10-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-023-05472-z
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Article ; Online: Liquid Chromatography-Mass Spectrometry Analysis of Frataxin Proteoforms in Whole Blood as Biomarkers of the Genetic Disease Friedreich's Ataxia.

Rojsajjakul, Teerapat / Wu, Linfeng / Grady, Connor B / Hwang, Wei-Ting / Mesaros, Clementina / Lynch, David R / Blair, Ian A

Analytical chemistry

2023 Volume 95, Issue 8, Page(s) 4251–4260

Abstract: Friedreich's ataxia (FRDA) is caused primarily by expanded GAA repeats in intron 1 of both alleles of ... ...

Abstract	Friedreich's ataxia (FRDA) is caused primarily by expanded GAA repeats in intron 1 of both alleles of the
MeSH term(s)	Animals ; Humans ; Biomarkers ; Chromatography, Liquid ; Friedreich Ataxia/diagnosis ; Friedreich Ataxia/genetics ; Mass Spectrometry ; Swine ; Frataxin
Chemical Substances	Biomarkers
Language	English
Publishing date	2023-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1508-8
ISSN	1520-6882 ; 0003-2700
ISSN (online)	1520-6882
ISSN	0003-2700
DOI	10.1021/acs.analchem.3c00091
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Article ; Online: Frataxin analysis using triple quadrupole mass spectrometry: application to a large heterogeneous clinical cohort.

Lynch, David R / Rojsajjakul, Teerapat / Subramony, S H / Perlman, Susan L / Keita, Medina / Mesaros, Clementina / Blair, Ian A

Journal of neurology

2023 Volume 271, Issue 4, Page(s) 1844–1849

Abstract: Background: Friedreich ataxia is a progressive multisystem disorder caused by deficiency of the protein frataxin; a small mitochondrial protein involved in iron sulfur cluster synthesis. Two types of frataxin exist: FXN-M, found in most cells, and FXN-E, ...

Abstract	Background: Friedreich ataxia is a progressive multisystem disorder caused by deficiency of the protein frataxin; a small mitochondrial protein involved in iron sulfur cluster synthesis. Two types of frataxin exist: FXN-M, found in most cells, and FXN-E, found almost exclusively in red blood cells. Treatments in clinical trials include frataxin restoration by gene therapy, protein replacement, and epigenetic therapies, all of which necessitate sensitive assays for assessing frataxin levels. Methods: In the present study, we have used a triple quadrupole mass spectrometry-based assay to examine the features of both types of frataxin levels in blood in a large heterogenous cohort of 106 patients with FRDA. Results: Frataxin levels (FXN-E and FXN M) were predicted by GAA repeat length in regression models (R Conclusion: The present data show that assay of FXN-M and FXN-E levels in blood provides an appropriate biofluid for assessing their repletion in particular clinical contexts.
MeSH term(s)	Humans ; Frataxin ; Friedreich Ataxia/genetics ; Mitochondrial Proteins/genetics ; Mass Spectrometry ; Iron-Binding Proteins/genetics ; Iron-Binding Proteins/metabolism
Chemical Substances	Frataxin ; Mitochondrial Proteins ; Iron-Binding Proteins
Language	English
Publishing date	2023-12-08
Publishing country	Germany
Document type	Journal Article
ZDB-ID	187050-6
ISSN	1432-1459 ; 0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
ISSN (online)	1432-1459
ISSN	0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
DOI	10.1007/s00415-023-12118-x
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Article: The androgen receptor.

Van-Duyne, Greg / Blair, Ian A / Sprenger, Cynthia / Moiseenkova-Bell, Vera / Plymate, Stephen / Penning, Trevor M

Vitamins and hormones

2023 Volume 123, Page(s) 439–481

Abstract: The Androgen Receptor (AR) is a ligand (androgen) activated transcription factor and a member of the nuclear receptor (NR) superfamily. It is required for male sex hormone function. AR-FL (full-length) has the domain structure of NRs, an N-terminal ... ...

Abstract	The Androgen Receptor (AR) is a ligand (androgen) activated transcription factor and a member of the nuclear receptor (NR) superfamily. It is required for male sex hormone function. AR-FL (full-length) has the domain structure of NRs, an N-terminal domain (NTD) required for transactivation, a DNA-binding domain (DBD), a nuclear localization signal (NLS) and a ligand-binding domain (LBD). Paradoxes exist in that endogenous ligands testosterone (T) and 5α-dihydrotestosterone (DHT) have differential effects on male sexual development while binding to the same receptor and transcriptional specificity is achieved even though the androgen response elements (AREs) are identical to those seen for the progesterone, glucocorticoid and mineralocorticoid receptors. A high resolution 3-dimensional structure of AR-FL by either cryo-EM or X-ray crystallography has remained elusive largely due to the intrinsic disorder of the NTD. AR function is regulated by post-translational modification leading to a large number of proteoforms. The interaction of these proteoforms in multiprotein complexes with co-activators and co-repressors driven by interdomain coupling mediates the AR transcriptional output. The AR is a drug target for selective androgen receptor modulators (SARMS) that either have anabolic or androgenic effects. Protstate cancer is treated with androgen deprivation therapy or by the use of AR antagonists that bind to the LBD. Drug resistance occurs due to adaptive AR upregulation and the appearance of splice variants that lack the LBD and become constitutively active. Bipolar T treatment and NTD-antagonists could surmount these resistance mechanisms, respectively. These recent advances in AR signaling are described.
MeSH term(s)	Male ; Humans ; Receptors, Androgen/genetics ; Androgens ; Androgen Antagonists ; Ligands ; Prostatic Neoplasms
Chemical Substances	Receptors, Androgen ; Androgens ; Androgen Antagonists ; Ligands
Language	English
Publishing date	2023-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	201161-x
ISSN	2162-2620 ; 0083-6729
ISSN (online)	2162-2620
ISSN	0083-6729
DOI	10.1016/bs.vh.2023.01.001
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Article: Analytical Methods for Mass Spectrometry-Based Metabolomics Studies.

Wang, Siyu / Blair, Ian A / Mesaros, Clementina

Advances in experimental medicine and biology

2019 Volume 1140, Page(s) 635–647

Abstract: The advancement of mass spectrometry-based analytical platform largely facilitates small-molecule metabolomics studies, which allows simultaneously analysis of a large number of metabolites from bio-samples and give a general picture of metabolic changes ...

Abstract	The advancement of mass spectrometry-based analytical platform largely facilitates small-molecule metabolomics studies, which allows simultaneously analysis of a large number of metabolites from bio-samples and give a general picture of metabolic changes related to diseases or environmental alteration. Due to the large diversity of cellular metabolites, globally and precisely examining metabolic profile remains the most challenging part in metabolomic experiment. Mass spectrometry coupled with liquid chromatography enhances sensitivity and resolving power of metabolites identification and quantification, as well as versatility of analyzing a wide array of metabolites. In this chapter, we discussed the technical aspects of each step in the workflow of metabolomics studies we aimed to give technical guidelines for metabolomics investigation design and approach.
MeSH term(s)	Chromatography, Liquid ; Mass Spectrometry ; Metabolome ; Metabolomics
Language	English
Publishing date	2019-07-26
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-15950-4_38
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