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Article ; Online: Lipid-laden foam cells in the pathology of atherosclerosis: shedding light on new therapeutic targets.

Galindo, Cristi L / Khan, Saifur / Zhang, Xiangyu / Yeh, Yu-Sheng / Liu, Ziyang / Razani, Babak

2023 Volume 27, Issue 12, Page(s) 1231–1245

Abstract: Introduction: Lipid-laden foam cells within atherosclerotic plaques are key players in all phases of lesion development including its progression, necrotic core formation, fibrous cap thinning, and eventually plaque rupture. Manipulating foam cell ... ...

Abstract	Introduction: Lipid-laden foam cells within atherosclerotic plaques are key players in all phases of lesion development including its progression, necrotic core formation, fibrous cap thinning, and eventually plaque rupture. Manipulating foam cell biology is thus an attractive therapeutic strategy at early, middle, and even late stages of atherosclerosis. Traditional therapies have focused on prevention, especially lowering plasma lipid levels. Despite these interventions, atherosclerosis remains a major cause of cardiovascular disease, responsible for the largest numbers of death worldwide. Areas covered: Foam cells within atherosclerotic plaques are comprised of macrophages, vascular smooth muscle cells, and other cell types which are exposed to high concentrations of lipoproteins accumulating within the subendothelial intimal layer. Macrophage-derived foam cells are particularly well studied and have provided important insights into lipid metabolism and atherogenesis. The contributions of foam cell-based processes are discussed with an emphasis on areas of therapeutic potential and directions for drug development. Exert opinion: As key players in atherosclerosis, foam cells are attractive targets for developing more specific, targeted therapies aimed at resolving atherosclerotic plaques. Recent advances in our understanding of lipid handling within these cells provide insights into how they might be manipulated and clinically translated to better treat atherosclerosis.
MeSH term(s)	Humans ; Foam Cells/metabolism ; Foam Cells/pathology ; Plaque, Atherosclerotic/drug therapy ; Plaque, Atherosclerotic/pathology ; Atherosclerosis/drug therapy ; Macrophages/metabolism ; Lipoproteins
Chemical Substances	Lipoproteins
Language	English
Publishing date	2023-12-30
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1080/14728222.2023.2288272
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Zs.A 5244: Show issues

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Article ; Online: metGWAS 1.0: an R workflow for network-driven over-representation analysis between independent metabolomic and meta-genome-wide association studies.

Khan, Saifur R / Obersterescu, Andreea / Gunderson, Erica P / Razani, Babak / Wheeler, Michael B / Cox, Brian J

Bioinformatics (Oxford, England)

2023 Volume 39, Issue 9

Abstract: Motivation: The method of genome-wide association studies (GWAS) and metabolomics combined provide an quantitative approach to pinpoint metabolic pathways and genes linked to specific diseases; however, such analyses require both genomics and ... ...

Abstract	Motivation: The method of genome-wide association studies (GWAS) and metabolomics combined provide an quantitative approach to pinpoint metabolic pathways and genes linked to specific diseases; however, such analyses require both genomics and metabolomics datasets from the same individuals/samples. In most cases, this approach is not feasible due to high costs, lack of technical infrastructure, unavailability of samples, and other factors. Therefore, an unmet need exists for a bioinformatics tool that can identify gene loci-associated polymorphic variants for metabolite alterations seen in disease states using standalone metabolomics. Results: Here, we developed a bioinformatics tool, metGWAS 1.0, that integrates independent GWAS data from the GWAS database and standalone metabolomics data using a network-based systems biology approach to identify novel disease/trait-specific metabolite-gene associations. The tool was evaluated using standalone metabolomics datasets extracted from two metabolomics-GWAS case studies. It discovered both the observed and novel gene loci with known single nucleotide polymorphisms when compared to the original studies. Availability and implementation: The developed metGWAS 1.0 framework is implemented in an R pipeline and available at: https://github.com/saifurbd28/metGWAS-1.0.
MeSH term(s)	Humans ; Genome-Wide Association Study ; Workflow ; Metabolomics ; Computational Biology ; Databases, Factual
Language	English
Publishing date	2023-08-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btad523
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Article ; Online: Integration of AI and traditional medicine in drug discovery.

Khan, Saifur R / Al Rijjal, Dana / Piro, Anthony / Wheeler, Michael B

Drug discovery today

2021 Volume 26, Issue 4, Page(s) 982–992

Abstract: AI integration in plant-based traditional medicine could be used to overcome drug discovery challenges. ...

Abstract	AI integration in plant-based traditional medicine could be used to overcome drug discovery challenges.
MeSH term(s)	Artificial Intelligence ; Drug Discovery/methods ; Drug Discovery/trends ; Humans ; Medicine, Traditional/methods ; Phytotherapy/methods
Language	English
Publishing date	2021-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2021.01.008
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Article: Heterogeneity in Early Postpartum Metabolic Profiles Among Women with GDM Who Progressed to Type 2 Diabetes During 10-Year Follow-Up: The SWIFT Study.

Khan, Saifur R / Rost, Hannes / Cox, Brian / Razani, Babak / Alexeeff, Stacey / Wheeler, Michael B / Gunderson, Erica P

medRxiv : the preprint server for health sciences

2023

Abstract: GDM is a strong risk factor for progression to T2D after pregnancy. Although both GDM and T2D exhibit heterogeneity, the link between the distinct heterogeneity of GDM and incident T2D has not been established. Herein, we evaluate early postpartum ... ...

Abstract	GDM is a strong risk factor for progression to T2D after pregnancy. Although both GDM and T2D exhibit heterogeneity, the link between the distinct heterogeneity of GDM and incident T2D has not been established. Herein, we evaluate early postpartum profiles of women with recent GDM who later developed incident T2D using a soft clustering method, followed by the integration of both clinical phenotypic variables and metabolomics to characterize these heterogeneous clusters/groups clinically and their molecular mechanisms. We identified three clusters based on two indices of glucose homeostasis at 6-9 weeks postpartum - HOMA-IR and HOMA-B among women who developed incident T2D during the 12-year follow-up. The clusters were classified as follows: pancreatic beta-cell dysfunction group (cluster-1), insulin resistant group (cluster-3), and a combination of both phenomena (cluster-2) comprising the majority of T2D. We also identified postnatal blood test parameters to distinguish the three clusters for clinical testing. Moreover, we compared these three clusters in their metabolomics profiles at the early stage of the disease to identify the mechanistic insights. A significantly higher concentration of a metabolite at the early stage of a T2D cluster than other clusters indicates its essentiality for the particular disease character. As such, the early-stage characters of T2D cluster-1 pathology include a higher concentration of sphingolipids, acyl-alkyl phosphatidylcholines, lysophosphatidylcholines, and glycine, indicating their essentiality for pancreatic beta-cell function. In contrast, the early-stage characteristics of T2D cluster-3 pathology include a higher concentration of diacyl phosphatidylcholines, acyl-carnitines, isoleucine, and glutamate, indicating their essentiality for insulin actions. Notably, all these biomolecules are found in the T2D cluster-2 with mediocre concentrations, indicating a true nature of a mixed group. In conclusion, we have deconstructed incident T2D heterogeneity and identified three clusters with their clinical testing procedures and molecular mechanisms. This information will aid in adopting proper interventions using a precision medicine approach.
Language	English
Publishing date	2023-06-16
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.13.23291346
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Article ; Online: Isoniazid and host immune system interactions: A proposal for a novel comprehensive mode of action.

Khan, Saifur R / Manialawy, Yousef / Siraki, Arno G

British journal of pharmacology

2019 Volume 176, Issue 24, Page(s) 4599–4608

Abstract: The known mode of action of isoniazid (INH) is to inhibit bacterial cell wall synthesis following activation by the bacterial catalase-peroxidase enzyme KatG in Mycobacterium tuberculosis (Mtb). This simplistic model fails to explain (a) how isoniazid ... ...

Abstract	The known mode of action of isoniazid (INH) is to inhibit bacterial cell wall synthesis following activation by the bacterial catalase-peroxidase enzyme KatG in Mycobacterium tuberculosis (Mtb). This simplistic model fails to explain (a) how isoniazid penetrates waxy granulomas with its very low lipophilicity, (b) how isoniazid kills latent Mtb lacking a typical cell wall, and (c) why isoniazid treatment time is remarkably long in contrast to most other antibiotics. To address these questions, a novel comprehensive mode of action of isoniazid has been proposed here. Briefly, isoniazid eradicates latent tuberculosis (TB) by prompting slow differentiation of pro-inflammatory monocytes and providing protection against reactive species-induced "self-necrosis" of phagocytes. In the case of active TB, different immune cells form INH-NAD
MeSH term(s)	Antitubercular Agents/pharmacology ; Bacterial Proteins/genetics ; Catalase/genetics ; Host Microbial Interactions/drug effects ; Host Microbial Interactions/immunology ; Humans ; Isoniazid/pharmacology ; Monocytes/drug effects ; Monocytes/immunology ; Mycobacterium tuberculosis/drug effects ; Mycobacterium tuberculosis/enzymology ; Oxidative Stress/drug effects ; Oxidative Stress/immunology ; Tuberculosis/blood ; Tuberculosis/drug therapy ; Tuberculosis/immunology
Chemical Substances	Antitubercular Agents ; Bacterial Proteins ; Catalase (EC 1.11.1.6) ; katG protein, Mycobacterium tuberculosis (EC 1.11.1.6) ; Isoniazid (V83O1VOZ8L)
Language	English
Publishing date	2019-11-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.14867
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Article ; Online: The magnesium transporter NIPAL1 is a pancreatic islet-expressed protein that conditionally impacts insulin secretion.

Manialawy, Yousef / Khan, Saifur R / Bhattacharjee, Alpana / Wheeler, Michael B

The Journal of biological chemistry

2020 Volume 295, Issue 29, Page(s) 9879–9892

Abstract: Type 2 diabetes is a chronic metabolic disease characterized by pancreatic β-cell dysfunction and peripheral insulin resistance. Among individuals with type 2 diabetes, ∼30% exhibit hypomagnesemia. Hypomagnesemia has been linked to insulin resistance ... ...

Abstract	Type 2 diabetes is a chronic metabolic disease characterized by pancreatic β-cell dysfunction and peripheral insulin resistance. Among individuals with type 2 diabetes, ∼30% exhibit hypomagnesemia. Hypomagnesemia has been linked to insulin resistance through reduced tyrosine kinase activity of the insulin receptor; however, its impact on pancreatic β-cell function is unknown. In this study, through analysis of several single-cell RNA-sequencing data sets in tandem with quantitative PCR validation in both murine and human islets, we identified
MeSH term(s)	Animals ; Cation Transport Proteins/biosynthesis ; Cation Transport Proteins/genetics ; Cell Line, Tumor ; Gene Expression Regulation ; Glucagon-Secreting Cells/cytology ; Glucagon-Secreting Cells/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/metabolism ; Magnesium/metabolism ; Male ; Mice
Chemical Substances	Cation Transport Proteins ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2020-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA120.013277
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Uc I Zs.108: Show issues

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Article ; Online: Unbiased data analytic strategies to improve biomarker discovery in precision medicine.

Khan, Saifur R / Manialawy, Yousef / Wheeler, Michael B / Cox, Brian J

Drug discovery today

2019 Volume 24, Issue 9, Page(s) 1735–1748

Abstract: Omics technologies promised improved biomarker discovery for precision medicine. The foremost problem of discovered biomarkers is irreproducibility between patient cohorts. From a data analytics perspective, the main reason for these failures is bias in ... ...

Abstract	Omics technologies promised improved biomarker discovery for precision medicine. The foremost problem of discovered biomarkers is irreproducibility between patient cohorts. From a data analytics perspective, the main reason for these failures is bias in statistical approaches and overfitting resulting from batch effects and confounding factors. The keys to reproducible biomarker discovery are: proper study design, unbiased data preprocessing and quality control analyses, and a knowledgeable application of statistics and machine learning algorithms. In this review, we discuss study design and analysis considerations and suggest standards from an expert point-of-view to promote unbiased decision-making in biomarker discovery in precision medicine.
MeSH term(s)	Biomarkers ; Computational Biology/methods ; Data Science/trends ; Electronic Data Processing/methods ; Humans ; Precision Medicine/trends ; Research Design/standards ; Research Design/trends
Chemical Substances	Biomarkers
Language	English
Publishing date	2019-05-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2019.05.018
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Article ; Online: Diminished Sphingolipid Metabolism, a Hallmark of Future Type 2 Diabetes Pathogenesis, Is Linked to Pancreatic β Cell Dysfunction.

Khan, Saifur R / Manialawy, Yousef / Obersterescu, Andreea / Cox, Brian J / Gunderson, Erica P / Wheeler, Michael B

iScience

2020 Volume 23, Issue 10, Page(s) 101566

Abstract: Gestational diabetes mellitus (GDM) is the top risk factor for future type 2 diabetes (T2D) development. Ethnicity profoundly influences who will transition from GDM to T2D, with high risk observed in Hispanic women. To better understand this risk, a ... ...

Abstract	Gestational diabetes mellitus (GDM) is the top risk factor for future type 2 diabetes (T2D) development. Ethnicity profoundly influences who will transition from GDM to T2D, with high risk observed in Hispanic women. To better understand this risk, a nested 1:1 pair-matched, Hispanic-specific, case-control design was applied to a prospective cohort with GDM history. Women who were non-diabetic 6-9 weeks postpartum (baseline) were monitored for the development of T2D. Metabolomics were performed on baseline plasma to identify metabolic pathways associated with T2D risk. Notably, diminished sphingolipid metabolism was highly associated with future T2D. Defects in sphingolipid metabolism were further implicated by integrating metabolomics and genome-wide association data, which identified two significantly enriched T2D-linked genes,
Language	English
Publishing date	2020-09-15
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2020.101566
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Article: Global protein expression dataset acquired during isoniazid-induced cytoprotection against H2O2 challenge in HL-60 cells.

Khan, Saifur R / Baghdasarian, Argishti / Fahlman, Richard P / Siraki, Arno G

Data in brief

2016 Volume 6, Page(s) 823–828

Abstract: Isoniazid (INH) is one of the first-line anti-tuberculosis drugs. Its effect on oxidative stress, however, is unknown. Here we used a model of oxidative stress by employing glucose/glucose oxidase (GOx), which (based on the availability of glucose and ... ...

Abstract	Isoniazid (INH) is one of the first-line anti-tuberculosis drugs. Its effect on oxidative stress, however, is unknown. Here we used a model of oxidative stress by employing glucose/glucose oxidase (GOx), which (based on the availability of glucose and oxygen) is known to produce H2O2. This reaction induces oxidative stress culminating in necrotic cell death in HL-60 cells (a human promyelocytic leukemia cell line). The changes in protein levels have been quantified using global proteome expression changes through stable isotope labeling by amino acids in cell culture (SILAC) followed by LC-MS/MS analysis. A total of 1459 and 1712 proteins were identified in forward and reverse experiments, respectively. However, only 390 proteins were reproducibly identified in both samples. These 390 proteins were taken into account for further analysis which has been described in "Cytoprotective effect of isoniazid against H2O2 derived injury in HL-60 cells" [1].
Language	English
Publishing date	2016-01-29
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2016.01.035
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Global protein expression dataset acquired during isoniazid-induced cytoprotection against H2O2 challenge in HL-60 cells

Khan, Saifur R. / Baghdasarian, Argishti / Fahlman, Richard P. / Siraki, Arno G.

Data in Brief. 2016 Mar., v. 6

2016

Abstract	Isoniazid (INH) is one of the first-line anti-tuberculosis drugs. Its effect on oxidative stress, however, is unknown. Here we used a model of oxidative stress by employing glucose/glucose oxidase (GOx), which (based on the availability of glucose and oxygen) is known to produce H₂O₂. This reaction induces oxidative stress culminating in necrotic cell death in HL-60 cells (a human promyelocytic leukemia cell line). The changes in protein levels have been quantified using global proteome expression changes through stable isotope labeling by amino acids in cell culture (SILAC) followed by LC–MS/MS analysis. A total of 1459 and 1712 proteins were identified in forward and reverse experiments, respectively. However, only 390 proteins were reproducibly identified in both samples. These 390 proteins were taken into account for further analysis which has been described in “Cytoprotective effect of isoniazid against H₂O₂ derived injury in HL-60 cells” [1].
Keywords	cell culture ; data collection ; glucose ; glucose oxidase ; humans ; isoniazid ; models ; necroptosis ; neoplasm cells ; oxidative stress ; oxygen ; protein synthesis ; proteome ; stable isotopes
Language	English
Dates of publication	2016-03
Size	p. 823-828.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2016.01.035
Database	NAL-Catalogue (AGRICOLA)

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