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Article ; Online: Autophagy in Atherosclerosis: Not All Foam Cells Are Created Equal.

Francis, Gordon A / Razani, Babak

2022 Volume 130, Issue 6, Page(s) 848–850

MeSH term(s)	Atherosclerosis ; Autophagy ; Foam Cells ; Humans
Language	English
Publishing date	2022-03-17
Publishing country	United States
Document type	Editorial ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.122.320857
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Article: Lead stimulates lymphocyte proliferation through enhanced T cell-B cell interaction.

Razani-Boroujerdi, S / Edwards, B / Sopori, M L

The Journal of pharmacology and experimental therapeutics

1999 Volume 288, Issue 2, Page(s) 714–719

Abstract: ... B cell populations. Pb failed to stimulate the proliferation of isolated T and B ... cells; however, the addition of gamma-irradiated B cells to T cell cultures or irradiated T cells to B cell cultures resulted ... facilitates the T cell-B cell interaction-dependent proliferation of lymphocytes through a signaling pathway(s ...

Abstract	We have studied the in vitro effects of lead (Pb) as Pb-acetate (0. 1-1000 ppm) on the activation of rat spleen (SP) cells. At a concentration of 0.5 to 200 ppm, Pb augmented the uptake of [3H]thymidine, progression of SP cells through the cell cycle, and allogeneic and syngeneic mixed lymphocyte reactions. However, at concentrations above 200 ppm, Pb inhibited the proliferation of these cells. To understand the cellular and molecular basis of these responses, we examined the effects of Pb on the proliferation of isolated T and/or B cell populations. Pb failed to stimulate the proliferation of isolated T and B cells; however, the addition of gamma-irradiated B cells to T cell cultures or irradiated T cells to B cell cultures resulted in Pb-induced incorporation of [3H]thymidine. On the other hand, macrophages were unable to reconstitute this response. Pb also induced a significant rise in the intracellular concentration of inositol 1,4,5-trisphosphate in SP cells; however, unlike the activation of lymphocytes through the antigen receptors, Pb did not significantly stimulate protein tyrosine kinase activity. These observations suggest that Pb facilitates the T cell-B cell interaction-dependent proliferation of lymphocytes through a signaling pathway(s) independent of the antigen receptor.
MeSH term(s)	Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/drug effects ; B-Lymphocytes/immunology ; Cell Communication/drug effects ; Cell Cycle/drug effects ; Dose-Response Relationship, Drug ; Inositol 1,4,5-Trisphosphate/metabolism ; Lead/pharmacology ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/physiology ; Lymphocyte Culture Test, Mixed ; Male ; Protein-Tyrosine Kinases/metabolism ; Rats ; Rats, Inbred Strains ; Spleen/cytology ; Spleen/drug effects ; Spleen/metabolism ; Stimulation, Chemical ; T-Lymphocytes/cytology ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology
Chemical Substances	Lead (2P299V784P) ; Inositol 1,4,5-Trisphosphate (85166-31-0) ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	1999-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
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Article ; Online: Amino Acid Metabolism and Atherosclerotic Cardiovascular Disease.

Anand, Sumit Kumar / Governale, Theresea-Anne / Zhang, Xiangyu / Razani, Babak / Yurdagul, Arif / Pattillo, Christopher B / Rom, Oren

The American journal of pathology

2024 Volume 194, Issue 4, Page(s) 510–524

Abstract: Despite significant advances in medical treatments and drug development, atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of death worldwide. Dysregulated lipid metabolism is a well-established driver of ASCVD. Unfortunately, even ... ...

Abstract	Despite significant advances in medical treatments and drug development, atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of death worldwide. Dysregulated lipid metabolism is a well-established driver of ASCVD. Unfortunately, even with potent lipid-lowering therapies, ASCVD-related deaths have continued to increase over the past decade, highlighting an incomplete understanding of the underlying risk factors and mechanisms of ASCVD. Accumulating evidence over the past decades indicates a correlation between amino acids and disease state. This review explores the emerging role of amino acid metabolism in ASCVD, uncovering novel potential biomarkers, causative factors, and therapeutic targets. Specifically, the significance of arginine and its related metabolites, homoarginine and polyamines, branched-chain amino acids, glycine, and aromatic amino acids, in ASCVD are discussed. These amino acids and their metabolites have been implicated in various processes characteristic of ASCVD, including impaired lipid metabolism, endothelial dysfunction, increased inflammatory response, and necrotic core development. Understanding the complex interplay between dysregulated amino acid metabolism and ASCVD provides new insights that may lead to the development of novel diagnostic and therapeutic approaches. Although further research is needed to uncover the precise mechanisms involved, it is evident that amino acid metabolism plays a role in ASCVD.
MeSH term(s)	Humans ; Cardiovascular Diseases ; Atherosclerosis ; Risk Factors ; Biomarkers ; Amino Acids/therapeutic use
Chemical Substances	Biomarkers ; Amino Acids
Language	English
Publishing date	2024-01-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2023.12.006
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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: PCSK9 Pleiotropism: In the Same Vein as Statins.

Park, Arick C / Zhang, Xiangyu / Yeh, Yu-Sheng / Razani, Babak

Circulation research

2022 Volume 131, Issue 11, Page(s) 890–892

MeSH term(s)	Proprotein Convertase 9/genetics ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Proprotein Convertases ; Serine Endopeptidases
Chemical Substances	PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Proprotein Convertases (EC 3.4.21.-) ; Serine Endopeptidases (EC 3.4.21.-)
Language	English
Publishing date	2022-11-10
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.122.322035
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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

Expert opinion on therapeutic targets

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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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: ... postpartum - HOMA-IR and HOMA-B among women who developed incident T2D during the 12-year follow-up ...

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: Preserving immune homeostasis with A20.

Razani, Bahram / Malynn, Barbara A / Ma, Averil

Advances in immunology

2020 Volume 148, Page(s) 1–48

Abstract: A20/TNFAIP3 is a TNF induced gene that plays a profound role in preserving cellular and organismal homeostasis (Lee, et al., 2000; Opipari etal., 1990). This protein has been linked to multiple human diseases via genetic, epigenetic, and an emerging ... ...

Abstract	A20/TNFAIP3 is a TNF induced gene that plays a profound role in preserving cellular and organismal homeostasis (Lee, et al., 2000; Opipari etal., 1990). This protein has been linked to multiple human diseases via genetic, epigenetic, and an emerging series of patients with mono-allelic coding mutations. Diverse cellular functions of this pleiotropically expressed protein include immune-suppressive, anti-inflammatory, and cell protective functions. The A20 protein regulates ubiquitin dependent cell signals; however, the biochemical mechanisms by which it performs these functions is surprisingly complex. Deciphering these cellular and biochemical facets of A20 dependent biology should greatly improve our understanding of murine and human disease pathophysiology as well as unveil new mechanisms of cell and tissue biology.
MeSH term(s)	Animals ; Autoimmunity ; Cell Death ; Homeostasis ; Humans ; Inflammation/immunology ; Mice ; Mutation/genetics ; Tumor Necrosis Factor alpha-Induced Protein 3/metabolism
Chemical Substances	TNFAIP3 protein, human (EC 3.4.19.12) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12)
Language	English
Publishing date	2020-10-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	80226-8
ISSN	1557-8445 ; 0065-2776
ISSN (online)	1557-8445
ISSN	0065-2776
DOI	10.1016/bs.ai.2020.10.001
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Article ; Online: Correction to: Subcutaneous Transplantation of White Adipose Tissue.

Yeh, Yu-Sheng / Iwase, Mari / Kawarasaki, Satoko / Kwon, Jungin / Rodriguez-Velez, Astrid / Zhang, Xiangyu / Jeong, Se-Jin / Goto, Tsuyoshi / Razani, Babak

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2662, Page(s) C1

Language	English
Publishing date	2023-05-29
Publishing country	United States
Document type	Published Erratum
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3167-6_22
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Article ; Online: Subcutaneous Transplantation of White Adipose Tissue.

Yeh, Yu-Sheng / Iwase, Mari / Kawarasaki, Satoko / Kwon, Jungin / Rodriguez-Velez, Astrid / Zhang, Xiangyu / Jeong, Se-Jin / Goto, Tsuyoshi / Razani, Babak

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2662, Page(s) 183–192

Abstract: In the research setting, white adipose tissue (WAT) transplantation, also known as fat transplantation, is often used to understand the physiological function of adipocytes or associated stromal vascular cells such as macrophages in the context of local ... ...

Abstract	In the research setting, white adipose tissue (WAT) transplantation, also known as fat transplantation, is often used to understand the physiological function of adipocytes or associated stromal vascular cells such as macrophages in the context of local and systemic metabolism. The mouse is the most common animal model used where WAT from a donor is transferred either to a subcutaneous site of the same organism or to a subcutaneous region of a recipient. Here, we describe in detail the procedure for heterologous fat transplantation, and, given the need for survival surgery, peri- and postoperative care and subsequent histological confirmation of fat grafts will also be discussed.
MeSH term(s)	Mice ; Animals ; Adipose Tissue, White/metabolism ; Adipocytes/metabolism ; Models, Animal ; Adipose Tissue/blood supply
Language	English
Publishing date	2023-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3167-6_16
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