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Article ; Online: Recent Cardiovascular Research highlights from the Americas.

Smart, Charles D / Madhur, Meena S

2019 Volume 115, Issue 2, Page(s) e22–e23

MeSH term(s)	Americas ; Animals ; Bibliometrics ; Biomedical Research ; Cardiology ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Cardiovascular System/metabolism ; Cardiovascular System/physiopathology ; Humans ; Periodicals as Topic ; Signal Transduction
Language	English
Publishing date	2019-01-22
Publishing country	England
Document type	Journal Article
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvy229
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Article ; Online: Immune Profiling Reveals Decreases in Circulating Regulatory and Exhausted T Cells in Human Hypertension.

Alexander, Matthew R / Dale, Bethany L / Smart, Charles D / Elijovich, Fernando / Wogsland, Cara E / Lima, Sierra M / Irish, Jonathan M / Madhur, Meena S

JACC. Basic to translational science

2023 Volume 8, Issue 3, Page(s) 319–336

Abstract: Evidence from nonhuman animal models demonstrates an important role for immune cells in hypertension, but immune cell changes in human hypertension are less clear. Using mass cytometry, we demonstrate novel and selective reductions in ... ...

Abstract	Evidence from nonhuman animal models demonstrates an important role for immune cells in hypertension, but immune cell changes in human hypertension are less clear. Using mass cytometry, we demonstrate novel and selective reductions in CCR10
Language	English
Publishing date	2023-01-04
Publishing country	United States
Document type	Journal Article
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2022.09.007
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Article ; Online: LNK/SH2B3 loss of function increases susceptibility to murine and human atrial fibrillation.

Cardiovascular research

2024

Abstract: Aims: The lymphocyte adaptor protein (LNK) is a negative regulator of cytokine and growth factor signaling. The rs3184504 variant in SH2B3 reduces LNK function and is linked to cardiovascular, inflammatory, and hematologic disorders including stroke. In ...

Abstract	Aims: The lymphocyte adaptor protein (LNK) is a negative regulator of cytokine and growth factor signaling. The rs3184504 variant in SH2B3 reduces LNK function and is linked to cardiovascular, inflammatory, and hematologic disorders including stroke. In mice, deletion of Lnk causes inflammation and oxidative stress. We hypothesized that Lnk-/- mice are susceptible to atrial fibrillation (AF) and that rs3184504 is associated with AF and AF-related stroke in humans. During inflammation, reactive lipid dicarbonyls are a major component of oxidative injury, and we further hypothesized that these mediators are critical drivers of the AF substrate in Lnk-/- mice. Methods and results: Lnk-/- or wild-type (WT) mice were treated with vehicle or 2-hydroxybenzylamine (2-HOBA), a dicarbonyl scavenger, for 3 months. Compared to WT, Lnk-/- mice displayed increased AF duration that was prevented by 2-HOBA. In the Lnk-/- atria, action potentials were prolonged with reduced transient outward K+ current, increased late Na+ current, and reduced peak Na+ current, proarrhythmic effects that were inhibited by 2-HOBA. Mitochondrial dysfunction, especially for complex I, was evident in Lnk-/- atria, while scavenging lipid dicarbonyls prevented this abnormality. Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were elevated in Lnk-/- plasma and atrial tissue, respectively, both of which caused electrical and bioenergetic remodeling in vitro. Inhibition of soluble TNF-α prevented electrical remodeling and AF susceptibility, while IL-1β inhibition improved mitochondrial respiration but had no effect on AF susceptibility. In a large database of genotyped patients, rs3184504 was associated with AF, as well as AF-related stroke. Conclusions: These findings identify a novel role for LNK in the pathophysiology of AF in both experimental mice and in humans. Moreover, reactive lipid dicarbonyls are critical to the inflammatory AF substrate in Lnk-/- mice and mediate the proarrhythmic effects of pro-inflammatory cytokines, primarily through electrical remodeling.
Language	English
Publishing date	2024-02-20
Publishing country	England
Document type	Journal Article
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvae036
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Article ; Online: A Single Nucleotide Polymorphism in

Alexander, Matthew R / Hank, Samuel / Dale, Bethany L / Himmel, Lauren / Zhong, Xue / Smart, Charles D / Fehrenbach, Daniel J / Chen, Yuhan / Prabakaran, Nitin / Tirado, Brian / Centrella, Megan / Ao, Mingfang / Du, Liping / Shyr, Yu / Levy, Daniel / Madhur, Meena S

Circulation research

2022 Volume 131, Issue 9, Page(s) 731–747

Abstract: Background: SH2B3 (SH2B adaptor protein 3) is an adaptor protein that negatively regulates cytokine signaling and cell proliferation. A common missense single nucleotide polymorphism in : Methods: We used CRISPR-Cas9 technology to create mice ... ...

Abstract	Background: SH2B3 (SH2B adaptor protein 3) is an adaptor protein that negatively regulates cytokine signaling and cell proliferation. A common missense single nucleotide polymorphism in Methods: We used CRISPR-Cas9 technology to create mice homozygous for the major (Arg/Arg) and minor (Trp/Trp) alleles of this Results: Trp/Trp mice exhibit 10 mmHg higher systolic BP during chronic Ang II infusion compared to Arg/Arg controls. Renal injury and perivascular fibrosis are exacerbated in Trp/Trp mice compared to Arg/Arg controls following Ang II infusion. Renal and ex vivo stimulated splenic CD8 Conclusions: Taken together, these results suggest that the Trp encoding allele of rs3184504 is causal for BP elevation and renal dysfunction, in part through loss of SH2B3-mediated repression of T cell IL-12 signaling leading to enhanced IFNg production.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Angiotensin II/metabolism ; Angiotensin II/toxicity ; Animals ; Arginine/adverse effects ; Arginine/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Fibrosis ; Genome-Wide Association Study ; Humans ; Hypertension/metabolism ; Hypertension, Renal/metabolism ; Interferon-gamma/metabolism ; Interleukin-12/adverse effects ; Interleukin-12/metabolism ; Kidney/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Polymorphism, Single Nucleotide ; Tryptophan
Chemical Substances	Adaptor Proteins, Signal Transducing ; Lnk protein, mouse ; Angiotensin II (11128-99-7) ; Interleukin-12 (187348-17-0) ; Interferon-gamma (82115-62-6) ; Tryptophan (8DUH1N11BX) ; Arginine (94ZLA3W45F)
Language	English
Publishing date	2022-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.320625
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Article ; Online: Growth Arrest Specific-6 and Axl Coordinate Inflammation and Hypertension.

Van Beusecum, Justin P / Barbaro, Natalia R / Smart, Charles D / Patrick, David M / Loperena, Roxana / Zhao, Shilin / de la Visitacion, Nestor / Ao, Mingfang / Xiao, Liang / Shibao, Cyndya A / Harrison, David G

Circulation research

2021 Volume 129, Issue 11, Page(s) 975–991

Abstract: Figure: see text]. ...

Abstract	[Figure: see text].
MeSH term(s)	Adult ; Aged ; Angiotensin II/metabolism ; Animals ; Cells, Cultured ; Dendritic Cells/metabolism ; Endothelial Cells/metabolism ; Female ; Humans ; Hypertension/metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Interleukin-1beta/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Monocytes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/metabolism
Chemical Substances	Intercellular Signaling Peptides and Proteins ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Proto-Oncogene Proteins ; growth arrest-specific protein 6 ; Angiotensin II (11128-99-7) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1)
Language	English
Publishing date	2021-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.319643
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Article ; Online: Hypertension: Do Inflammation and Immunity Hold the Key to Solving this Epidemic?

Madhur, Meena S / Elijovich, Fernando / Alexander, Matthew R / Pitzer, Ashley / Ishimwe, Jeanne / Van Beusecum, Justin P / Patrick, David M / Smart, Charles D / Kleyman, Thomas R / Kingery, Justin / Peck, Robert N / Laffer, Cheryl L / Kirabo, Annet

Circulation research

2021 Volume 128, Issue 7, Page(s) 908–933

Abstract: Elevated cardiovascular risk including stroke, heart failure, and heart attack is present even after normalization of blood pressure in patients with hypertension. Underlying immune cell activation is a likely culprit. Although immune cells are important ...

Abstract	Elevated cardiovascular risk including stroke, heart failure, and heart attack is present even after normalization of blood pressure in patients with hypertension. Underlying immune cell activation is a likely culprit. Although immune cells are important for protection against invading pathogens, their chronic overactivation may lead to tissue damage and high blood pressure. Triggers that may initiate immune activation include viral infections, autoimmunity, and lifestyle factors such as excess dietary salt. These conditions activate the immune system either directly or through their impact on the gut microbiome, which ultimately produces chronic inflammation and hypertension. T cells are central to the immune responses contributing to hypertension. They are activated in part by binding specific antigens that are presented in major histocompatibility complex molecules on professional antigen-presenting cells, and they generate repertoires of rearranged T-cell receptors. Activated T cells infiltrate tissues and produce cytokines including interleukin 17A, which promote renal and vascular dysfunction and end-organ damage leading to hypertension. In this comprehensive review, we highlight environmental, genetic, and microbial associated mechanisms contributing to both innate and adaptive immune cell activation leading to hypertension. Targeting the underlying chronic immune cell activation in hypertension has the potential to mitigate the excess cardiovascular risk associated with this common and deadly disease.
MeSH term(s)	Antihypertensive Agents/therapeutic use ; B-Lymphocytes/immunology ; Complement System Proteins/immunology ; Cytokines/immunology ; Dendritic Cells/immunology ; Drug Resistance ; Female ; Gastrointestinal Microbiome/immunology ; Heart Disease Risk Factors ; Host Microbial Interactions ; Humans ; Hypertension/drug therapy ; Hypertension/immunology ; Immune System Phenomena ; Immunity, Cellular/physiology ; Immunity, Innate ; Inflammasomes/immunology ; Inflammation/genetics ; Inflammation/immunology ; Lymphocyte Activation/immunology ; Macrophages/immunology ; Male ; Monocytes/immunology ; Sex Factors ; Sodium Chloride, Dietary/adverse effects ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes, Regulatory/immunology ; Virus Diseases/immunology
Chemical Substances	Antihypertensive Agents ; Cytokines ; Inflammasomes ; Sodium Chloride, Dietary ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2021-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.318052
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Article ; Online: Class switching and high-affinity immunoglobulin G production by B cells is dispensable for the development of hypertension in mice.

Chen, Yuhan / Dale, Bethany L / Alexander, Matthew R / Xiao, Liang / Ao, Mingfang / Pandey, Arvind K / Smart, Charles D / Davis, Gwendolyn K / Madhur, Meena S

Cardiovascular research

2020 Volume 117, Issue 4, Page(s) 1217–1228

Abstract: Aims: Elevated serum immunoglobulins have been associated with experimental and human hypertension for decades but whether immunoglobulins and B cells play a causal role in hypertension pathology is unclear. In this study, we sought to determine the ... ...

Abstract	Aims: Elevated serum immunoglobulins have been associated with experimental and human hypertension for decades but whether immunoglobulins and B cells play a causal role in hypertension pathology is unclear. In this study, we sought to determine the role of B cells and high-affinity class-switched immunoglobulins on hypertension and hypertensive end-organ damage to determine if they might represent viable therapeutic targets for this disease. Methods and results: We purified serum immunoglobulin G (IgG) from mice exposed to vehicle or angiotensin (Ang) II to induce hypertension and adoptively transferred these to wild type (WT) recipient mice receiving a subpressor dose of Ang II. We found that transfer of IgG from hypertensive animals does not affect blood pressure, endothelial function, renal inflammation, albuminuria, or T cell-derived cytokine production compared with transfer of IgG from vehicle infused animals. As an alternative approach to investigate the role of high-affinity, class-switched immunoglobulins, we studied mice with genetic deletion of activation-induced deaminase (Aicda-/-). These mice have elevated levels of IgM but virtual absence of class-switched immunoglobulins such as IgG subclasses and IgA. Neither male nor female Aicda-/- mice were protected from Ang II-induced hypertension and renal/vascular damage. To determine if IgM or non-immunoglobulin-dependent innate functions of B cells play a role in hypertension, we studied mice with severe global B-cell deficiency due to deletion of the membrane exon of the IgM heavy chain (µMT-/-). µMT-/- mice were also not protected from hypertension or end-organ damage induced by Ang II infusion or deoxycorticosterone acetate-salt treatment. Conclusions: These results suggest that B cells and serum immunoglobulins do not play a causal role in hypertension pathology.
MeSH term(s)	Angiotensin II ; Animals ; Antibody Affinity ; Aorta/immunology ; Aorta/metabolism ; Aorta/pathology ; Blood Pressure/immunology ; Cells, Cultured ; Cytidine Deaminase/genetics ; Cytidine Deaminase/metabolism ; Desoxycorticosterone Acetate ; Disease Models, Animal ; Female ; Hypertension/blood ; Hypertension/genetics ; Hypertension/immunology ; Hypertension/physiopathology ; Immunoglobulin Class Switching ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Heavy Chains/immunology ; Immunoglobulin Heavy Chains/metabolism ; Immunoglobulin M/genetics ; Immunoglobulin M/immunology ; Immunoglobulin M/metabolism ; Kidney/immunology ; Kidney/metabolism ; Kidney/pathology ; Male ; Memory B Cells/immunology ; Memory B Cells/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Sodium Chloride, Dietary ; Mice
Chemical Substances	Immunoglobulin G ; Immunoglobulin Heavy Chains ; Immunoglobulin M ; Sodium Chloride, Dietary ; Angiotensin II (11128-99-7) ; Desoxycorticosterone Acetate (6E0A168OB8) ; AICDA (activation-induced cytidine deaminase) (EC 3.5.4.-) ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2020-06-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvaa187
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Article ; Online: Predicting susceptibility to SARS-CoV-2 infection based on structural differences in ACE2 across species.

Alexander, Matthew R / Schoeder, Clara T / Brown, Jacquelyn A / Smart, Charles D / Moth, Chris / Wikswo, John P / Capra, John A / Meiler, Jens / Chen, Wenbiao / Madhur, Meena S

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2020 Volume 34, Issue 12, Page(s) 15946–15960

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the global pandemic of coronavirus disease-2019 (COVID-19). SARS-CoV-2 is a zoonotic disease, but little is known about variations in species susceptibility that could identify ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the global pandemic of coronavirus disease-2019 (COVID-19). SARS-CoV-2 is a zoonotic disease, but little is known about variations in species susceptibility that could identify potential reservoir species, animal models, and the risk to pets, wildlife, and livestock. Certain species, such as domestic cats and tigers, are susceptible to SARS-CoV-2 infection, while other species such as mice and chickens are not. Most animal species, including those in close contact with humans, have unknown susceptibility. Hence, methods to predict the infection risk of animal species are urgently needed. SARS-CoV-2 spike protein binding to angiotensin-converting enzyme 2 (ACE2) is critical for viral cell entry and infection. Here we integrate species differences in susceptibility with multiple in-depth structural analyses to identify key ACE2 amino acid positions including 30, 83, 90, 322, and 354 that distinguish susceptible from resistant species. Using differences in these residues across species, we developed a susceptibility score that predicts an elevated risk of SARS-CoV-2 infection for multiple species including horses and camels. We also demonstrate that SARS-CoV-2 is nearly optimal for binding ACE2 of humans compared to other animals, which may underlie the highly contagious transmissibility of this virus among humans. Taken together, our findings define potential ACE2 and SARS-CoV-2 residues for therapeutic targeting and identification of animal species on which to focus research and protection measures for environmental and public health.
MeSH term(s)	Amino Acid Sequence ; Angiotensin-Converting Enzyme 2/chemistry ; Angiotensin-Converting Enzyme 2/genetics ; Animals ; COVID-19/genetics ; Camelus ; Genetic Predisposition to Disease ; Glycosylation ; Horses ; Humans ; Models, Molecular ; Phylogeny ; Protein Binding ; Protein Structure, Tertiary ; Receptors, Virus/chemistry ; Receptors, Virus/genetics ; SARS-CoV-2 ; Sequence Alignment ; Species Specificity
Chemical Substances	Receptors, Virus ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Keywords	covid19
Language	English
Publishing date	2020-10-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202001808R
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Article ; Online: Isolevuglandins disrupt PU.1-mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus.

JCI insight

2022 Volume 7, Issue 13

Abstract: We describe a mechanism responsible for systemic lupus erythematosus (SLE). In humans with SLE and in 2 SLE murine models, there was marked enrichment of isolevuglandin-adducted proteins (isoLG adducts) in monocytes and dendritic cells. We found that ... ...

Abstract	We describe a mechanism responsible for systemic lupus erythematosus (SLE). In humans with SLE and in 2 SLE murine models, there was marked enrichment of isolevuglandin-adducted proteins (isoLG adducts) in monocytes and dendritic cells. We found that antibodies formed against isoLG adducts in both SLE-prone mice and humans with SLE. In addition, isoLG ligation of the transcription factor PU.1 at a critical DNA binding site markedly reduced transcription of all C1q subunits. Treatment of SLE-prone mice with the specific isoLG scavenger 2-hydroxybenzylamine (2-HOBA) ameliorated parameters of autoimmunity, including plasma cell expansion, circulating IgG levels, and anti-dsDNA antibody titers. 2-HOBA also lowered blood pressure, attenuated renal injury, and reduced inflammatory gene expression uniquely in C1q-expressing dendritic cells. Thus, isoLG adducts play an essential role in the genesis and maintenance of systemic autoimmunity and hypertension in SLE.
MeSH term(s)	Animals ; Antibodies, Antinuclear ; Autoimmunity ; Complement C1q/genetics ; Hypertension ; Lipids ; Lupus Erythematosus, Systemic ; Mice
Chemical Substances	Antibodies, Antinuclear ; Lipids ; anti-dsDNA autoantibody ; isolevuglandin ; Complement C1q (80295-33-6)
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.136678
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Article ; Online: Predicting susceptibility to SARS‐CoV‐2 infection based on structural differences in ACE2 across species

Alexander, Matthew R. / Schoeder, Clara T. / Brown, Jacquelyn A. / Smart, Charles D. / Moth, Chris / Wikswo, John P. / Capra, John A. / Meiler, Jens / Chen, Wenbiao / Madhur, Meena S.

The FASEB Journal ; ISSN 0892-6638 1530-6860

2020

Keywords	Biotechnology ; Genetics ; Biochemistry ; Molecular Biology ; covid19
Language	English
Publisher	Wiley
Publishing country	us
Document type	Article ; Online
DOI	10.1096/fj.202001808r
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