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Article ; Online: The predictive potential of circulating microRNA for future cardiovascular events.

Johnson, Jason L

2020 Volume 117, Issue 1, Page(s) 1–3

MeSH term(s)	Cardiovascular Diseases/diagnosis ; Circulating MicroRNA/genetics ; Humans ; Hyperlipoproteinemia Type II ; MicroRNAs/genetics
Chemical Substances	Circulating MicroRNA ; MicroRNAs
Language	English
Publishing date	2020-05-12
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvaa145
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Article ; Online: Investigation of Atherosclerotic Plaque Vulnerability.

George, Sarah J / Johnson, Jason L

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

2022 Volume 2419, Page(s) 521–535

Abstract: Histochemical and immunohistochemical approaches permit the detection and evaluation of proteins and cell types within murine brachiocephalic artery atherosclerotic plaques, that can be subsequently analyzed to provide inferences on atherosclerotic ... ...

Abstract	Histochemical and immunohistochemical approaches permit the detection and evaluation of proteins and cell types within murine brachiocephalic artery atherosclerotic plaques, that can be subsequently analyzed to provide inferences on atherosclerotic plaque vulnerability. Here we describe the specific histochemical techniques deployed to examine the expression of elastin, fibrillar collagens, and neutral lipids, alongside immunohistochemistry protocols for the identification of macrophages (CD68) and vascular smooth muscle cells (α-smooth muscle actin). We will also describe how analyses derived from these methods can be combined to determine evidence of previous plaque rupture and susceptibility to rupture.
MeSH term(s)	Animals ; Immunohistochemistry ; Macrophages/metabolism ; Mice ; Myocytes, Smooth Muscle/metabolism ; Plaque, Atherosclerotic/metabolism
Language	English
Publishing date	2022-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1924-7_32
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Article ; Online: Elucidating the contributory role of microRNA to cardiovascular diseases (a review).

Johnson, Jason L

Vascular pharmacology

2018 Volume 114, Page(s) 31–48

Abstract: Cardiovascular diseases encompassing atherosclerosis, aortic aneurysms, restenosis, and pulmonary arterial hypertension, remain the leading cause of morbidity and mortality worldwide. In response to a range of stimuli, the dynamic interplay between ... ...

Abstract	Cardiovascular diseases encompassing atherosclerosis, aortic aneurysms, restenosis, and pulmonary arterial hypertension, remain the leading cause of morbidity and mortality worldwide. In response to a range of stimuli, the dynamic interplay between biochemical and biomechanical mechanisms affect the behaviour and function of multiple cell types, driving the development and progression of cardiovascular diseases. Accumulating evidence has highlighted microRNAs (miRs) as significant regulators and micro-managers of key cellular and molecular pathophysiological processes involved in predominant cardiovascular diseases, including cell mitosis, motility and viability, lipid metabolism, generation of inflammatory mediators, and dysregulated proteolysis. Human pathological and clinical studies have aimed to identify select microRNA which may serve as biomarkers of disease and their progression, which are discussed within this review. In addition, I provide comprehensive coverage of in vivo investigations elucidating the modulation of distinct microRNA on the pathophysiology of atherosclerosis, abdominal aortic aneurysms, restenosis, and pulmonary arterial hypertension. Collectively, clinical and animal studies have begun to unravel the complex and often diverse effects microRNAs and their targets impart during the development of cardiovascular diseases and revealed promising therapeutic strategies through which modulation of microRNA function may be applied clinically.
MeSH term(s)	Animals ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Cardiovascular Diseases/therapy ; Cardiovascular System/metabolism ; Cardiovascular System/pathology ; Gene Expression Regulation ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Signal Transduction
Chemical Substances	MicroRNAs
Language	English
Publishing date	2018-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2082846-9
ISSN	1879-3649 ; 1537-1891 ; 1879-3649
ISSN (online)	1879-3649 ; 1537-1891
ISSN	1879-3649
DOI	10.1016/j.vph.2018.10.010
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Zs.A 591: Show issues

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Article: The contribution of matrix metalloproteinases and their inhibitors to the development, progression, and rupture of abdominal aortic aneurysms.

Atkinson, Georgia / Bianco, Rosaria / Di Gregoli, Karina / Johnson, Jason L

Frontiers in cardiovascular medicine

2023 Volume 10, Page(s) 1248561

Abstract: Abdominal aortic aneurysms (AAAs) account for up to 8% of deaths in men aged 65 years and over and 2.2% of women. Patients with AAAs often have atherosclerosis, and intimal atherosclerosis is generally present in AAAs. Accordingly, AAAs are considered a ... ...

Abstract	Abdominal aortic aneurysms (AAAs) account for up to 8% of deaths in men aged 65 years and over and 2.2% of women. Patients with AAAs often have atherosclerosis, and intimal atherosclerosis is generally present in AAAs. Accordingly, AAAs are considered a form of atherosclerosis and are frequently referred to as atherosclerotic aneurysms. Pathological observations advocate inflammatory cell infiltration alongside adverse extracellular matrix degradation as key contributing factors to the formation of human atherosclerotic AAAs. Therefore, macrophage production of proteolytic enzymes is deemed responsible for the damaging loss of ECM proteins, especially elastin and fibrillar collagens, which characterise AAA progression and rupture. Matrix metalloproteinases (MMPs) and their regulation by tissue inhibitors metalloproteinases (TIMPs) can orchestrate not only ECM remodelling, but also moderate the proliferation, migration, and apoptosis of resident aortic cells, alongside the recruitment and subsequent behaviour of inflammatory cells. Accordingly, MMPs are thought to play a central regulatory role in the development, progression, and eventual rupture of abdominal aortic aneurysms (AAAs). Together, clinical and animal studies have shed light on the complex and often diverse effects MMPs and TIMPs impart during the development of AAAs. This dichotomy is underlined from evidence utilising broad-spectrum MMP inhibition in animal models and clinical trials which have failed to provide consistent protection from AAA progression, although more encouraging results have been observed through deployment of selective inhibitors. This review provides a summary of the supporting evidence connecting the contribution of individual MMPs to AAA development, progression, and eventual rupture. Topics discussed include structural, functional, and cell-specific diversity of MMP members; evidence from animal models of AAA and comparisons with findings in humans; the dual role of MMPs and the requirement to selectively target individual MMPs; and the advances in identifying aberrant MMP activity. As evidenced, our developing understanding of the multifaceted roles individual MMPs perform during the progression and rupture of AAAs, should motivate clinical trials assessing the therapeutic potential of selective MMP inhibitors, which could restrict AAA-related morbidity and mortality worldwide.
Language	English
Publishing date	2023-09-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2023.1248561
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Article ; Online: Metalloproteinases in atherosclerosis.

Johnson, Jason L

European journal of pharmacology

2017 Volume 816, Page(s) 93–106

Abstract: Atherosclerosis underlies most cardiovascular diseases, and is accepted as a primary cause of mortality worldwide. Proteases have been implicated in the development and progression of atherosclerosis, due to their ability to provoke focal destruction of ... ...

Abstract	Atherosclerosis underlies most cardiovascular diseases, and is accepted as a primary cause of mortality worldwide. Proteases have been implicated in the development and progression of atherosclerosis, due to their ability to provoke focal destruction of the vascular extracellular matrix. Members of the metalloproteinase family, especially matrix metalloproteinases (MMPs), and their endogenous tissue inhibitors (TIMPs) have been suggested to perform complex dual roles during late-stage progression and rupture of atherosclerotic plaques. Proposed favourable actions of metalloproteinases include the promotion of vascular smooth muscle growth and survival which stabilises plaques, while conversely extracellular matrix destruction alongside interminable monocyte/macrophage accumulation can encourage plaque rupture. This review provides a summary of the cogent evidence connecting the contribution of individual metalloproteinases to atherosclerotic plaque development, progression, and instability. Topics discussed include structural, functional and cell-specific diversity of MMP members; evidence from animal models of atherosclerosis and comparisons with findings in humans; the dual role of MMPs and the requirement to selectively target individual MMPs; and the need for efficient surrogate markers of MMP inhibition. Accordingly, as our knowledge of the complex roles individual MMPs play especially during the progression and rupture of atherosclerotic plaques expands, new impetus is required for clinical trials evaluating the therapeutic potential of selective MMP inhibition, which could limit cardiovascular morbidity and mortality worldwide.
MeSH term(s)	Animals ; Atherosclerosis/enzymology ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Humans ; Metalloproteases/genetics ; Metalloproteases/metabolism
Chemical Substances	Metalloproteases (EC 3.4.-)
Language	English
Publishing date	2017-09-09
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2017.09.007
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Zs.A 522: Show issues

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Article ; Online: Monitoring Cellular Proliferation and Apoptosis in Atherosclerosis Plaques and Intimal Thickenings.

Wadey, Kerry S / Johnson, Jason L / George, Sarah J

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

2022 Volume 2419, Page(s) 507–519

Abstract: Immunohistochemistry for specific proteins characteristic of proliferative or apoptotic cells allows for monitoring of these cell behaviors in biological tissues samples, including atherosclerotic plaques and intimal thickenings. Proliferating cell ... ...

Abstract	Immunohistochemistry for specific proteins characteristic of proliferative or apoptotic cells allows for monitoring of these cell behaviors in biological tissues samples, including atherosclerotic plaques and intimal thickenings. Proliferating cell nuclear antigen (PCNA) and Ki-67 are widely used markers of cell proliferation and cleaved caspase-3 is a well-established marker of apoptosis that can be detected in tissue samples using immunohistochemistry. This technique enables quantification of the abundance of these proteins and provides information on the distribution of these biomarkers in tissues. By combining with immunohistochemistry for specific cell type markers, it is also possible to determine which cell types are proliferating or undergoing apoptosis. Here, we detail protocols for immunohistochemistry of PCNA, Ki-67, and cleaved caspase-3 for evaluation of cellular proliferation and apoptosis in atherosclerotic plaques in vivo. In addition, we outline methods for the quantification and localization of cell proliferation using bromodeoxyuridine/5-bromo-2'-deoxyuridine (BrdU) and ethynyldeoxyuridine/5-ethynyl-2 ́-deoxyuridine(EdU) labeled tissue samples collected from animals exposed to BrdU or EdU.
MeSH term(s)	Animals ; Apoptosis ; Atherosclerosis ; Bromodeoxyuridine/metabolism ; Cell Division ; Cell Proliferation ; Ki-67 Antigen/metabolism ; Plaque, Atherosclerotic ; Proliferating Cell Nuclear Antigen/metabolism
Chemical Substances	Ki-67 Antigen ; Proliferating Cell Nuclear Antigen ; Bromodeoxyuridine (G34N38R2N1)
Language	English
Publishing date	2022-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1924-7_31
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Article ; Online: Use of Mouse Carotid Artery Ligation Model of Intimal Thickening to Probe Vascular Smooth Muscle Cell Remodeling and Function in Atherosclerosis.

Williams, Helen / Brown, Bethan A / Johnson, Jason L / George, Sarah J

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

2022 Volume 2419, Page(s) 537–560

Abstract: The thickening of the intima is a critical underlying component of atherosclerosis. Consequently, robust and reproducible animal models of intimal thickening are essential for a greater understanding of the mechanisms underlying the process of intimal ... ...

Abstract	The thickening of the intima is a critical underlying component of atherosclerosis. Consequently, robust and reproducible animal models of intimal thickening are essential for a greater understanding of the mechanisms underlying the process of intimal thickening and to evaluate new approaches for the reduction of intimal thickening and thereby atherosclerosis. The ligation of the carotid artery in the mouse causes the thickening of the intimal layer of the artery. This model is relatively simple and is reproducible and therefore is a preferred and well-established model of intimal thickening. Here, we detail a protocol for carotid artery ligation in the mouse and methods for histological examination and quantification of intimal thickening.
MeSH term(s)	Animals ; Atherosclerosis/pathology ; Carotid Arteries/pathology ; Carotid Arteries/surgery ; Disease Models, Animal ; Mice ; Muscle, Smooth, Vascular/physiology ; Myocytes, Smooth Muscle/pathology
Language	English
Publishing date	2022-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1924-7_33
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Article ; Online: Inhibition of Intimal Thickening By PRH (Proline-Rich Homeodomain) in Mice.

Reolizo, Lien M / Williams, Helen / Wadey, Kerry / Frankow, Aleksandra / Li, Ze / Gaston, Kevin / Jayaraman, Padma-Sheela / Johnson, Jason L / George, Sarah J

Arteriosclerosis, thrombosis, and vascular biology

2023 Volume 43, Issue 3, Page(s) 456–473

Abstract: Background: Late vein graft failure is caused by intimal thickening resulting from endothelial cell (EC) damage and inflammation which promotes vascular smooth muscle cell (VSMC) dedifferentiation, migration, and proliferation. Nonphosphorylatable PRH ( ... ...

Abstract	Background: Late vein graft failure is caused by intimal thickening resulting from endothelial cell (EC) damage and inflammation which promotes vascular smooth muscle cell (VSMC) dedifferentiation, migration, and proliferation. Nonphosphorylatable PRH (proline-rich homeodomain) S163C:S177C offers enhanced stability and sustained antimitotic effect. Therefore, we investigated whether adenovirus-delivered PRH S163C:S177C protein attenuates intimal thickening via VSMC phenotype modification without detrimental effects on ECs. Methods: PRH S163C:S177C was expressed in vitro (human saphenous vein-VSMCs and human saphenous vein-ECs) and in vivo (ligated mouse carotid arteries) by adenoviruses. Proliferation, migration, and apoptosis were quantified and phenotype was assessed using Western blotting for contractile filament proteins and collagen gel contraction. EC inflammation was quantified using VCAM (vascular cell adhesion protein)-1, ICAM (intercellular adhesion molecule)-1, interleukin-6, and monocyte chemotactic factor-1 measurement and monocyte adhesion. Next Generation Sequencing was utilized to identify novel downstream mediators of PRH action and these and intimal thickening were investigated in vivo. Results: PRH S163C:S177C inhibited proliferation, migration, and apoptosis and promoted contractile phenotype (enhanced contractile filament proteins and collagen gel contraction) compared with virus control in human saphenous vein-VSMCs. PRH S163C:S177C expression in human saphenous vein-ECs significantly reduced apoptosis, without affecting cell proliferation and migration, while reducing TNF (tumor necrosis factor)-α-induced VCAM-1 and ICAM-1 and monocyte adhesion and suppressing interleukin-6 and monocyte chemotactic factor-1 protein levels. PRH S163C:S177C expression in ligated murine carotid arteries significantly impaired carotid artery ligation-induced neointimal proliferation and thickening without reducing endothelial coverage. Next Generation Sequencing revealed STAT-1 (signal transducer and activator of transcription 1) and HDAC-9 (histone deacetylase 9) as mediators of PRH action and was supported by in vitro and in vivo analyses. Conclusions: We observed PRH S163C:S177C attenuated VSMC proliferation, and migration and enhanced VSMC differentiation at least in part via STAT-1 and HDAC-9 signaling while promoting endothelial repair and anti-inflammatory properties. These findings highlight the potential for PRH S163C:S177C to preserve endothelial function whilst suppressing intimal thickening, and reducing late vein graft failure.
MeSH term(s)	Mice ; Animals ; Humans ; Interleukin-6/metabolism ; Tunica Intima/pathology ; Cell Proliferation ; Neointima/pathology ; Chemotactic Factors/metabolism ; Chemotactic Factors/pharmacology ; Myocytes, Smooth Muscle/metabolism ; Cell Movement
Chemical Substances	Interleukin-6 ; Chemotactic Factors
Language	English
Publishing date	2023-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.122.318367
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Zs.A 1705: Show issues

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Article ; Online: Monitoring Cellular Proliferation, Migration, and Apoptosis Associated with Atherosclerosis Plaques In Vitro.

Wadey, Kerry S / Somos, Alexandros / Cross, Stephen J / Reolizo, Lien M / Johnson, Jason L / George, Sarah J

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

2022 Volume 2419, Page(s) 133–167

Abstract: Bromodeoxyuridine/5-bromo-2'-deoxyuridine (BrdU) is a nucleoside analog of thymidine and its incorporation into DNA during replication within S-phase of the cell cycle is used to quantify cell proliferation. Quantification of incorporated BrdU is ... ...

Abstract	Bromodeoxyuridine/5-bromo-2'-deoxyuridine (BrdU) is a nucleoside analog of thymidine and its incorporation into DNA during replication within S-phase of the cell cycle is used to quantify cell proliferation. Quantification of incorporated BrdU is considered the most direct measure of cell proliferation, and here we describe BrdU incorporation into cultured vascular smooth muscle cells (VSMCs) and endothelial cells in vitro. Incorporation of fluorescent-labeled ethynyldeoxyuridine/5-ethynyl-2'-deoxyuridine (EdU) is a novel alternative to BrdU assays and presents significant advantages. This method of detection of EdU based on a simple "click" chemical reaction, which covalently bonds EdU to a fluorescent dye is also outlined in this chapter with a protocol for quantitative analysis of EdU incorporation using a Fiji-based macro. We also describe how proliferation can be assessed by quantification of classical proliferative markers such as phopsho-Ser807/811 retinoblastoma (Rb), proliferating cell nuclear antigen (PCNA) and cyclin D1 by Western blotting. As these markers are involved in different aspects of the cell cycle regulation, examining their expression levels can not only reveal the relative population of proliferating cells but can also improve our understanding of the mechanism of action of a given treatment or intervention. The scratch wound assay is a simple and cost-effective technique to quantify cell migration. A protocol which involves creating a wound in a cell cultured monolayer and measuring the distance migrated by the cells after a predefined time period is also described. Gap creation can also be achieved via physical cell exclusion where cells are seeded in distinct reservoirs of a cell culture insert which reveal a gap upon removal. Cell migration may then be quantified by monitoring the rate of gap closure. The presence of cleaved caspase-3 is a marker of programmed cell death (apoptosis). To detect cleaved caspase-3 in vitro, immunocytochemistry and fluorescence can be performed as outlined in this chapter.
MeSH term(s)	Apoptosis ; Atherosclerosis ; Bromodeoxyuridine/metabolism ; Cell Proliferation ; Deoxyuridine ; Endothelial Cells/metabolism ; Humans
Chemical Substances	Bromodeoxyuridine (G34N38R2N1) ; Deoxyuridine (W78I7AY22C)
Language	English
Publishing date	2022-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1924-7_9
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Article ; Online: Non-coding RNAs in cardiovascular cell biology and atherosclerosis.

Fasolo, Francesca / Di Gregoli, Karina / Maegdefessel, Lars / Johnson, Jason L

Cardiovascular research

2019 Volume 115, Issue 12, Page(s) 1732–1756

Abstract: Atherosclerosis underlies the predominant number of cardiovascular diseases and remains a leading cause of morbidity and mortality worldwide. The development, progression and formation of clinically relevant atherosclerotic plaques involves the ... ...

Abstract	Atherosclerosis underlies the predominant number of cardiovascular diseases and remains a leading cause of morbidity and mortality worldwide. The development, progression and formation of clinically relevant atherosclerotic plaques involves the interaction of distinct and over-lapping mechanisms which dictate the roles and actions of multiple resident and recruited cell types including endothelial cells, vascular smooth muscle cells, and monocyte/macrophages. The discovery of non-coding RNAs (ncRNAs) including microRNAs, long non-coding RNAs, and circular RNAs, and their identification as key mechanistic regulators of mRNA and protein expression has piqued interest in their potential contribution to atherosclerosis. Accruing evidence has revealed ncRNAs regulate pivotal cellular and molecular processes during all stages of atherosclerosis including cell invasion, growth, and survival; cellular uptake and efflux of lipids, expression and release of pro- and anti-inflammatory intermediaries, and proteolytic balance. The expression profile of ncRNAs within atherosclerotic lesions and the circulation have been determined with the aim of identifying individual or clusters of ncRNAs which may be viable therapeutic targets alongside deployment as biomarkers of atherosclerotic plaque progression. Consequently, numerous in vivo studies have been convened to determine the effects of moderating the function or expression of select ncRNAs in well-characterized animal models of atherosclerosis. Together, clinicopathological findings and studies in animal models have elucidated the multifaceted and frequently divergent effects ncRNAs impose both directly and indirectly on the formation and progression of atherosclerosis. From these findings' potential novel therapeutic targets and strategies have been discovered which may pave the way for further translational studies and possibly taken forward for clinical application.
MeSH term(s)	Animals ; Arteries/metabolism ; Arteries/pathology ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Gene Expression Regulation ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Plaque, Atherosclerotic ; RNA, Circular/genetics ; RNA, Circular/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; RNA, Untranslated/genetics ; RNA, Untranslated/metabolism ; Signal Transduction
Chemical Substances	MicroRNAs ; RNA, Circular ; RNA, Long Noncoding ; RNA, Untranslated
Language	English
Publishing date	2019-08-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvz203
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