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Article ; Online: 1.55 µm wavelength band photonic crystal surface emitting laser with n-side photonic crystal and operation at up to 85 °C.

Moodie, David / Boylan, Karl / Hattasan, Nannicha / Rihani, Samir / Pearce, Stuart / Qi, Lu / Dosanjh, Sukhjiban / Repiso Menendez, Eva / Silva, Matteo / Spalding, Richard / Burlinson, Stephen / Gillanders, Martin / Turner, David / Berry, Graham

Optics express

2024 Volume 32, Issue 6, Page(s) 10295–10301

Abstract: We describe the structure, fabrication, and measured performance of a 1543 nm wavelength photonic crystal surface emitting laser. An asymmetric double lattice design was used to achieve single mode lasing with side mode suppression ratios >40 dB. The ... ...

Abstract	We describe the structure, fabrication, and measured performance of a 1543 nm wavelength photonic crystal surface emitting laser. An asymmetric double lattice design was used to achieve single mode lasing with side mode suppression ratios >40 dB. The photonic crystal was formed using encapsulated air holes in an n-doped InGaAsP layer with an InGaAlAs active layer then grown above it. In this way a laser with a low series resistance of 0.32 Ω capable of pulsed output powers of 171 mW at 25 °C and 40 mW at 85 °C was demonstrated.
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	1491859-6
ISSN	1094-4087 ; 1094-4087
ISSN (online)	1094-4087
ISSN	1094-4087
DOI	10.1364/OE.521265
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Article ; Online: Foam cell formation: A new target for fighting atherosclerosis and cardiovascular disease.

Maguire, Eithne M / Pearce, Stuart W A / Xiao, Qingzhong

Vascular pharmacology

2018 Volume 112, Page(s) 54–71

Abstract: During atherosclerosis, the gradual accumulation of lipids into the subendothelial space of damaged arteries results in several lipid modification processes followed by macrophage uptake in the arterial wall. The way in which these modified lipoproteins ... ...

Abstract	During atherosclerosis, the gradual accumulation of lipids into the subendothelial space of damaged arteries results in several lipid modification processes followed by macrophage uptake in the arterial wall. The way in which these modified lipoproteins are dealt with determines the likelihood of cholesterol accumulation within the monocyte-derived macrophage and thus its transformation into the foam cell that makes up the characteristic fatty streak observed in the early stages of atherosclerosis. The unique expression of chemokine receptors and cellular adhesion molecules expressed on the cell surface of monocytes points to a particular extravasation route that they can take to gain entry into atherosclerotic site, in order to undergo differentiation into the phagocytic macrophage. Indeed several GWAS and animal studies have identified key genes and proteins required for monocyte recruitment as well cholesterol handling involving lipid uptake, cholesterol esterification and cholesterol efflux. A re-examination of the previously accepted paradigm of macrophage foam cell origin has been called into question by recent studies demonstrating shared expression of scavenger receptors, cholesterol transporters and pro-inflammatory cytokine release by alternative cell types present in the neointima, namely; endothelial cells, vascular smooth muscle cells and stem/progenitor cells. Thus, therapeutic targets aimed at a more heterogeneous foam cell population with shared functions, such as enhanced protease activity, and signalling pathways, mediated by non-coding RNA molecules, may provide greater therapeutic outcome in patients. Finally, studies targeting each aspect of foam cell formation and death using both genetic knock down and pharmacological inhibition have provided researchers with a clearer understanding of the cellular processes at play, as well as helped researchers to identify key molecular targets, which may hold significant therapeutic potential in the future.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Atherosclerosis/drug therapy ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Cardiovascular Agents/pharmacology ; Cholesterol/metabolism ; Foam Cells/drug effects ; Foam Cells/metabolism ; Foam Cells/pathology ; Genetic Predisposition to Disease ; Humans ; Molecular Targeted Therapy ; Necrosis ; Phenotype ; Plaque, Atherosclerotic ; Risk Factors ; Signal Transduction/drug effects
Chemical Substances	Cardiovascular Agents ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2018-08-14
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.2018.08.002
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Article: Matrix Metalloproteinase in Abdominal Aortic Aneurysm and Aortic Dissection.

Maguire, Eithne M / Pearce, Stuart W A / Xiao, Rui / Oo, Aung Y / Xiao, Qingzhong

Pharmaceuticals (Basel, Switzerland)

2019 Volume 12, Issue 3

Abstract: Abdominal Aortic Aneurysm (AAA) affects 4-5% of men over 65, and Aortic Dissection (AD) is a life-threatening aortic pathology associated with high morbidity and mortality. Initiators of AAA and AD include smoking and arterial hypertension, whilst key ... ...

Abstract	Abdominal Aortic Aneurysm (AAA) affects 4-5% of men over 65, and Aortic Dissection (AD) is a life-threatening aortic pathology associated with high morbidity and mortality. Initiators of AAA and AD include smoking and arterial hypertension, whilst key pathophysiological features of AAA and AD include chronic inflammation, hypoxia, and large modifications to the extra cellular matrix (ECM). As it stands, only surgical methods are available for preventing aortic rupture in patients, which often presents difficulties for recovery. No pharmacological treatment is available, as such researchers are attempting to understand the cellular and molecular pathophysiology of AAA and AD. Upregulation of matrix metalloproteinase (MMPs), particularly MMP-2 and MMP-9, has been identified as a key event occurring during aneurysmal growth. As such, several animal models of AAA and AD have been used to investigate the therapeutic potential of suppressing MMP-2 and MMP-9 activity as well as modulating the activity of other MMPs, and TIMPs involved in the pathology. Whilst several studies have offered promising results, targeted delivery of MMP inhibition still needs to be developed in order to avoid surgery in high risk patients.
Language	English
Publishing date	2019-08-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph12030118
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Article ; Online: Causal Role for Neutrophil Elastase in Thoracic Aortic Dissection in Mice.

Yang, Mei / Zhou, Xinmiao / Pearce, Stuart W A / Yang, Zhisheng / Chen, Qishan / Niu, Kaiyuan / Liu, Chenxin / Luo, Jun / Li, Dan / Shao, Yue / Zhang, Cheng / Chen, Dan / Wu, Qingchen / Cutillas, Pedro R / Zhao, Lin / Xiao, Qingzhong / Zhang, Li

Arteriosclerosis, thrombosis, and vascular biology

2023 Volume 43, Issue 10, Page(s) 1900–1920

Abstract: Background: Thoracic aortic dissection (TAD) is a life-threatening aortic disease without effective medical treatment. Increasing evidence has suggested a role for NE (neutrophil elastase) in vascular diseases. In this study, we aimed at investigating a ...

Abstract	Background: Thoracic aortic dissection (TAD) is a life-threatening aortic disease without effective medical treatment. Increasing evidence has suggested a role for NE (neutrophil elastase) in vascular diseases. In this study, we aimed at investigating a causal role for NE in TAD and exploring the molecular mechanisms involved. Methods: β-aminopropionitrile monofumarate was administrated in mice to induce TAD. NE deficiency mice, pharmacological inhibitor GW311616A, and adeno-associated virus-2-mediated in vivo gene transfer were applied to explore a causal role for NE and associated target gene in TAD formation. Multiple functional assays and biochemical analyses were conducted to unravel the underlying cellular and molecular mechanisms of NE in TAD. Results: NE aortic gene expression and plasma activity was significantly increased during β-aminopropionitrile monofumarate-induced TAD and in patients with acute TAD. NE deficiency prevents β-aminopropionitrile monofumarate-induced TAD onset/development, and GW311616A administration ameliorated TAD formation/progression. Decreased levels of neutrophil extracellular traps, inflammatory cells, and MMP (matrix metalloproteinase)-2/9 were observed in NE-deficient mice. TBL1x (F-box-like/WD repeat-containing protein TBL1x) has been identified as a novel substrate and functional downstream target of NE in TAD. Loss-of-function studies revealed that NE mediated inflammatory cell transendothelial migration by modulating TBL1x-LTA4H (leukotriene A4 hydrolase) signaling and that NE regulated smooth muscle cell phenotype modulation under TAD pathological condition by regulating TBL1x-MECP2 (methyl CpG-binding protein 2) signal axis. Further mechanistic studies showed that TBL1x inhibition decreased the binding of TBL1x and HDAC3 (histone deacetylase 3) to Conclusions: We unravel a critical role of NE and its target TBL1x in regulating inflammatory cell migration and smooth muscle cell phenotype modulation in the context of TAD. Our findings suggest that the NE-TBL1x signal axis represents a valuable therapeutic for treating high-risk TAD patients.
MeSH term(s)	Animals ; Humans ; Mice ; Aminopropionitrile/toxicity ; Aortic Aneurysm, Thoracic/chemically induced ; Aortic Aneurysm, Thoracic/genetics ; Aortic Aneurysm, Thoracic/metabolism ; Aortic Dissection/chemically induced ; Aortic Dissection/genetics ; Dissection, Thoracic Aorta ; Leukocyte Elastase/genetics ; Leukocyte Elastase/adverse effects
Chemical Substances	Aminopropionitrile (151-18-8) ; Leukocyte Elastase (EC 3.4.21.37) ; Elane protein, mouse (EC 3.4.21.37)
Language	English
Publishing date	2023-08-17
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.123.319281
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Zs.A 1705: Show issues

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Article ; Online: A novel small molecule TLR4 antagonist (IAXO-102) negatively regulates non-hematopoietic toll like receptor 4 signalling and inhibits aortic aneurysms development.

Huggins, Christopher / Pearce, Stuart / Peri, Francesco / Neumann, Frank / Cockerill, Gillian / Pirianov, Grisha

Atherosclerosis

2015 Volume 242, Issue 2, Page(s) 563–570

Abstract: Objectives: The toll-like receptors (TLRs), including TLR4, have been shown to play a crucial role in vascular inflammatory diseases, such as atherosclerosis and aneurysm. The main goal of this study was to determine the potential of IAXO-102 (Innaxon, ... ...

Abstract	Objectives: The toll-like receptors (TLRs), including TLR4, have been shown to play a crucial role in vascular inflammatory diseases, such as atherosclerosis and aneurysm. The main goal of this study was to determine the potential of IAXO-102 (Innaxon, Tewkesbury), a novel small molecule TLR4 antagonist, to modulate non-hematopoietic TLR4 proinflammatory signalling and inhibit experimental abdominal aortic aneurysm (AAA) development. Methods: Human umbilical vein endothelial cells (HUVEC) and Angiotensin II-induced experimental AAA development were our in vitro and in vivo models respectively. Western blotting, antibody array and ELISA approaches were used to explore the effect of IAXO-102 on TLR4 functional activity on two levels: modulation of TLR4-induced mitogen activated protein kinases (MAPK) and p65 NF-kB phosphorylation and expression of TLR4 dependent proinflammatory proteins. Results: Following activation of TLR4, in vitro/in vivo data revealed that IAXO-102 inhibited MAPK and p65 NF-kB phosphorylation associated with down regulation of the expression of TLR4 and TLR4 dependent proinflammatory proteins. Furthermore, IAXO-102 decreased Angiotensin II-induced aortic expansion, rupture and incidence of AAA. Conclusions: These results demonstrate the ability of IAXO-102 to negatively regulate TLR4 signalling and to inhibit experimental AAA development, suggesting the potential therapeutic use of this TLR4 antagonist for pharmacological intervention of AAA.
MeSH term(s)	Amino Sugars/pharmacology ; Animals ; Aorta/metabolism ; Aortic Aneurysm, Abdominal/drug therapy ; Aortic Aneurysm, Abdominal/prevention & control ; Apolipoproteins E/genetics ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation ; Glycolipids/pharmacology ; Human Umbilical Vein Endothelial Cells ; Humans ; Incidence ; Inflammation ; MAP Kinase Signaling System ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phosphorylation ; Signal Transduction ; Toll-Like Receptor 4/antagonists & inhibitors ; Toll-Like Receptor 4/metabolism ; Transcription Factor RelA/metabolism
Chemical Substances	Amino Sugars ; Apolipoproteins E ; Glycolipids ; IAXO-102 ; TLR4 protein, human ; Toll-Like Receptor 4 ; Transcription Factor RelA
Language	English
Publishing date	2015-08-08
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2015.08.010
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Article ; Online: Power Budget Analysis for Waveguide-Enhanced Raman Spectroscopy.

Wang, Zilong / Pearce, Stuart J / Lin, Yung-Chun / Zervas, Michalis N / Bartlett, Philip N / Wilkinson, James S

Applied spectroscopy

2016 Volume 70, Issue 8, Page(s) 1384–1391

Abstract: Waveguide-enhanced Raman spectroscopy (WERS) is emerging as an attractive alternative to plasmonic surface-enhanced Raman spectroscopy approaches as it can provide more reproducible quantitative spectra on a robust chip without the need for ... ...

Abstract	Waveguide-enhanced Raman spectroscopy (WERS) is emerging as an attractive alternative to plasmonic surface-enhanced Raman spectroscopy approaches as it can provide more reproducible quantitative spectra on a robust chip without the need for nanostructured plasmonic materials. Realizing portable WERS systems with high sensitivity using low-cost laser diodes and compact spectrometers requires a detailed analysis of the power budget from laser to spectrometer chip. In this paper, we describe theoretical optimization of planar waveguides for maximum Raman excitation efficiency, demonstrate WERS for toluene on a silicon process compatible high index contrast tantalum pentoxide waveguide, measure the absolute conversion efficiency from pump power to received power in an individual Raman line, and compare this with a power budget analysis of the complete system including collection with an optical fiber and interfacing to a compact spectrometer. Optimized 110 nm thick Ta2O5 waveguides on silica substrates excited at a wavelength of 637 nm are shown experimentally to yield overall system power conversion efficiency of ∼0.5 × 10(-12) from the pump power in the waveguide to the collected Raman power in the 1002 cm(-1) Raman line of toluene, in comparison with a calculated efficiency of 3.9 × 10(-12) Collection efficiency is dictated by the numerical and physical apertures of the spectral detection system but may be improved by further engineering the spatial and angular Raman scattering distributions.
Language	English
Publishing date	2016-08
Publishing country	United States
Document type	Journal Article
ISSN	1943-3530
ISSN (online)	1943-3530
DOI	10.1177/0003702816654042
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Article ; Online: Genetic and Pharmacologic Inhibition of the Neutrophil Elastase Inhibits Experimental Atherosclerosis.

Wen, Guanmei / An, Weiwei / Chen, Jiangyong / Maguire, Eithne M / Chen, Qishan / Yang, Feng / Pearce, Stuart W A / Kyriakides, Maria / Zhang, Li / Ye, Shu / Nourshargh, Sussan / Xiao, Qingzhong

Journal of the American Heart Association

2018 Volume 7, Issue 4

Abstract: Background: To investigate whether neutrophil elastase (NE) plays a causal role in atherosclerosis, and the molecular mechanisms involved.: Methods and results: NE genetic-deficient mice (Apolipoprotein E: Conclusions: We outlined a pathogenic ... ...

Abstract	Background: To investigate whether neutrophil elastase (NE) plays a causal role in atherosclerosis, and the molecular mechanisms involved. Methods and results: NE genetic-deficient mice (Apolipoprotein E Conclusions: We outlined a pathogenic role for NE in foam cell formation and atherosclerosis development. Consequently, inhibition of NE may represent a potential therapeutic approach to treating cardiovascular disease.
MeSH term(s)	ATP Binding Cassette Transporter 1/metabolism ; Animals ; Aorta/drug effects ; Aorta/enzymology ; Aorta/pathology ; Aortic Diseases/enzymology ; Aortic Diseases/genetics ; Aortic Diseases/pathology ; Aortic Diseases/prevention & control ; Atherosclerosis/enzymology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Cells, Cultured ; Cholesterol/blood ; Cytokines/blood ; Disease Models, Animal ; Foam Cells/drug effects ; Foam Cells/metabolism ; Foam Cells/pathology ; Inflammation Mediators/blood ; Leukocyte Elastase/antagonists & inhibitors ; Leukocyte Elastase/deficiency ; Leukocyte Elastase/genetics ; Male ; Mice, Inbred C57BL ; Mice, Knockout, ApoE ; Neutrophils/drug effects ; Neutrophils/enzymology ; Piperidines/pharmacology ; Plaque, Atherosclerotic ; Proteolysis ; Serine Proteinase Inhibitors/pharmacology
Chemical Substances	ABCA1 protein, mouse ; ATP Binding Cassette Transporter 1 ; Cytokines ; GW 311616 ; Inflammation Mediators ; Piperidines ; Serine Proteinase Inhibitors ; Cholesterol (97C5T2UQ7J) ; Leukocyte Elastase (EC 3.4.21.37)
Language	English
Publishing date	2018-02-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.117.008187
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Article ; Online: Pioglitazone Identifies a New Target for Aneurysm Treatment: Role of Egr1 in an Experimental Murine Model of Aortic Aneurysm.

Charolidi, Nicoletta / Pirianov, Grisha / Torsney, Evelyn / Pearce, Stuart / Laing, Ken / Nohturfft, Axel / Cockerill, Gillian W

Journal of vascular research

2015 Volume 52, Issue 2, Page(s) 81–93

Abstract: Peroxisome proliferator-activated receptor x03B3; agonists have been shown to inhibit angiotensin II (AngII)-induced experimental abdominal aortic aneurysms. Macrophage infiltration to the vascular wall is an early event in this pathology, and therefore ... ...

Abstract	Peroxisome proliferator-activated receptor x03B3; agonists have been shown to inhibit angiotensin II (AngII)-induced experimental abdominal aortic aneurysms. Macrophage infiltration to the vascular wall is an early event in this pathology, and therefore we explored the effects of the peroxisome proliferator-activated receptor x03B3; agonist pioglitazone on AngII-treated macrophages. Using microarray-based expression profiling of phorbol ester-stimulated THP-1 cells, we found that a number of aneurysm-related gene changes effected by AngII were modulated following the addition of pioglitazone. Among those genes, polycystic kidney disease 1 (PKD1) was significantly up-regulated (multiple testing corrected p < 0.05). The analysis of the PKD1 proximal promoter revealed a putative early growth response 1 (EGR1) binding site, which was confirmed by chromatin immunoprecipitation (ChIP) and quantitative PCR. Further analysis of publicly available ChIP-sequencing data revealed that this putative binding site overlapped with a conserved EGR1 binding peak present in 5 other cell lines. Quantitative real-time PCR showed that EGR1 suppressed PKD1, while AngII significantly up-regulated PKD1, an effect counteracted by pioglitazone. Conversely, in EGR1 short hairpin RNA lentivirally transduced THP-1 cells, reduced EGR1 led to a significant up-regulation of PKD1, especially after treatment with pioglitazone. In vivo, deficiency of Egr1 in the haematopoietic compartment of mice completely abolished the incidence of CaCl2-induced aneurysm formation.
MeSH term(s)	Angiotensin II/pharmacology ; Animals ; Aortic Aneurysm, Abdominal/chemically induced ; Aortic Aneurysm, Abdominal/genetics ; Aortic Aneurysm, Abdominal/metabolism ; Aortic Aneurysm, Abdominal/prevention & control ; Base Sequence ; Binding Sites ; Calcium Chloride ; Cell Line, Tumor ; Disease Models, Animal ; Early Growth Response Protein 1/deficiency ; Early Growth Response Protein 1/genetics ; Early Growth Response Protein 1/metabolism ; Female ; Gene Expression Profiling/methods ; Gene Expression Regulation ; Humans ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Mice, Knockout ; Molecular Sequence Data ; PPAR gamma/agonists ; PPAR gamma/metabolism ; Pioglitazone ; Promoter Regions, Genetic ; RNA Interference ; Signal Transduction/drug effects ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism ; Thiazolidinediones/pharmacology ; Time Factors ; Transfection
Chemical Substances	EGR1 protein, human ; Early Growth Response Protein 1 ; Egr1 protein, mouse ; PPAR gamma ; TRPP Cation Channels ; Thiazolidinediones ; polycystic kidney disease 1 protein ; Angiotensin II (11128-99-7) ; Calcium Chloride (M4I0D6VV5M) ; Pioglitazone (X4OV71U42S)
Language	English
Publishing date	2015-06-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000430986
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Article ; Online: Highly sensitive biosensor based on UV-imprinted layered polymeric-inorganic composite waveguides.

Wang, Meng / Hiltunen, Jussi / Liedert, Christina / Pearce, Stuart / Charlton, Martin / Hakalahti, Leena / Karioja, Pentti / Myllylä, Risto

Optics express

2012 Volume 20, Issue 18, Page(s) 20309–20317

Abstract: An evanescent field sensor utilizing layered polymeric-inorganic composite waveguide configuration was developed in this work. The composite waveguide structure consists of a UV-imprint patterned polymer inverted rib waveguide with a Ta2O5 thin film ... ...

Abstract	An evanescent field sensor utilizing layered polymeric-inorganic composite waveguide configuration was developed in this work. The composite waveguide structure consists of a UV-imprint patterned polymer inverted rib waveguide with a Ta2O5 thin film sputter-deposited on top of the low refractive index polymer layers. The results suggest that the polymer based sensor can achieve a detection limit of 3 × 10(-7) RIU for refractive index sensing and corresponding limit of about 100 fg/mm2 for molecular adsorption detection. Besides enhancing the sensitivity significantly, the inorganic coating on the polymer layer was found to block water absorption effectively into the waveguide resulting in a stabilized sensor operation. The ability to use the developed sensor in specific molecular detection was confirmed by investigating antibody - antigen binding reactions. The results of this work demonstrate that high performance sensing capability can be obtained with the developed composite waveguide sensor.
MeSH term(s)	Biosensing Techniques/instrumentation ; Equipment Design ; Equipment Failure Analysis ; Immunoassay/instrumentation ; Inorganic Chemicals/chemistry ; Molecular Imprinting/instrumentation ; Molecular Imprinting/methods ; Polymers/chemistry ; Refractometry/instrumentation ; Surface Plasmon Resonance/instrumentation
Chemical Substances	Inorganic Chemicals ; Polymers
Language	English
Publishing date	2012-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1491859-6
ISSN	1094-4087 ; 1094-4087
ISSN (online)	1094-4087
ISSN	1094-4087
DOI	10.1364/OE.20.020309
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Article: Pioglitazone Identifies a New Target for Aneurysm Treatment: Role of Egr1 in an Experimental Murine Model of Aortic Aneurysm

Charolidi, Nicoletta / Pirianov, Grisha / Torsney, Evelyn / Pearce, Stuart / Laing, Ken / Nohturfft, Axel / Cockerill, Gillian W.

Journal of Vascular Research

2015 Volume 52, Issue 2, Page(s) 81–93

Abstract: Peroxisome proliferator-activated receptor γ agonists have been shown to inhibit angiotensin II (AngII)-induced experimental abdominal aortic aneurysms. Macrophage infiltration to the vascular wall is an early event in this pathology, and therefore we ... ...

Institution	Institute of Cardiovascular and Cell Sciences, St. George's, University of London, London, UK
Abstract	Peroxisome proliferator-activated receptor γ agonists have been shown to inhibit angiotensin II (AngII)-induced experimental abdominal aortic aneurysms. Macrophage infiltration to the vascular wall is an early event in this pathology, and therefore we explored the effects of the peroxisome proliferator-activated receptor γ agonist pioglitazone on AngII-treated macrophages. Using microarray-based expression profiling of phorbol ester-stimulated THP-1 cells, we found that a number of aneurysm-related gene changes effected by AngII were modulated following the addition of pioglitazone. Among those genes, polycystic kidney disease 1 (PKD1) was significantly up-regulated (multiple testing corrected p < 0.05). The analysis of the PKD1 proximal promoter revealed a putative early growth response 1 (EGR1) binding site, which was confirmed by chromatin immunoprecipitation (ChIP) and quantitative PCR. Further analysis of publicly available ChIP-sequencing data revealed that this putative binding site overlapped with a conserved EGR1 binding peak present in 5 other cell lines. Quantitative real-time PCR showed that EGR1 suppressed PKD1, while AngII significantly up-regulated PKD1, an effect counteracted by pioglitazone. Conversely, in EGR1 short hairpin RNA lentivirally transduced THP-1 cells, reduced EGR1 led to a significant up-regulation of PKD1, especially after treatment with pioglitazone. In vivo, deficiency of Egr1 in the haematopoietic compartment of mice completely abolished the incidence of CaCl2-induced aneurysm formation.
Keywords	Aneurysm ; Polycystic kidney disease ; Angiotensin II ; Macrophage ; Pioglitazone
Language	English
Publishing date	2015-06-20
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Research Paper
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000430986
Database	Karger publisher's database

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