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Article ; Online: Fluid shear stress regulates placental growth factor expression via heme oxygenase 1 and iron.

Rashdan, Nabil A / Zhai, Bo / Lovern, Pamela C

2021 Volume 11, Issue 1, Page(s) 14912

Abstract: Increased fluid shear stress (FSS) is a key initiating stimulus for arteriogenesis, the outward remodeling of collateral arterioles in response to upstream occlusion. Placental growth factor (PLGF) is an important arteriogenic mediator. We previously ... ...

Abstract	Increased fluid shear stress (FSS) is a key initiating stimulus for arteriogenesis, the outward remodeling of collateral arterioles in response to upstream occlusion. Placental growth factor (PLGF) is an important arteriogenic mediator. We previously showed that elevated FSS increases PLGF in a reactive oxygen species (ROS)-dependent fashion both in vitro and ex vivo. Heme oxygenase 1 (HO-1) is a cytoprotective enzyme that is upregulated by stress and has arteriogenic effects. In the current study, we used isolated murine mesentery arterioles and co-cultures of human coronary artery endothelial cells (EC) and smooth muscle cells (SMC) to test the hypothesis that HO-1 mediates the effects of FSS on PLGF. HO-1 mRNA was increased by conditions of increased flow and shear stress in both co-cultures and vessels. Both inhibition of HO-1 with zinc protoporphyrin and HO-1 knockdown abolished the effect of FSS on PLGF. Conversely, induction of HO-1 activity increased PLGF. To determine which HO-1 product upregulates PLGF, co-cultures were treated with a CO donor (CORM-A1), biliverdin, ferric ammonium citrate (FAC), or iron-nitrilotriacetic acid (iron-NTA). Of these FAC and iron-NTA induced an increase PLGF expression. This study demonstrates that FSS acts through iron to induce pro-arteriogenic PLGF, suggesting iron supplementation as a novel potential treatment for revascularization.
MeSH term(s)	Animals ; Blood Circulation/physiology ; Cells, Cultured ; Coculture Techniques ; Coronary Vessels ; Endothelial Cells/metabolism ; Gene Expression ; Heme Oxygenase-1/genetics ; Heme Oxygenase-1/metabolism ; Heme Oxygenase-1/physiology ; Humans ; Iron/metabolism ; Mesenteric Arteries ; Mice ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Placenta Growth Factor/metabolism ; RNA, Messenger/metabolism ; Reactive Oxygen Species/metabolism ; Shear Strength/physiology
Chemical Substances	PGF protein, human ; RNA, Messenger ; Reactive Oxygen Species ; Placenta Growth Factor (144589-93-5) ; Iron (E1UOL152H7) ; Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2021-07-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-94559-w
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Article ; Online: Hydrogen peroxide in the ER: A tale of triage.

Rashdan, Nabil A / Pattillo, Christopher B

Redox biology

2019 Volume 28, Page(s) 101358

Abstract: Oxidative protein folding in the endoplasmic reticulum (ER) is a significant source of hydrogen peroxide ( ... ...

Abstract	Oxidative protein folding in the endoplasmic reticulum (ER) is a significant source of hydrogen peroxide (H
MeSH term(s)	Animals ; Aquaporins/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Oxidation-Reduction ; Protein Folding
Chemical Substances	AQP11 protein, human ; Aquaporins ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2019-10-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2019.101358
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Article ; Online: Neurogranin expression regulates mitochondrial function and redox balance in endothelial cells.

Jorgensen, Ashton N / Rashdan, Nabil A / Rao, K N Shashanka / Delgadillo, Luisa F / Kolluru, Gopi K / Krzywanski, David M / Pattillo, Christopher B / Kevil, Christopher G / Nam, Hyung W

Redox biology

2024 Volume 70, Page(s) 103085

Abstract: Endothelial dysfunction and endothelial activation are common early events in vascular diseases and can arise from mitochondrial dysfunction. Neurogranin (Ng) is a 17kD protein well known to regulate intracellular ... ...

Abstract	Endothelial dysfunction and endothelial activation are common early events in vascular diseases and can arise from mitochondrial dysfunction. Neurogranin (Ng) is a 17kD protein well known to regulate intracellular Ca
MeSH term(s)	Animals ; Humans ; Mice ; Endothelial Cells/metabolism ; Hydrogen Peroxide/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Diseases/metabolism ; Neurogranin/metabolism ; Nitric Oxide/metabolism ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism
Chemical Substances	Hydrogen Peroxide (BBX060AN9V) ; Neurogranin (132654-77-4) ; Nitric Oxide (31C4KY9ESH) ; Reactive Oxygen Species
Language	English
Publishing date	2024-02-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2024.103085
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Article ; Online: Fluid shear stress upregulates placental growth factor in the vessel wall via NADPH oxidase 4.

Rashdan, Nabil A / Lloyd, Pamela G

American journal of physiology. Heart and circulatory physiology

2015 Volume 309, Issue 10, Page(s) H1655–66

Abstract: Placental growth factor (PLGF), a potent stimulator of arteriogenesis, is upregulated during outward arterial remodeling. Increased fluid shear stress (FSS) is a key physiological stimulus for arteriogenesis. However, the role of FSS in regulating PLGF ... ...

Abstract	Placental growth factor (PLGF), a potent stimulator of arteriogenesis, is upregulated during outward arterial remodeling. Increased fluid shear stress (FSS) is a key physiological stimulus for arteriogenesis. However, the role of FSS in regulating PLGF expression is unknown. To test the hypothesis that FSS regulates PLGF expression in vascular cells and to identify the signaling pathways involved, human coronary artery endothelial cells (HCAEC) and human coronary artery smooth muscle cells were cultured on either side of porous Transwell inserts. HCAEC were then exposed to pulsatile FSS of 0.07 Pa ("normal," mimicking flow through quiescent collaterals), 1.24 Pa ("high," mimicking increased flow in remodeling collaterals), or 0.00 Pa ("static") for 2 h. High FSS increased secreted PLGF protein ∼1.4-fold compared with static control (n = 5, P < 0.01), while normal FSS had no significant effect on PLGF. Similarly, high flow stimulated PLGF mRNA expression nearly twofold in isolated mouse mesenteric arterioles. PLGF knockdown using siRNA revealed that HCAEC were the primary source of PLGF in cocultures (n = 5, P < 0.01). Both H2O2 and nitric oxide production were increased by FSS compared with static control (n = 5, P < 0.05). N(G)-nitro-l-arginine methyl ester (100 μM) had no significant effect on the FSS-induced increase in PLGF. In contrast, both catalase (500 U/ml) and diphenyleneiodonium (5 μM) attenuated the effects of FSS on PLGF protein in cocultures. Diphenyleneiodonium also blocked the effect of high flow to upregulate PLGF mRNA in isolated arterioles. Further studies identified NADPH oxidase 4 as a source of reactive oxygen species for this pathway. We conclude that FSS regulates PLGF expression via NADPH oxidase 4 and reactive oxygen species signaling.
MeSH term(s)	Animals ; Arterioles/drug effects ; Arterioles/metabolism ; Catalase/pharmacology ; Cells, Cultured ; Coculture Techniques ; Collateral Circulation ; Coronary Vessels/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Gene Expression Profiling ; Humans ; Hydrogen Peroxide/metabolism ; Mice ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; NADPH Oxidase 4 ; NADPH Oxidases/drug effects ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitrates/metabolism ; Nitrites/metabolism ; Onium Compounds/pharmacology ; Placenta Growth Factor ; Pregnancy Proteins/drug effects ; Pregnancy Proteins/genetics ; Pregnancy Proteins/metabolism ; Pulsatile Flow ; RNA, Messenger/drug effects ; RNA, Messenger/metabolism ; Reactive Oxygen Species/metabolism ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; Stress, Mechanical ; Up-Regulation ; Vascular Remodeling
Chemical Substances	Nitrates ; Nitrites ; Onium Compounds ; PGF protein, human ; Pgf protein, mouse ; Pregnancy Proteins ; RNA, Messenger ; Reactive Oxygen Species ; Placenta Growth Factor (144589-93-5) ; diphenyleneiodonium (6HJ411TU98) ; Hydrogen Peroxide (BBX060AN9V) ; Catalase (EC 1.11.1.6) ; NADPH Oxidase 4 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; NOX4 protein, human (EC 1.6.3.-) ; Nox4 protein, mouse (EC 1.6.3.-) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2015-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00408.2015
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Article ; Online: Hyperglycemia-induced effects on glycocalyx components in the retina.

Kaur, Gaganpreet / Rogers, Janet / Rashdan, Nabil A / Cruz-Topete, Diana / Pattillo, Christopher B / Hartson, Steven D / Harris, Norman R

Experimental eye research

2021 Volume 213, Page(s) 108846

Abstract: Purpose: Diabetic retinopathy is a vision-threatening complication of diabetes characterized by endothelial injury and vascular dysfunction. The loss of the endothelial glycocalyx, a dynamic layer lining all endothelial cells, contributes to several ... ...

Abstract	Purpose: Diabetic retinopathy is a vision-threatening complication of diabetes characterized by endothelial injury and vascular dysfunction. The loss of the endothelial glycocalyx, a dynamic layer lining all endothelial cells, contributes to several microvascular pathologies, including an increase in vascular permeability, leukocyte plugging, and capillary occlusion, and may drive the progression of retinopathy. Previously, a significant decrease in glycocalyx thickness has been observed in diabetic retinas. However, the effects of diabetes on specific components of the retinal glycocalyx have not yet been studied. Therefore, the aim of our study was to investigate changes in synthesis, expression, and shedding of retinal glycocalyx components induced by hyperglycemia, which could provide a novel therapeutic target for diabetic retinopathy. Methods: Primary rat retinal microvascular endothelial cells (RRMECs) were grown under normal glucose (5 mM) or high-glucose (25 mM) conditions for 6 days. The mRNA and protein levels of the glycocalyx components were examined using qRT-PCR and Western blot analysis, respectively. Further, mass spectrometry was used to analyze protein intensities of core proteins. In addition, the streptozotocin-induced Type 1 diabetic rat model was used to study changes in the expression of the retinal glycocalyx in vivo. The shedding of the glycocalyx was studied in both culture medium and in plasma using Western blot analysis. Results: A significant increase in the shedding of syndecan-1 and CD44 was observed both in vitro and in vivo under high-glucose conditions. The mRNA levels of syndecan-3 were significantly lower in the RRMECs grown under high glucose conditions, whereas those of syndecan-1, syndecan-2, syndecan-4, glypican-1, glypican-3, and CD44 were significantly higher. The protein expression of syndecan-3 and glypican-1 in RRMECs was reduced considerably following exposure to high glucose, whereas that of syndecan-1 and CD44 increased significantly. In addition, mass spectrometry data also suggests a significant increase in syndecan-4 and a significant decrease in glypican-3 protein levels with high glucose stimulation. In vivo, our data also suggest a significant decrease in the mRNA transcripts of syndecan-3 and an increase in mRNA levels of glypican-1 and CD44 in the retinas of diabetic rats. The diabetic rats exhibited a significant reduction in the retinal expression of syndecan-3 and CD44. However, the expression of syndecan-1 and glypican-1 increased significantly in the diabetic retina. Conclusions: One of the main findings of our study was the considerable diversity of glucose-induced changes in expression and shedding of various components of endothelial glycocalyx, for example, increased endothelial and retinal syndecan-1, but decreased endothelial and retinal syndecan-3. This indicates that the reported decrease in the retinal glycocalyx in diabetes in not a result of a non-specific shedding mechanism. Moreover, mRNA measurements indicated a similar diversity, with increases in endothelial and/or retinal levels of syndecan-1, glypican-1, and CD44, but a decrease for syndecan-3, with these increases in mRNA potentially a compensatory reaction to the overall loss of glycocalyx.
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Blotting, Western ; Cells, Cultured ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Type 1/metabolism ; Diabetic Retinopathy/metabolism ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Enzyme-Linked Immunosorbent Assay ; Glucose/pharmacology ; Glycocalyx/metabolism ; Glypicans/metabolism ; Hyaluronan Receptors/metabolism ; Hyperglycemia/metabolism ; Insulin/blood ; Male ; Mass Spectrometry ; RNA, Messenger/genetics ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Retina/metabolism ; Retinal Vessels/cytology ; Syndecans/metabolism
Chemical Substances	Blood Glucose ; Glypicans ; Hyaluronan Receptors ; Insulin ; RNA, Messenger ; Syndecans ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-11-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2021.108846
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Article ; Online: Spatially Resolved Metabolites in Stable and Unstable Human Atherosclerotic Plaques Identified by Mass Spectrometry Imaging.

Seeley, Erin H / Liu, Zhipeng / Yuan, Shuai / Stroope, Chad / Cockerham, Elizabeth / Rashdan, Nabil A / Delgadillo, Luisa F / Finney, Alexandra C / Kumar, Dhananjay / Das, Sandeep / Razani, Babak / Liu, Wanqing / Traylor, James / Orr, A Wayne / Rom, Oren / Pattillo, Christopher B / Yurdagul, Arif

Arteriosclerosis, thrombosis, and vascular biology

2023 Volume 43, Issue 9, Page(s) 1626–1635

Abstract: Background: Impairments in carbohydrate, lipid, and amino acid metabolism drive features of plaque instability. However, where these impairments occur within the atheroma remains largely unknown. Therefore, we sought to characterize the spatial ... ...

Abstract	Background: Impairments in carbohydrate, lipid, and amino acid metabolism drive features of plaque instability. However, where these impairments occur within the atheroma remains largely unknown. Therefore, we sought to characterize the spatial distribution of metabolites within stable and unstable atherosclerosis in both the fibrous cap and necrotic core. Methods: Atherosclerotic tissue specimens from 9 unmatched individuals were scored based on the Stary classification scale and subdivided into stable and unstable atheromas. After performing mass spectrometry imaging on these samples, we identified over 850 metabolite-related peaks. Using MetaboScape, METASPACE, and Human Metabolome Database, we confidently annotated 170 of these metabolites and found over 60 of these were different between stable and unstable atheromas. We then integrated these results with an RNA-sequencing data set comparing stable and unstable human atherosclerosis. Results: Upon integrating our mass spectrometry imaging results with the RNA-sequencing data set, we discovered that pathways related to lipid metabolism and long-chain fatty acids were enriched in stable plaques, whereas reactive oxygen species, aromatic amino acid, and tryptophan metabolism were increased in unstable plaques. In addition, acylcarnitines and acylglycines were increased in stable plaques whereas tryptophan metabolites were enriched in unstable plaques. Evaluating spatial differences in stable plaques revealed lactic acid in the necrotic core, whereas pyruvic acid was elevated in the fibrous cap. In unstable plaques, 5-hydroxyindoleacetic acid was enriched in the fibrous cap. Conclusions: Our work here represents the first step to defining an atlas of metabolic pathways involved in plaque destabilization in human atherosclerosis. We anticipate this will be a valuable resource and open new avenues of research in cardiovascular disease.
MeSH term(s)	Humans ; Plaque, Atherosclerotic/chemistry ; Tryptophan ; Atherosclerosis/diagnostic imaging ; Mass Spectrometry ; Necrosis ; RNA
Chemical Substances	Tryptophan (8DUH1N11BX) ; RNA (63231-63-0)
Language	English
Publishing date	2023-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.122.318684
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Article ; Online: A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification.

Zhu, Dongxing / Rashdan, Nabil A / Chapman, Karen E / Hadoke, Patrick Wf / MacRae, Vicky E

Vascular pharmacology

2016 Volume 86, Page(s) 87–93

Abstract: Vascular calcification, which is common in the elderly and in patients with atherosclerosis, diabetes and chronic renal disease, increases the risk of cardiovascular morbidity and mortality. It is a complex, active and highly regulated cellular process ... ...

Abstract	Vascular calcification, which is common in the elderly and in patients with atherosclerosis, diabetes and chronic renal disease, increases the risk of cardiovascular morbidity and mortality. It is a complex, active and highly regulated cellular process that resembles physiological bone formation. It has previously been established that pharmacological doses of glucocorticoids facilitate arterial calcification. However, the consequences for vascular calcification of endogenous glucocorticoid elevation have yet to be established. Glucocorticoids (cortisol, corticosterone) are released from the adrenal gland, but can also be generated within cells from 11-keto metabolites of glucocorticoids (cortisone, 11-dehydrocorticosterone [11-DHC]) by the enzyme, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). In the current study we hypothesized that endogenous glucocorticoids facilitate vascular smooth muscle cell (VSMC) calcification and investigated the receptor-mediated mechanism underpinning this process. In vitro studies revealed increased phosphate-induced calcification in mouse VSMCs following treatment for 7days with corticosterone (100nM; 7.98 fold; P<0.01), 11-DHC (100nM; 7.14 fold; P<0.05) and dexamethasone (10nM; 7.16 fold; P<0.05), a synthetic glucocorticoid used as a positive control. Inhibition of 11β-HSD isoenzymes by 10μM carbenoxolone reduced the calcification induced by 11-DHC (0.37 fold compared to treatment with 11-DHC alone; P<0.05). The glucocorticoid receptor (GR) antagonist mifepristone (10μM) had no effect on VSMC calcification in response to corticosterone or 11-DHC. In contrast, the mineralocorticoid receptor (MR) antagonist eplerenone (10μM) significantly decreased corticosterone- (0.81 fold compared to treatment with corticosterone alone; P<0.01) and 11-DHC-driven (0.64 fold compared to treatment with 11-DHC alone; P<0.01) VSMC calcification, suggesting this glucocorticoid effect is MR-driven and not GR-driven. Neither corticosterone nor 11-DHC altered the mRNA levels of the osteogenic markers PiT-1, Osx and Bmp2. However, DAPI staining of pyknotic nuclei and flow cytometry analysis of surface Annexin V expression showed that corticosterone induced apoptosis in VSMCs. This study suggests that in mouse VSMCs, corticosterone acts through the MR to induce pro-calcification effects, and identifies 11β-HSD-inhibition as a novel potential treatment for vascular calcification.
MeSH term(s)	11-beta-Hydroxysteroid Dehydrogenase Type 1/antagonists & inhibitors ; 11-beta-Hydroxysteroid Dehydrogenase Type 1/metabolism ; Animals ; Apoptosis ; Corticosterone/administration & dosage ; Corticosterone/metabolism ; Disease Models, Animal ; Eplerenone ; Flow Cytometry ; Glucocorticoids/administration & dosage ; Glucocorticoids/metabolism ; Mice ; Mice, Inbred C57BL ; Mifepristone/pharmacology ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/pathology ; Myocytes, Smooth Muscle/pathology ; Phosphates/administration & dosage ; RNA, Messenger/metabolism ; Receptors, Glucocorticoid/antagonists & inhibitors ; Receptors, Glucocorticoid/metabolism ; Receptors, Mineralocorticoid/drug effects ; Receptors, Mineralocorticoid/metabolism ; Spironolactone/analogs & derivatives ; Spironolactone/pharmacology ; Vascular Calcification/pathology
Chemical Substances	Glucocorticoids ; Phosphates ; RNA, Messenger ; Receptors, Glucocorticoid ; Receptors, Mineralocorticoid ; Spironolactone (27O7W4T232) ; Mifepristone (320T6RNW1F) ; Eplerenone (6995V82D0B) ; 11-beta-Hydroxysteroid Dehydrogenase Type 1 (EC 1.1.1.146) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2016-05-03
Publishing country	United States
Document type	Journal Article
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.2016.04.005
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Zs.A 591: Show issues

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Article ; Online: New perspectives on rare connective tissue calcifying diseases.

Rashdan, Nabil A / Rutsch, Frank / Kempf, Hervé / Váradi, András / Lefthériotis, Georges / MacRae, Vicky E

Current opinion in pharmacology

2016 Volume 28, Page(s) 14–23

Abstract: Connective tissue calcifying diseases (CTCs) are characterized by abnormal calcium deposition in connective tissues. CTCs are caused by multiple factors including chronic diseases (Type II diabetes mellitus, chronic kidney disease), the use of ... ...

Abstract	Connective tissue calcifying diseases (CTCs) are characterized by abnormal calcium deposition in connective tissues. CTCs are caused by multiple factors including chronic diseases (Type II diabetes mellitus, chronic kidney disease), the use of pharmaceuticals (e.g. warfarin, glucocorticoids) and inherited rare genetic diseases such as pseudoxanthoma elasticum (PXE), generalized arterial calcification in infancy (GACI) and Keutel syndrome (KTLS). This review explores our current knowledge of these rare inherited CTCs, and highlights the most promising avenues for pharmaceutical intervention. Advancing our understanding of rare inherited forms of CTC is not only essential for the development of therapeutic strategies for patients suffering from these diseases, but also fundamental to delineating the mechanisms underpinning acquired chronic forms of CTC.
MeSH term(s)	Animals ; Calcinosis/drug therapy ; Calcinosis/etiology ; Calcinosis/physiopathology ; Calcium/metabolism ; Chronic Disease ; Connective Tissue/pathology ; Connective Tissue Diseases/drug therapy ; Connective Tissue Diseases/etiology ; Connective Tissue Diseases/physiopathology ; Drug Design ; Humans
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2016-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2016.02.002
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Zs.A 5608: Show issues

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Article ; Online: A novel fluorescein-bisphosphonate based diagnostic tool for the detection of hydroxyapatite in both cell and tissue models.

Sim, Alisia M / Rashdan, Nabil A / Cui, Lin / Moss, Alastair J / Nudelman, Fabio / Dweck, Marc R / MacRae, Vicky E / Hulme, Alison N

Scientific reports

2018 Volume 8, Issue 1, Page(s) 17360

Abstract: A rapid and efficient method for the detection of hydroxyapatite (HAP) has been developed which shows superiority to existing well-established methods. This fluorescein-bisphosphonate probe is highly selective for HAP over other calcium minerals and is ... ...

Abstract	A rapid and efficient method for the detection of hydroxyapatite (HAP) has been developed which shows superiority to existing well-established methods. This fluorescein-bisphosphonate probe is highly selective for HAP over other calcium minerals and is capable of detecting lower levels of calcification in cellular models than either hydrochloric acid-based calcium leaching assays or the Alizarin S stain. The probe has been shown to be effective in both in vitro vascular calcification models and in vitro bone calcification models. Moreover we have demonstrated binding of this probe to vascular calcification in rat aorta and to areas of microcalcification, in human vascular tissue, beyond the resolution of computed tomography in human atherosclerotic plaques. Fluorescein-BP is therefore a highly sensitive and specific imaging probe for the detection of vascular calcification, with the potential to improve not only ex vivo assessments of HAP deposition but also the detection of vascular microcalcification in humans.
MeSH term(s)	Aged ; Animals ; Calcification, Physiologic/physiology ; Calcium/metabolism ; Diphosphonates/metabolism ; Durapatite/metabolism ; Female ; Fluorescein/metabolism ; Humans ; Male ; Middle Aged ; Muscle, Smooth, Vascular/metabolism ; Osteogenesis/physiology ; Plaque, Atherosclerotic/metabolism ; Rats ; Vascular Calcification/diagnosis ; Vascular Calcification/metabolism
Chemical Substances	Diphosphonates ; Durapatite (91D9GV0Z28) ; Calcium (SY7Q814VUP) ; Fluorescein (TPY09G7XIR)
Language	English
Publishing date	2018-11-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-35454-9
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Article ; Online: Induction of glutathione biosynthesis by glycine-based treatment mitigates atherosclerosis.

Redox biology

2022 Volume 52, Page(s) 102313

Abstract: Lower circulating levels of glycine are consistently reported in association with cardiovascular disease (CVD), but the causative role and therapeutic potential of glycine in atherosclerosis, the underlying cause of most CVDs, remain to be established. ... ...

Abstract	Lower circulating levels of glycine are consistently reported in association with cardiovascular disease (CVD), but the causative role and therapeutic potential of glycine in atherosclerosis, the underlying cause of most CVDs, remain to be established. Here, following the identification of reduced circulating glycine in patients with significant coronary artery disease (sCAD), we investigated a causative role of glycine in atherosclerosis by modulating glycine availability in atheroprone mice. We further evaluated the atheroprotective potential of DT-109, a recently identified glycine-based compound with dual lipid/glucose-lowering properties. Glycine deficiency enhanced, while glycine supplementation attenuated, atherosclerosis development in apolipoprotein E-deficient (Apoe
MeSH term(s)	Animals ; Apolipoproteins E/genetics ; Atherosclerosis/drug therapy ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Disease Models, Animal ; Glutamate-Cysteine Ligase ; Glutathione/metabolism ; Glycine/pharmacology ; Glycine/therapeutic use ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Plaque, Atherosclerotic/metabolism ; Superoxides
Chemical Substances	Apolipoproteins E ; Superoxides (11062-77-4) ; Glutamate-Cysteine Ligase (EC 6.3.2.2) ; Glutathione (GAN16C9B8O) ; Glycine (TE7660XO1C)
Language	English
Publishing date	2022-04-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102313
Database	MEDical Literature Analysis and Retrieval System OnLINE

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