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Article ; Online: Diosmin and its glycocalyx restorative and anti-inflammatory effects on injured blood vessels.

Mitra, Ronodeep / Nersesyan, Alina / Pentland, Kaleigh / Melin, M Mark / Levy, Robert M / Ebong, Eno E

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

2022 Volume 36, Issue 12, Page(s) e22630

Abstract: The endothelium, a crucial homeostatic organ, regulates vascular permeability and tone. Under physiological conditions, endothelial stimulation induces vasodilator endothelial nitric oxide (eNO) release and prevents adhesion molecule accessibility and ... ...

Abstract	The endothelium, a crucial homeostatic organ, regulates vascular permeability and tone. Under physiological conditions, endothelial stimulation induces vasodilator endothelial nitric oxide (eNO) release and prevents adhesion molecule accessibility and leukocyte adhesion and migration into vessel walls. Endothelium dysfunction is a principal event in cardiovascular disorders, including atherosclerosis. Minimal attention is given to an important endothelial cell structure, the endothelial glycocalyx (GCX), a negatively charged heterogeneous polysaccharide that serves as a protective covering for endothelial cells and enables endothelial cells to transduce mechanical stimuli into various biological and chemical activities. Endothelial GCX shedding thus plays a role in endothelial dysfunction, for example by increasing vascular permeability and decreasing vessel tone. Consequently, there is increasing interest in developing therapies that focus on GCX repair to limit downstream endothelium dysfunction and prevent further downstream cardiovascular events. Here, we present diosmin (3',5,7-trihydroxy-4'-methoxyflavone-7-rhamnoglucoside), a flavone glycoside of diosmetin, which downregulates adhesive molecule expression, decreases inflammation and capillary permeability, and upregulates eNO expression. Due to these pleiotropic effects of diosmin on the vasculature, a possible unidentified mechanism of action is through GCX restoration. We hypothesize that diosmin positively affects GCX integrity along with GCX-related endothelial functions. Our hypothesis was tested in a partial ligation left carotid artery (LCA) mouse model, where the right carotid artery was the control for each mouse. Diosmin (50 mg/kg) was administered daily for 7 days, 72 h after ligation. Within the ligated mice LCAs, diosmin treatment elevated the activated eNO synthase level, inhibited inflammatory cell uptake, decreased vessel wall thickness, increased vessel diameter, and increased GCX coverage of the vessel wall. ELISA showed a decrease in hyaluronan concentration in plasma samples of diosmin-treated mice, signifying reduced GCX shedding. In summary, diosmin supported endothelial GCX integrity, to which we attribute diosmin's preservation of endothelial function as indicated by attenuated expression of inflammatory factors and restored vascular tone.
MeSH term(s)	Mice ; Animals ; Glycocalyx/metabolism ; Diosmin/pharmacology ; Diosmin/metabolism ; Endothelial Cells/metabolism ; Atherosclerosis/metabolism ; Nitric Oxide/metabolism ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/metabolism ; Endothelium, Vascular/metabolism
Chemical Substances	Diosmin (7QM776WJ5N) ; Nitric Oxide (31C4KY9ESH) ; Anti-Inflammatory Agents
Language	English
Publishing date	2022-10-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202200053RR
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 296: Show issues

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Article ; Online: Lack of Laminar Shear Stress Facilitates the Endothelial Uptake of Very Small Superparamagnetic Iron Oxide Nanoparticles by Modulating the Endothelial Surface Layer.

Twamley, Shailey Gale / Gimber, Niclas / Sánchez-Ibarra, Héctor Eduardo / Christaller, Tobias / Isakzai, Victoria / Kratz, Harald / Mitra, Ronodeep / Kampen, Lena / Stach, Anke / Heilmann, Heike / Söhl-Kielczynski, Berit / Ebong, Eno Essien / Schmoranzer, Jan / Münster-Wandowski, Agnieszka / Ludwig, Antje

International journal of nanomedicine

2024 Volume 19, Page(s) 3123–3142

Abstract: Purpose: To study whether the absence of laminar shear stress (LSS) enables the uptake of very small superparamagnetic iron oxide nanoparticles (VSOP) in endothelial cells by altering the composition, size, and barrier function of the endothelial ... ...

Abstract	Purpose: To study whether the absence of laminar shear stress (LSS) enables the uptake of very small superparamagnetic iron oxide nanoparticles (VSOP) in endothelial cells by altering the composition, size, and barrier function of the endothelial surface layer (ESL). Methods and results: A quantitative particle exclusion assay with living human umbilical endothelial cells using spinning disc confocal microscopy revealed that the dimension of the ESL was reduced in cells cultivated in the absence of LSS. By combining gene expression analysis, flow cytometry, high pressure freezing/freeze substitution immuno-transmission electron microscopy, and confocal laser scanning microscopy, we investigated changes in ESL composition. We found that increased expression of the hyaluronan receptor CD44 by absence of shear stress did not affect the uptake rate of VSOPs. We identified collagen as a previously neglected component of ESL that contributes to its barrier function. Experiments with inhibitor halofuginone and small interfering RNA (siRNA) demonstrated that suppression of collagen expression facilitates VSOP uptake in endothelial cells grown under LSS. Conclusion: The absence of laminar shear stress disturbs the barrier function of the ESL, facilitating membrane accessibility and endocytic uptake of VSOP. Collagen, a previously neglected component of ESL, contributes to its barrier function.
MeSH term(s)	Humans ; Endothelial Cells/metabolism ; Endothelium ; Magnetic Iron Oxide Nanoparticles ; Gene Expression Profiling ; Collagen/metabolism ; Stress, Mechanical ; Cells, Cultured
Chemical Substances	Collagen (9007-34-5)
Language	English
Publishing date	2024-04-02
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2364941-0
ISSN	1178-2013 ; 1176-9114
ISSN (online)	1178-2013
ISSN	1176-9114
DOI	10.2147/IJN.S437714
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Zs.A 6606: Show issues

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Article: Regeneration and Assessment of the Endothelial Glycocalyx To Address Cardiovascular Disease

Banerjee, Selina / Mwangi, John G. / Stanley, Theodora K. / Mitra, Ronodeep / Ebong, Eno E.

Industrial & engineering chemistry process design and development. 2021 Nov. 24, v. 60, no. 48

2021

Abstract: Endothelial cell (EC) glycocalyx (GCX) loss permits blood circulating particle infiltration of the vessel walls and leads to vascular dysfunction, atherosclerosis, and serious downstream cardiovascular events, motivating EC GCX regeneration to treat ... ...

Abstract	Endothelial cell (EC) glycocalyx (GCX) loss permits blood circulating particle infiltration of the vessel walls and leads to vascular dysfunction, atherosclerosis, and serious downstream cardiovascular events, motivating EC GCX regeneration to treat cardiovascular disease. This review discusses the benefits and drawbacks of current options for EC GCX regeneration and assessment. Existing pharmaceutical therapies are being explored for their applicability to EC GCX regeneration, while nutraceuticals are under development as primary EC GCX regeneration approaches, and novel therapies continue to emerge. Promotion of increased efficacy of these therapies by using novel targeted drug delivery approaches is proposed. In addition, development of intravital (and intravascular, if possible) detection tools for assessment of GCX health and GCX regeneration efficacy is recommended. The work presented in this review encourages continued development of GCX regeneration and detection approaches, which could lead to breakthrough solutions for addressing cardiovascular disease.
Keywords	atherosclerosis ; blood ; chemistry ; dietary supplements ; drugs ; endothelial cells ; process design
Language	English
Dates of publication	2021-1124
Size	p. 17328-17347.
Publishing place	American Chemical Society
Document type	Article
ZDB-ID	1484436-9
ISSN	1520-5045 ; 0888-5885
ISSN (online)	1520-5045
ISSN	0888-5885
DOI	10.1021/acs.iecr.1c03074
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Endothelial barrier reinforcement relies on flow-regulated glycocalyx, a potential therapeutic target.

Harding, Ian C / Mitra, Ronodeep / Mensah, Solomon A / Nersesyan, Alina / Bal, Nandita N / Ebong, Eno E

Biorheology

2019 Volume 56, Issue 2-3, Page(s) 131–149

Abstract: Background: The onset of many disease processes depends on the function of the endothelial cell (EC) glycocalyx (GCX) which acts as a flow-dependent barrier to cellular infiltration and molecular transport across the blood vessel wall.: Objective: ... ...

Abstract	Background: The onset of many disease processes depends on the function of the endothelial cell (EC) glycocalyx (GCX) which acts as a flow-dependent barrier to cellular infiltration and molecular transport across the blood vessel wall. Objective: This review aims to examine these processes with the potential end goal of implementing GCX repair to restore EC barrier function and slow the progression of disease. Methods: Cell and mouse studies were employed to examine the state of EC GCX in healthy versus disruptive flow conditions. Correlations of observations of the GCX with a number of EC functions were sought with an emphasis on studies of trans-endothelial barrier integrity against vessel wall infiltration of cells and molecules from the circulation. To demonstrate the importance of GCX as a regulator of trans-endothelial infiltration, assays were performed using ECs with an intact GCX and compared to assays of ECs with an experimentally degraded GCX. Studies were also conducted of ECs in which a degraded GCX was repaired. Results: In healthy flow conditions, the EC GCX was found to be thick and substantially covered the endothelial surface. GCX expression dropped significantly in complex flow conditions and coincided with a disease-like cellular and molecular accumulation in the endothelium or within the blood vessel wall. Therapeutic repair of the GCX abolished this accumulation. Conclusions: Regenerating the degraded GCX reverses EC barrier dysfunction and may attenuate the progression of vascular disease.
MeSH term(s)	Animals ; Capillary Permeability/physiology ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Glycocalyx/metabolism ; Hemodynamics/physiology ; Humans ; Mice ; Vascular Diseases/metabolism ; Vascular Diseases/therapy
Language	English
Publishing date	2019-04-15
Publishing country	Netherlands
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. ; Review
ZDB-ID	82015-5
ISSN	1878-5034 ; 0006-355X
ISSN (online)	1878-5034
ISSN	0006-355X
DOI	10.3233/BIR-180205
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Zs.A 394: Show issues

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Article ; Online: Pro-atherosclerotic disturbed flow disrupts caveolin-1 expression, localization, and function via glycocalyx degradation

Ian C. Harding / Ronodeep Mitra / Solomon A. Mensah / Ira M. Herman / Eno E. Ebong

Journal of Translational Medicine, Vol 16, Iss 1, Pp 1-

2018 Volume 20

Abstract: Abstract Background Endothelial-dependent atherosclerosis develops in a non-random pattern in regions of vessel bending and bifurcations, where blood flow exhibits disturbed flow (DF) patterns. In contrast, uniform flow (UF), normal endothelium, and ... ...

Abstract	Abstract Background Endothelial-dependent atherosclerosis develops in a non-random pattern in regions of vessel bending and bifurcations, where blood flow exhibits disturbed flow (DF) patterns. In contrast, uniform flow (UF), normal endothelium, and healthy vessel walls co-exist within straight vessels. In clarifying how flow protectively or atherogenically regulates endothelial cell behavior, involvement of the endothelial surface glycocalyx has been suggested due to reduced expression in regions of atherosclerosis development. Here, we hypothesized that pro-atherosclerotic endothelial dysfunction occurs as a result of DF-induced reduction in glycocalyx expression and subsequently impairs endothelial sensitivity to flow. Specifically, we propose that glycocalyx degradation can induce pro-atherosclerotic endothelial dysfunction through decreased caveolin-1 and endothelial nitric oxide synthase expression and localization. Methods We studied endothelial cells in atherosclerotic-prone DF and atherosclerotic-resistant UF conditions in parallel plate flow culture and in C57Bl/6 mice. The effects of flow conditioning on endothelial cell behavior were quantified using immunocytochemistry. The glycocalyx was fluorescently labeled for wheat germ agglutinin, which serves as a general glycocalyx label, and heparan sulfate, a major glycocalyx component. Additionally, mechanosensitivity was assessed by immunocytochemical fluorescence expression and function of caveolin-1, the protein that forms the mechanosignaling caveolar invaginations on the endothelial surface, total endothelial-type nitric oxide synthase (eNOS), which synthesizes nitric oxide, and serine 1177 phosphorylated eNOS (eNOS-pS1177), which is the active form of eNOS. Caveolin function and eNOS expression and activation were correlated to glycocalyx expression. Heparinase III enzyme was used to degrade a major glycocalyx component, HS, to identify the role of the glycocalyx in caveoin-1 and eNOS-pS1177 regulation. Results Results confirmed that DF reduces ...
Keywords	Atherosclerosis ; Endothelial cells ; Fluid shear stress ; Glycocalyx ; Caveolin ; Endothelial-type nitric oxide synthase ; Medicine ; R
Subject code	570
Language	English
Publishing date	2018-12-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Pro-atherosclerotic disturbed flow disrupts caveolin-1 expression, localization, and function via glycocalyx degradation.

Harding, Ian C / Mitra, Ronodeep / Mensah, Solomon A / Herman, Ira M / Ebong, Eno E

Journal of translational medicine

2018 Volume 16, Issue 1, Page(s) 364

Abstract: Background: Endothelial-dependent atherosclerosis develops in a non-random pattern in regions of vessel bending and bifurcations, where blood flow exhibits disturbed flow (DF) patterns. In contrast, uniform flow (UF), normal endothelium, and healthy ... ...

Abstract	Background: Endothelial-dependent atherosclerosis develops in a non-random pattern in regions of vessel bending and bifurcations, where blood flow exhibits disturbed flow (DF) patterns. In contrast, uniform flow (UF), normal endothelium, and healthy vessel walls co-exist within straight vessels. In clarifying how flow protectively or atherogenically regulates endothelial cell behavior, involvement of the endothelial surface glycocalyx has been suggested due to reduced expression in regions of atherosclerosis development. Here, we hypothesized that pro-atherosclerotic endothelial dysfunction occurs as a result of DF-induced reduction in glycocalyx expression and subsequently impairs endothelial sensitivity to flow. Specifically, we propose that glycocalyx degradation can induce pro-atherosclerotic endothelial dysfunction through decreased caveolin-1 and endothelial nitric oxide synthase expression and localization. Methods: We studied endothelial cells in atherosclerotic-prone DF and atherosclerotic-resistant UF conditions in parallel plate flow culture and in C57Bl/6 mice. The effects of flow conditioning on endothelial cell behavior were quantified using immunocytochemistry. The glycocalyx was fluorescently labeled for wheat germ agglutinin, which serves as a general glycocalyx label, and heparan sulfate, a major glycocalyx component. Additionally, mechanosensitivity was assessed by immunocytochemical fluorescence expression and function of caveolin-1, the protein that forms the mechanosignaling caveolar invaginations on the endothelial surface, total endothelial-type nitric oxide synthase (eNOS), which synthesizes nitric oxide, and serine 1177 phosphorylated eNOS (eNOS-pS1177), which is the active form of eNOS. Caveolin function and eNOS expression and activation were correlated to glycocalyx expression. Heparinase III enzyme was used to degrade a major glycocalyx component, HS, to identify the role of the glycocalyx in caveoin-1 and eNOS-pS1177 regulation. Results: Results confirmed that DF reduces caveolin-1 expression and abolishes most of its subcellular localization preferences, when compared to the effect of UF. DF down-regulates caveolin-1 mechanosignaling, as indicated by its reduced colocalization with serine 1177 phosphorylated endothelial-type nitric oxide synthase (eNOS-pS1177), a vasoregulatory signaling molecule whose activity is regulated by its residence in caveolae. As expected, DF inhibited glycocalyx expression compared to UF. In the absence of heparan sulfate, a major glycocalyx component, UF-conditioned endothelial cells exhibited near DF-like caveolin-1 expression, localization, and colocalization with eNOS-pS1177. Conclusions: This is the first demonstration of a flow-defined role of the glycocalyx in caveolae expression and function related to vasculoprotective endothelial mechanosensitivity that defends against atherosclerosis. The results suggest that a glycocalyx-based therapeutic targeted to areas of atherosclerosis development could prevent disease initiation and progression.
MeSH term(s)	Adipose Tissue ; Animals ; Atherosclerosis/metabolism ; Caveolin 1/metabolism ; Endothelial Cells/metabolism ; Glycocalyx/metabolism ; Hemorheology ; Heparitin Sulfate/metabolism ; Male ; Mice, Inbred C57BL ; Models, Biological ; Nitric Oxide Synthase Type III/metabolism ; Rats ; Signal Transduction
Chemical Substances	Caveolin 1 ; Heparitin Sulfate (9050-30-0) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2018-12-18
Publishing country	England
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.
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/s12967-018-1721-2
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Article ; Online: Targeted Intravenous Nanoparticle Delivery: Role of Flow and Endothelial Glycocalyx Integrity.

Cheng, Ming J / Mitra, Ronodeep / Okorafor, Chinedu C / Nersesyan, Alina A / Harding, Ian C / Bal, Nandita N / Kumar, Rajiv / Jo, Hanjoong / Sridhar, Srinivas / Ebong, Eno E

Annals of biomedical engineering

2020 Volume 48, Issue 7, Page(s) 1941–1954

Abstract: Therapies for atherosclerotic cardiovascular disease should target early disease stages and specific vascular sites where disease occurs. Endothelial glycocalyx (GCX) degradation compromises endothelial barrier function and increases vascular ... ...

Abstract	Therapies for atherosclerotic cardiovascular disease should target early disease stages and specific vascular sites where disease occurs. Endothelial glycocalyx (GCX) degradation compromises endothelial barrier function and increases vascular permeability. This initiates pro-atherosclerotic lipids and inflammatory cells to penetrate vessel walls, and at the same time this can be leveraged for targeted drug delivery. In prior cell culture studies, GCX degradation significantly increased endothelial cell uptake of nanoparticle vehicles that are designed for drug delivery, compared to the effects of intact GCX. The present study assessed if the cell culture findings translate to selective nanoparticle uptake in animal vessels. In mice, the left carotid artery (LCA) was partially ligated to disturb blood flow, which induces GCX degradation, endothelial dysfunction, and atherosclerosis. After ligation, the LCA vessel wall exhibited a loss of continuity of the GCX layer on the intima. 10-nm gold nanospheres (GNS) coated with polyethylene glycol (PEG) were delivered intravenously. GCX degradation in the ligated LCA correlated to increased GNS infiltration of the ligated LCA wall. This suggests that GCX dysfunction, which coincides with atherosclerosis, can indeed be targeted for enhanced drug delivery, offering a new approach in cardiovascular disease therapy.
MeSH term(s)	Animals ; Atherosclerosis/drug therapy ; Carotid Arteries/pathology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/pathology ; Glycocalyx/pathology ; Gold ; Human Umbilical Vein Endothelial Cells ; Humans ; Male ; Metal Nanoparticles/administration & dosage ; Mice ; Mice, Inbred C57BL ; Polyethylene Glycols
Chemical Substances	Polyethylene Glycols (3WJQ0SDW1A) ; Gold (7440-57-5)
Language	English
Publishing date	2020-02-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	185984-5
ISSN	1573-9686 ; 0191-5649 ; 0090-6964
ISSN (online)	1573-9686
ISSN	0191-5649 ; 0090-6964
DOI	10.1007/s10439-020-02474-4
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Zs.A 1018: Show issues

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Article ; Online: Glycocalyx in Atherosclerosis-Relevant Endothelium Function and as a Therapeutic Target.

Mitra, Ronodeep / O'Neil, Gerard Leland / Harding, Ian Chandler / Cheng, Ming Jie / Mensah, Solomon Arko / Ebong, Eno Essien

Current atherosclerosis reports

2017 Volume 19, Issue 12, Page(s) 63

Abstract: Purpose of review: The cell surface-attached extracellular glycocalyx (GCX) layer is a major contributor to endothelial cell (EC) function and EC-dependent vascular health and is a first line of defense against vascular diseases including ... ...

Abstract	Purpose of review: The cell surface-attached extracellular glycocalyx (GCX) layer is a major contributor to endothelial cell (EC) function and EC-dependent vascular health and is a first line of defense against vascular diseases including atherosclerosis. Here, we highlight our findings regarding three GCX-dependent EC functions, which are altered when GCX is shed and in atherosclerosis. We discuss why the GCX is a viable option for the prevention and treatment of atherosclerosis. Recent findings: GCX regulated EC activities such as barrier and filtration function, active cell-to-cell communication, and vascular tone mediation contribute to function of the entire vascular wall. Atheroprone vessel regions, including bifurcation sites, exhibit breakdown in GCX. This GCX degradation allows increased lipid flux and thereby promotes lipid deposition in the vessel walls, a hallmark of atherosclerosis. GCX degradation also alters EC-to-EC communication while increasing EC-to-inflammatory cell interactions that enable inflammatory cells to migrate into the vessel wall. Inflammatory macrophages and foam cells, to be specific, appear in early stages of atherosclerosis. Furthermore, GCX degradation deregulates vascular tone, by causing ECs to reduce their expression of endothelial nitric oxide synthase (eNOS) which produces the vasodilator, nitric oxide. Loss of vasodilation supports vasoconstriction, which promotes the progression of atherosclerosis. Common medicinal atherosclerosis therapies include lipid lowering and anti-platelet therapies. None of these treatments specifically target the endothelial GCX, although the GCX is at the front-line in atherosclerosis combat. This review demonstrates the viability of targeting the GCX therapeutically, to support proper EC functionality and prevent and/or treat atherosclerosis.
MeSH term(s)	Animals ; Atherosclerosis/etiology ; Atherosclerosis/metabolism ; Atherosclerosis/physiopathology ; Atherosclerosis/therapy ; Endothelial Cells/metabolism ; Endothelial Cells/physiology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiology ; Endothelium, Vascular/physiopathology ; Glycocalyx/metabolism ; Glycocalyx/physiology ; Humans ; Models, Animal ; Molecular Targeted Therapy
Language	English
Publishing date	2017-11-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057369-8
ISSN	1534-6242 ; 1523-3804
ISSN (online)	1534-6242
ISSN	1523-3804
DOI	10.1007/s11883-017-0691-9
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Zs.A 5534: Show issues

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Article ; Online: The comparative effects of high fat diet or disturbed blood flow on glycocalyx integrity and vascular inflammation.

Mitra, Ronodeep / Qiao, Ju / Madhavan, Sudharsan / O'Neil, Gerard L / Ritchie, Bailey / Kulkarni, Praveen / Sridhar, Srinivas / van de Ven, Anne L / Kemmerling, Erica M Cherry / Ferris, Craig / Hamilton, James A / Ebong, Eno E

Translational medicine communications

2018 Volume 3

Abstract: Background and aims: Endothelial surface glycocalyx shedding plays a role in endothelial dysfunction and increases vessel wall permeability, which can lead to inflammation and atherogenesis. We sought to elucidate whether a high fat diet (HFD) or ... ...

Abstract	Background and aims: Endothelial surface glycocalyx shedding plays a role in endothelial dysfunction and increases vessel wall permeability, which can lead to inflammation and atherogenesis. We sought to elucidate whether a high fat diet (HFD) or disturbed blood flow conditions, both of which are atherogenic risk factors, would contribute more detrimentally to pre-atherosclerotic loss of endothelial glycocalyx integrity and vascular inflammation. Methods: Six to seven week-old C57BL/6-background apolipoprotein-E-knockout (ApoE-KO) male mice were either fed a chow diet, fed a modified Western HFD, and/or subjected to a partial left carotid artery (LCA) ligation procedure to induce disturbed blood flow patterns in the LCA. Mice were sacrificed after 1 week of experimental conditions. Both LCA and right carotid artery (RCA) vessels were dissected and preserved to compare glycocalyx coverage and thickness as well as macrophage accumulation in carotid arterial walls amongst and between cohorts. Results: Glycocalyx coverage of the endothelium was significantly reduced in the LCAs of HFD fed mice when compared to the control. More significant reduction in glycocalyx coverage occurred in the LCAs of mice exposed to disturbed flow by partial LCA ligation when compared to the control. No differences were found in glycocalyx coverage of RCAs from all cohorts. Regarding inflammation, no difference in macrophage accumulation in carotid arterial walls was observed when comparing the LCAs and RCAs of control and HFD fed mice. However, macrophage infiltration in vessel walls showed a 20-fold increase in the LCAs exposed to disturbed flow following ligation, when compared to control LCAs, while no such statistical difference was observed between the RCAs of the group. Conclusions: In our mouse model, endothelial glycocalyx integrity was compromised more by disturbed blood flow patterns than by exposure of the carotid vessel to HFD conditions. The pathophysiological implications include endothelial dysfunction, which correlates to macrophage infiltration in vessel walls and promotes atherogenesis.
Language	English
Publishing date	2018-11-22
Publishing country	England
Document type	Journal Article
ISSN	2396-832X
ISSN (online)	2396-832X
DOI	10.1186/s41231-018-0029-9
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Article ; Online: Characterization of aortic root geometry in transcatheter aortic valve replacement patients.

Madukauwa-David, Immanuel David / Midha, Prem A / Sharma, Rahul / McLain, Kylee / Mitra, Ronodeep / Crawford, Kaylyn / Yoon, Sung-Han / Makkar, Raj R / Yoganathan, Ajit P

Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions

2018 Volume 93, Issue 1, Page(s) 134–140

Abstract: Purpose: The study aimed to characterize the geometry of the aortic root pre- and post-transcatheter aortic valve replacement (TAVR) and investigate differences in pre- and post-TAVR anatomy.: Background: A greater understanding of how aortic root ... ...

Abstract	Purpose: The study aimed to characterize the geometry of the aortic root pre- and post-transcatheter aortic valve replacement (TAVR) and investigate differences in pre- and post-TAVR anatomy. Background: A greater understanding of how aortic root geometry changes after TAVR is needed to facilitate further investigation into the hemodynamic profiles of the post-TAVR aortic root. Methods: Anatomical measurements were conducted on de-identified, retrospective post-TAVR 4DCT scans of 109 patients with aortic stenosis obtained from the RESOLVE study. The diameter of the aortic root was measured at the level of the annulus, left ventricular outflow tract (LVOT), sinus of Valsalva, sinotubular junction (STJ) and ascending aorta. The heights of the STJ and coronary arteries were also measured. Results: All aortic root dimensions were normally distributed across the cohort and changed significantly between pre- and post-TAVR conditions (P < 0.01). Post-TAVR dimensions changed significantly from peak systole to end diastole (P < 0.01). Regression models were obtained for all aortic root dimensions in terms of annulus diameter with excellent coefficient of determination (R Conclusions: There are significant differences between pre- and post-TAVR as well as peak systolic and end diastolic aortic root anatomy. Appropriate anatomical dimensions should be selected for benchtop testing as the geometry varies greatly throughout the cardiac cycle.
MeSH term(s)	Aged ; Aged, 80 and over ; Aortic Valve/diagnostic imaging ; Aortic Valve/physiopathology ; Aortic Valve/surgery ; Aortic Valve Stenosis/diagnostic imaging ; Aortic Valve Stenosis/physiopathology ; Aortic Valve Stenosis/surgery ; Female ; Four-Dimensional Computed Tomography ; Humans ; Male ; Multidetector Computed Tomography ; Predictive Value of Tests ; Retrospective Studies ; Transcatheter Aortic Valve Replacement ; Treatment Outcome ; United States
Language	English
Publishing date	2018-09-28
Publishing country	United States
Document type	Journal Article ; Multicenter Study
ZDB-ID	1459995-8
ISSN	1522-726X ; 1522-1946
ISSN (online)	1522-726X
ISSN	1522-1946
DOI	10.1002/ccd.27805
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In stock of ZB MED Cologne/Königswinter

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Full text online

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In stock of ZB MED Cologne/Königswinter

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Order via subito

Inter-library loan at ZB MED

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In stock of ZB MED Cologne/Königswinter

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