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Article: A Next-Generation 3D Tissue-Engineered Model of the Human Brain Microvasculature to Study the Blood-Brain Barrier.

Galpayage Dona, Kalpani N Udeni / Ramirez, Servio H / Andrews, Allison M

2023 Volume 10, Issue 7

Abstract: More than a billion people are affected by neurological disorders, and few have effective therapeutic options. A key challenge that has prevented promising preclinically proven strategies is the translation gap to the clinic. Humanized tissue engineering ...

Abstract	More than a billion people are affected by neurological disorders, and few have effective therapeutic options. A key challenge that has prevented promising preclinically proven strategies is the translation gap to the clinic. Humanized tissue engineering models that recreate the brain environment may aid in bridging this translational gap. Here, we showcase the methodology that allows for the practical fabrication of a comprehensive microphysicological system (MPS) of the blood-brain barrier (BBB). Compared to other existing 2D and 3D models of the BBB, this model features relevant cytoarchitecture and multicellular arrangement, with branching and network topologies of the vascular bed. This process utilizes 3D bioprinting with digital light processing to generate a vasculature lumen network surrounded by embedded human astrocytes. The lumens are then cellularized with primary human brain microvascular endothelial cells and pericytes. To initiate mechanotransduction pathways and complete maturation, vascular structures are continuously perfused for 7 days. Constructs are validated for complete endothelialization with viability dyes prior to functional assessments that include barrier integrity (permeability) and immune-endothelial interactions. This MPS has applications for the study of novel therapeutics, toxins, and elucidating mechanisms of pathophysiology.
Language	English
Publishing date	2023-07-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2746191-9
ISSN	2306-5354
ISSN	2306-5354
DOI	10.3390/bioengineering10070817
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Article ; Online: Effects of Drag-Reducing Polymers on Hemodynamics and Whole Blood-Endothelial Interactions in 3D-Printed Vascular Topologies.

Paone, Louis S / Szkolnicki, Matthew / DeOre, Brandon J / Tran, Kiet A / Goldman, Noah / Andrews, Allison M / Ramirez, Servio H / Galie, Peter A

ACS applied materials & interfaces

2024 Volume 16, Issue 12, Page(s) 14457–14466

Abstract: Most in vitro models use culture medium to apply fluid shear stress to endothelial cells, which does not capture the interaction between blood and endothelial cells. Here, we describe a new system to characterize whole blood flow through a 3D-printed, ... ...

Abstract	Most in vitro models use culture medium to apply fluid shear stress to endothelial cells, which does not capture the interaction between blood and endothelial cells. Here, we describe a new system to characterize whole blood flow through a 3D-printed, endothelialized vascular topology that induces flow separation at a bifurcation. Drag-reducing polymers, which have been previously studied as a potential therapy to reduce the pressure drop across the vascular bed, are evaluated for their effect on mitigating the disturbed flow. Polymer concentrations of 1000 ppm prevented recirculation and disturbed flow at the wall. Proteomic analysis of plasma collected from whole blood recirculated through the vascularized channel with and without drag-reducing polymers provides insight into the effects of flow regimes on levels of proteins indicative of the endothelial-blood interaction. The results indicate that blood flow alters proteins associated with coagulation, inflammation, and other processes. Overall, these proof-of-concept experiments demonstrate the importance of using whole blood flow to study the endothelial response to perfusion.
MeSH term(s)	Polymers/pharmacology ; Endothelial Cells ; Proteomics ; Hemodynamics/physiology ; Printing, Three-Dimensional ; Stress, Mechanical
Chemical Substances	Polymers
Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Journal Article
ISSN	1944-8252
ISSN (online)	1944-8252
DOI	10.1021/acsami.3c17099
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Article: Engineered Dual Antioxidant Enzyme Complexes Targeting ICAM-1 on Brain Endothelium Reduce Brain Injury-Associated Neuroinflammation.

Leonard, Brian M / Shuvaev, Vladimir V / Bullock, Trent A / Galpayage Dona, Kalpani N Udeni / Muzykantov, Vladimir R / Andrews, Allison M / Ramirez, Servio H

Bioengineering (Basel, Switzerland)

2024 Volume 11, Issue 3

Abstract: The neuroinflammatory cascade triggered by traumatic brain injury (TBI) represents a clinically important point for therapeutic intervention. Neuroinflammation generates oxidative stress in the form of high-energy reactive oxygen and nitrogen species, ... ...

Abstract	The neuroinflammatory cascade triggered by traumatic brain injury (TBI) represents a clinically important point for therapeutic intervention. Neuroinflammation generates oxidative stress in the form of high-energy reactive oxygen and nitrogen species, which are key mediators of TBI pathology. The role of the blood-brain barrier (BBB) is essential for proper neuronal function and is vulnerable to oxidative stress. Results herein explore the notion that attenuating oxidative stress at the vasculature after TBI may result in improved BBB integrity and neuroprotection. Utilizing amino-chemistry, a biological construct (designated "dual conjugate" for short) was generated by covalently binding two antioxidant enzymes (superoxide dismutase 1 (SOD-1) and catalase (CAT)) to antibodies specific for ICAM-1. Bioengineering of the conjugate preserved its targeting and enzymatic functions, as evaluated by real-time bioenergetic measurements (via the Seahorse-XF platform), in brain endothelial cells exposed to increasing concentrations of hydrogen peroxide or a superoxide anion donor. Results showed that the dual conjugate effectively mitigated the mitochondrial stress due to oxidative damage. Furthermore, dual conjugate administration also improved BBB and endothelial protection under oxidative insult in an in vitro model of TBI utilizing a software-controlled stretching device that induces a 20% in mechanical strain on the endothelial cells. Additionally, the dual conjugate was also effective in reducing indices of neuroinflammation in a controlled cortical impact (CCI)-TBI animal model. Thus, these studies provide proof of concept that targeted dual antioxidant biologicals may offer a means to regulate oxidative stress-associated cellular damage during neurotrauma.
Language	English
Publishing date	2024-02-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2746191-9
ISSN	2306-5354
ISSN	2306-5354
DOI	10.3390/bioengineering11030200
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Article ; Online: Activation of CB2R by synthetic CB2R agonist, PM289, improves brain endothelial barrier properties, decreases inflammatory response and enhances endothelial repair.

Bullock, Trent A / Galpayage Dona, Kalpani N Udeni / Hale, Jonathan F / Morales, Paula / Jagerovic, Nadine / Andrews, Allison M / Ramirez, Servio H

NeuroImmune pharmacology and therapeutics

2023 Volume 2, Issue 4, Page(s) 387–400

Abstract: The Cannabinoid 2 Receptor (CB2R) has been found to provide immunological modulation in different cell types. More recently, detection of CB2R in the cerebral endothelium suggests a possible role in the resolution of inflammation at the level of the ... ...

Abstract	The Cannabinoid 2 Receptor (CB2R) has been found to provide immunological modulation in different cell types. More recently, detection of CB2R in the cerebral endothelium suggests a possible role in the resolution of inflammation at the level of the blood-brain-barrier (BBB). Here, the notion that CB2R upregulation in brain endothelial cells could be exploited to promote vascular protection and BBB integrity was evaluated. Targeting and activation of CB2R was accomplished by a novel and highly specific chromenopyrazole based CB2R agonist, PM289. This study demonstrates that CB2R upregulation is induced as early as 8 h in the cortical vasculature in an experimental mouse model of TBI. Unlike CB2R, CB1R was marginally detected and not significantly induced. In the human brain endothelial cell line, hCMEC/D3 cells, similar induction of CB2R was observed upon stimulation with TNFα. Analysis of transendothelial electrical resistance shows that PM289 markedly prevented the barrier-leakiness induced by TNFα. The BBB is also responsible for maintaining an immunological barrier. The five-fold increase in ICAM1 expression in stimulated endothelial cells was significantly diminished due to CB2R activation. Utilizing wounding assays, results showed that wound repair could be accomplished in nearly half the time when the novel CB2R agonist is present compared to the untreated control. Lastly, mechanistically, the effects of CB2R may be explained by the observed inhibition of the p65 NFκB subunit. Overall, these studies support the notion that targeting and activating CB2R in the brain vasculature could aid in BBB and vascular protection in the context of neuroinflammation.
Language	English
Publishing date	2023-10-16
Publishing country	Germany
Document type	Journal Article
ISSN	2750-6665
ISSN (online)	2750-6665
DOI	10.1515/nipt-2023-0016
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Article ; Online: Microparticle-Induced Activation of the Vascular Endothelium Requires Caveolin-1/Caveolae.

Andrews, Allison M / Rizzo, Victor

PloS one

2016 Volume 11, Issue 2, Page(s) e0149272

Abstract: Microparticles (MPs) are small membrane fragments shed from normal as well as activated, apoptotic or injured cells. Emerging evidence implicates MPs as a causal and/or contributing factor in altering normal vascular cell phenotype through initiation of ... ...

Abstract	Microparticles (MPs) are small membrane fragments shed from normal as well as activated, apoptotic or injured cells. Emerging evidence implicates MPs as a causal and/or contributing factor in altering normal vascular cell phenotype through initiation of proinflammatory signal transduction events and paracrine delivery of proteins, mRNA and miRNA. However, little is known regarding the mechanism by which MPs influence these events. Caveolae are important membrane microdomains that function as centers of signal transduction and endocytosis. Here, we tested the concept that the MP-induced pro-inflammatory phenotype shift in endothelial cells (ECs) depends on caveolae. Consistent with previous reports, MP challenge activated ECs as evidenced by upregulation of intracellular adhesion molecule-1 (ICAM-1) expression. ICAM-1 upregulation was mediated by activation of NF-κB, Poly [ADP-ribose] polymerase 1 (PARP-1) and the epidermal growth factor receptor (EGFR). This response was absent in ECs lacking caveolin-1/caveolae. To test whether caveolae-mediated endocytosis, a dynamin-2 dependent process, is a feature of the proinflammatory response, EC's were pretreated with the dynamin-2 inhibitor dynasore. Similar to observations in cells lacking caveolin-1, inhibition of endocytosis significantly attenuated MPs effects including, EGFR phosphorylation, activation of NF-κB and upregulation of ICAM-1 expression. Thus, our results indicate that caveolae play a role in mediating the pro-inflammatory signaling pathways which lead to EC activation in response to MPs.
MeSH term(s)	Animals ; Caveolae/metabolism ; Caveolin 1/genetics ; Caveolin 1/metabolism ; Cell Line ; Cell-Derived Microparticles/metabolism ; Endocytosis/drug effects ; Endothelial Cells ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; ErbB Receptors/metabolism ; Gene Knockout Techniques ; Intercellular Adhesion Molecule-1/genetics ; Intercellular Adhesion Molecule-1/metabolism ; Mice ; NF-kappa B/metabolism ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Caveolin 1 ; NF-kappa B ; Tumor Necrosis Factor-alpha ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2016-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0149272
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Article ; Online: SARS-CoV-2 Spike Protein Disrupts Blood-Brain Barrier Integrity via RhoA Activation.

DeOre, Brandon J / Tran, Kiet A / Andrews, Allison M / Ramirez, Servio H / Galie, Peter A

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2021 Volume 16, Issue 4, Page(s) 722–728

Abstract: The SARS-CoV-2 spike protein has been shown to disrupt blood-brain barrier (BBB) function, but its pathogenic mechanism of action is unknown. Whether angiotensin converting enzyme 2 (ACE2), the viral binding site for SARS-CoV-2, contributes to the spike ... ...

Abstract	The SARS-CoV-2 spike protein has been shown to disrupt blood-brain barrier (BBB) function, but its pathogenic mechanism of action is unknown. Whether angiotensin converting enzyme 2 (ACE2), the viral binding site for SARS-CoV-2, contributes to the spike protein-induced barrier disruption also remains unclear. Here, a 3D-BBB microfluidic model was used to interrogate mechanisms by which the spike protein may facilitate barrier dysfunction. The spike protein upregulated the expression of ACE2 in response to laminar shear stress. Moreover, interrogating the role of ACE2 showed that knock-down affected endothelial barrier properties. These results identify a possible role of ACE2 in barrier homeostasis. Analysis of RhoA, a key molecule in regulating endothelial cytoskeleton and tight junction complex dynamics, reveals that the spike protein triggers RhoA activation. Inhibition of RhoA with C3 transferase rescues its effect on tight junction disassembly. Overall, these results indicate a possible means by which the engagement of SARS-CoV-2 with ACE2 facilitates disruption of the BBB via RhoA activation. Understanding how SARS-CoV-2 dysregulates the BBB may lead to strategies to prevent the neurological deficits seen in COVID-19 patients.
MeSH term(s)	Blood-Brain Barrier/metabolism ; COVID-19 ; Humans ; Protein Binding ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus ; rhoA GTP-Binding Protein
Chemical Substances	Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; RHOA protein, human (124671-05-2) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2021-10-23
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-021-10029-0
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Article ; Online: Extracellular vesicles: mediators and biomarkers of pathology along CNS barriers.

Ramirez, Servio H / Andrews, Allison M / Paul, Debayon / Pachter, Joel S

Fluids and barriers of the CNS

2018 Volume 15, Issue 1, Page(s) 19

Abstract: Extracellular vesicles (EVs) are heterogeneous, nano-sized vesicles that are shed into the blood and other body fluids, which disperse a variety of bioactive molecules (e.g., protein, mRNA, miRNA, DNA and lipids) to cellular targets over long and short ... ...

Abstract	Extracellular vesicles (EVs) are heterogeneous, nano-sized vesicles that are shed into the blood and other body fluids, which disperse a variety of bioactive molecules (e.g., protein, mRNA, miRNA, DNA and lipids) to cellular targets over long and short distances. EVs are thought to be produced by nearly every cell type, however this review will focus specifically on EVs that originate from cells at the interface of CNS barriers. Highlighted topics include, EV biogenesis, the production of EVs in response to neuroinflammation, role in intercellular communication and their utility as a therapeutic platform. In this review, novel concepts regarding the use of EVs as biomarkers for BBB status and as facilitators for immune neuroinvasion are also discussed. Future directions and prospective are covered along with important unanswered questions in the field of CNS endothelial EV biology.
MeSH term(s)	Central Nervous System/blood supply ; Central Nervous System/metabolism ; Exosomes/metabolism ; Extracellular Vesicles/metabolism ; Humans ; Inflammation/metabolism
Language	English
Publishing date	2018-07-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-018-0104-7
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Article ; Online: The psychoactive drug of abuse mephedrone differentially disrupts blood-brain barrier properties.

Buzhdygan, Tetyana P / Rodrigues, Cassidy R / McGary, Hannah M / Khan, Jana A / Andrews, Allison M / Rawls, Scott M / Ramirez, Servio H

Journal of neuroinflammation

2021 Volume 18, Issue 1, Page(s) 63

Abstract: Background: Synthetic cathinones are a category of psychostimulants belonging to the growing number of designer drugs also known as "Novel Psychoactive Substances" (NPS). In recent years, NPS have gained popularity in the recreational drug market due to ...

Abstract	Background: Synthetic cathinones are a category of psychostimulants belonging to the growing number of designer drugs also known as "Novel Psychoactive Substances" (NPS). In recent years, NPS have gained popularity in the recreational drug market due to their amphetamine-like stimulant effects, low cost, ease of availability, and lack of detection by conventional toxicology screening. All these factors have led to an increase in NPS substance abuse among the young adults, followed by spike of overdose-related fatalities and adverse effects, severe neurotoxicity, and cerebral vascular complications. Much remains unknown about how synthetic cathinones negatively affect the CNS and the status of the blood-brain barrier (BBB). Methods: We used in vitro models of the BBB and primary human brain microvascular endothelial cells (hBMVEC) to investigate the effects of the synthetic cathinone, 4-methyl methcathinone (mephedrone), on BBB properties. Results: We showed that mephedrone exposure resulted in the loss of barrier properties and endothelial dysfunction of primary hBMVEC. Increased permeability and decreased transendothelial electrical resistance of the endothelial barrier were attributed to changes in key proteins involved in the tight junction formation. Elevated expression of matrix metalloproteinases, angiogenic growth factors, and inflammatory cytokines can be explained by TLR-4-dependent activation of NF-κB signaling. Conclusions: In this first characterization of the effects of a synthetic cathinone on human brain endothelial cells, it appears clear that mephedrone-induced damage of the BBB is not limited by the disruption of the barrier properties but also include endothelial activation and inflammation. This may especially be important in comorbid situations of mephedrone abuse and HIV-1 infections. In this context, mephedrone could negatively affect HIV-1 neuroinvasion and NeuroAIDS progression.
MeSH term(s)	Blood-Brain Barrier/drug effects ; Cells, Cultured ; Designer Drugs/pharmacology ; Endothelial Cells/drug effects ; Humans ; Methamphetamine/analogs & derivatives ; Methamphetamine/pharmacology ; Psychotropic Drugs/pharmacology
Chemical Substances	Designer Drugs ; Psychotropic Drugs ; Methamphetamine (44RAL3456C) ; mephedrone (8BA8T27317)
Language	English
Publishing date	2021-03-01
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-021-02116-z
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Article ; Online: An Engineered Adeno-Associated Virus Capsid Mediates Efficient Transduction of Pericytes and Smooth Muscle Cells of the Brain Vasculature.

Ramirez, Servio H / Hale, Jonathan F / McCarthy, Siobhan / Cardenas, Christian L / Dona, Kalpani N Udeni Galpayage / Hanlon, Killian S / Hudry, Eloise / Cruz, Demitri De La / Ng, Carrie / Das, Sabyasachi / Nguyen, Diane M / Nammour, Josette / Bennett, Rachel E / Andrews, Allison M / Musolino, Patricia L / Maguire, Casey A

Human gene therapy

2023 Volume 34, Issue 15-16, Page(s) 682–696

Abstract: Neurodegeneration and cerebrovascular disease share an underlying microvascular dysfunction that may be remedied by selective transgene delivery. To date, limited options exist in which cellular components of the brain vasculature can be effectively ... ...

Abstract	Neurodegeneration and cerebrovascular disease share an underlying microvascular dysfunction that may be remedied by selective transgene delivery. To date, limited options exist in which cellular components of the brain vasculature can be effectively targeted by viral vector therapeutics. In this study, we characterize the first engineered adeno-associated virus (AAV) capsid mediating high transduction of cerebral vascular pericytes and smooth muscle cells (SMCs). We performed two rounds of
MeSH term(s)	Humans ; Capsid/metabolism ; Dependovirus/metabolism ; Transduction, Genetic ; Pericytes/metabolism ; Capsid Proteins/metabolism ; Brain/metabolism ; Myocytes, Smooth Muscle/metabolism ; Genetic Vectors/genetics
Chemical Substances	Capsid Proteins
Language	English
Publishing date	2023-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1028152-6
ISSN	1557-7422 ; 1043-0342
ISSN (online)	1557-7422
ISSN	1043-0342
DOI	10.1089/hum.2022.211
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Article: Endothelial Targeted Strategies to Combat Oxidative Stress: Improving Outcomes in Traumatic Brain Injury.

Lutton, Evan M / Farney, S Katie / Andrews, Allison M / Shuvaev, Vladimir V / Chuang, Gwo-Yu / Muzykantov, Vladimir R / Ramirez, Servio H

Frontiers in neurology

2019 Volume 10, Page(s) 582

Abstract: The endothelium is a thin monolayer of specialized cells that lines the luminal wall of blood vessels and constitutes the critical innermost portion of the physical barrier between the blood and the brain termed the blood-brain barrier (BBB). Aberrant ... ...

Abstract	The endothelium is a thin monolayer of specialized cells that lines the luminal wall of blood vessels and constitutes the critical innermost portion of the physical barrier between the blood and the brain termed the blood-brain barrier (BBB). Aberrant changes in the endothelium occur in many neuropathological states, including those with high morbidity and mortality that lack targeted therapeutic interventions, such as traumatic brain injury (TBI). Utilizing ligands of surface determinants expressed on brain endothelium to target and combat injury mechanisms at damaged endothelium offers a new approach to the study of TBI and new avenues for clinical advancement. Many factors influence the targets that are expressed on endothelium. Therefore, the optimization of binding sites and ideal design features of nanocarriers are controllable factors that permit the engineering of nanotherapeutic agents with applicability that is specific to a known disease state. Following TBI, damaged endothelial cells upregulate cell adhesion molecules, including ICAM-1, and are key sites of reactive oxygen species (ROS) generation, including hydrogen peroxide. Reactive oxygen species along with pro-inflammatory mediators are known to contribute to endothelial damage and loss of BBB integrity. The use of targeted endothelial nanomedicine, with conjugates of the antioxidant enzyme catalase linked to anti-ICAM-1 antibodies, has recently been demonstrated to minimize oxidative stress at the BBB and reduce neuropathological outcomes following TBI. Here, we discuss targeted endothelial nanomedicine and its potential to provide benefits in TBI outcomes and future directions of this approach.
Language	English
Publishing date	2019-06-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2019.00582
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