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Article ; Online: Epigenetics and stroke: role of DNA methylation and effect of aging on blood-brain barrier recovery.

Phillips, Chelsea M / Stamatovic, Svetlana M / Keep, Richard F / Andjelkovic, Anuska V

2023 Volume 20, Issue 1, Page(s) 14

Abstract: Incomplete recovery of blood-brain barrier (BBB) function contributes to stroke outcomes. How the BBB recovers after stroke remains largely unknown. Emerging evidence suggests that epigenetic factors play a significant role in regulating post-stroke BBB ... ...

Abstract	Incomplete recovery of blood-brain barrier (BBB) function contributes to stroke outcomes. How the BBB recovers after stroke remains largely unknown. Emerging evidence suggests that epigenetic factors play a significant role in regulating post-stroke BBB recovery. This study aimed to evaluate the epigenetic and transcriptional profile of cerebral microvessels after thromboembolic (TE) stroke to define potential causes of limited BBB recovery. RNA-sequencing and reduced representation bisulfite sequencing (RRBS) analyses were performed using microvessels isolated from young (6 months) and old (18 months) mice seven days poststroke compared to age-matched sham controls. DNA methylation profiling of poststroke brain microvessels revealed 11,287 differentially methylated regions (DMR) in old and 9818 DMR in young mice, corresponding to annotated genes. These DMR were enriched in genes encoding cell structural proteins (e.g., cell junction, and cell polarity, actin cytoskeleton, extracellular matrix), transporters and channels (e.g., potassium transmembrane transporter, organic anion and inorganic cation transporters, calcium ion transport), and proteins involved in endothelial cell processes (e.g., angiogenesis/vasculogenesis, cell signaling and transcription regulation). Integrated analysis of methylation and RNA sequencing identified changes in cell junctions (occludin), actin remodeling (ezrin) as well as signaling pathways like Rho GTPase (RhoA and Cdc42ep4). Aging as a hub of aberrant methylation affected BBB recovery processes by profound alterations (hypermethylation and repression) in structural protein expression (e.g., claudin-5) as well as activation of a set of genes involved in endothelial to mesenchymal transformation (e.g., Sox9, Snai1), repression of angiogenesis and epigenetic regulation. These findings revealed that DNA methylation plays an important role in regulating BBB repair after stroke, through regulating processes associated with BBB restoration and prevalently with processes enhancing BBB injury.
MeSH term(s)	Animals ; Mice ; DNA Methylation ; Epigenesis, Genetic ; Blood-Brain Barrier ; Stroke/genetics ; Membrane Transport Proteins ; Aging
Chemical Substances	Membrane Transport Proteins
Language	English
Publishing date	2023-02-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-023-00414-7
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Article ; Online: An In Vivo Mouse Model to Study Blood-Brain Barrier Destabilization in the Chronic Phase of Stroke.

Stamatovic, Svetlana M / Phillips, Chelsea M / Keep, Richard F / Andjelkovic, Anuska V

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

2022 Volume 2492, Page(s) 289–305

Abstract: Cerebral ischemic injury evokes a complex cascade of pathophysiological events at the blood-vascular-parenchymal interface. These evolve over time and space and result in progressive neurological damage. Emerging evidence suggests that blood-brain ... ...

Abstract	Cerebral ischemic injury evokes a complex cascade of pathophysiological events at the blood-vascular-parenchymal interface. These evolve over time and space and result in progressive neurological damage. Emerging evidence suggests that blood-brain barrier (BBB) recovery and reestablishment of BBB impermeability are incomplete and that these could influence stroke injury recovery, increase the risk of new stroke occurrence, and be a solid substrate for developing vascular dementia. Recent work from the author's laboratory has established the existence of incomplete BBB recovery in chronic stroke conditions that was induced by structural alterations to brain endothelial junctional complexes and persistent BBB leakage. The experimental methodology presented here is focused on modelling chronic stroke injury using an in vivo thromboembolic mouse stroke model and how to evaluate the kinetics and magnitude of BBB hyperpermeability in chronic stroke conditions using a combination of magnetic resonance imaging, tracer studies, and immunohistochemistry.
MeSH term(s)	Animals ; Biological Transport ; Blood-Brain Barrier/pathology ; Brain/pathology ; Brain Ischemia/pathology ; Disease Models, Animal ; Mice ; Stroke/pathology
Language	English
Publishing date	2022-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2289-6_17
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Article ; Online: Cerebral Cavernous Malformation Pathogenesis: Investigating Lesion Formation and Progression with Animal Models.

Phillips, Chelsea M / Stamatovic, Svetlana M / Keep, Richard F / Andjelkovic, Anuska V

International journal of molecular sciences

2022 Volume 23, Issue 9

Abstract: Cerebral cavernous malformation (CCM) is a cerebromicrovascular disease that affects up to 0.5% of the population. Vessel dilation, decreased endothelial cell-cell contact, and loss of junctional complexes lead to loss of brain endothelial barrier ... ...

Abstract	Cerebral cavernous malformation (CCM) is a cerebromicrovascular disease that affects up to 0.5% of the population. Vessel dilation, decreased endothelial cell-cell contact, and loss of junctional complexes lead to loss of brain endothelial barrier integrity and hemorrhagic lesion formation. Leakage of hemorrhagic lesions results in patient symptoms and complications, including seizures, epilepsy, focal headaches, and hemorrhagic stroke. CCMs are classified as sporadic (sCCM) or familial (fCCM), associated with loss-of-function mutations in
MeSH term(s)	Animals ; Hemangioma, Cavernous, Central Nervous System/genetics ; Hemangioma, Cavernous, Central Nervous System/pathology ; Mice ; Microtubule-Associated Proteins/metabolism ; Models, Animal ; Mutation ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Zebrafish/genetics ; Zebrafish/metabolism
Chemical Substances	Microtubule-Associated Proteins ; Proto-Oncogene Proteins
Language	English
Publishing date	2022-04-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23095000
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Article ; Online: 20 kDa isoform of connexin-43 augments spatial reorganization of the brain endothelial junctional complex and lesion leakage in cerebral cavernous malformation type-3.

Phillips, Chelsea M / Johnson, Allison M / Stamatovic, Svetlana M / Keep, Richard F / Andjelkovic, Anuska V

Neurobiology of disease

2023 Volume 186, Page(s) 106277

Abstract: Cerebral cavernous malformation type-3 (CCM3) is a type of brain vascular malformation caused by mutations in programmed cell death protein-10 (PDCD10). It is characterized by early life occurrence of hemorrhagic stroke and profound blood-brain barrier ... ...

Abstract	Cerebral cavernous malformation type-3 (CCM3) is a type of brain vascular malformation caused by mutations in programmed cell death protein-10 (PDCD10). It is characterized by early life occurrence of hemorrhagic stroke and profound blood-brain barrier defects. The pathogenic mechanisms responsible for microvascular hyperpermeability and lesion progression in CCM3 are still largely unknown. The current study examined brain endothelial barrier structural defects formed in the absence of CCM3 in vivo and in vitro that may lead to CCM3 lesion leakage. We found significant upregulation of a 20 kDa isoform of connexin 43 (GJA1-20 k) in brain endothelial cells (BEC) in both non-leaky and leaky lesions, as well as in an in vitro CCM3 knockdown model (CCM3KD-BEC). Morphological, biochemical, FRET, and FRAP analyses of CCM3KD-BEC found GJA1-20 k regulates full-length GJA1 biogenesis, prompting uncontrolled gap junction growth. Furthermore, by binding to a tight junction scaffolding protein, ZO-1, GJA1-20 k interferes with Cx43/ZO-1 interactions and gap junction/tight junction crosstalk, promoting ZO-1 dissociation from tight junction complexes and diminishing claudin-5/ZO-1 interaction. As a consequence, the tight junction complex is destabilized, allowing "replacement" of tight junctions with gap junctions leading to increased brain endothelial barrier permeability. Modifying cellular levels of GJA1-20 k rescued brain endothelial barrier integrity re-establishing the spatial organization of gap and tight junctional complexes. This study highlights generation of potential defects at the CCM3-affected brain endothelial barrier which may underlie prolonged vascular leakiness.
MeSH term(s)	Humans ; Blood-Brain Barrier ; Brain ; Connexin 43 ; Endothelial Cells ; Hemangioma, Cavernous, Central Nervous System
Chemical Substances	Connexin 43 ; GJA1 protein, human
Language	English
Publishing date	2023-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106277
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Article ; Online: Blood-Brain Barrier Dysfunction in Normal Aging and Neurodegeneration: Mechanisms, Impact, and Treatments.

Andjelkovic, Anuska V / Situ, Muyu / Citalan-Madrid, Ali Francisco / Stamatovic, Svetlana M / Xiang, Jianming / Keep, Richard F

Stroke

2023 Volume 54, Issue 3, Page(s) 661–672

Abstract: Cerebral endothelial cells and their linking tight junctions form a unique, dynamic and multi-functional interface, the blood-brain barrier (BBB). The endothelium is regulated by perivascular cells and components forming the neurovascular unit. This ... ...

Abstract	Cerebral endothelial cells and their linking tight junctions form a unique, dynamic and multi-functional interface, the blood-brain barrier (BBB). The endothelium is regulated by perivascular cells and components forming the neurovascular unit. This review examines BBB and neurovascular unit changes in normal aging and in neurodegenerative disorders, particularly focusing on Alzheimer disease, cerebral amyloid angiopathy and vascular dementia. Increasing evidence indicates BBB dysfunction contributes to neurodegeneration. Mechanisms underlying BBB dysfunction are outlined (endothelium and neurovascular unit mediated) as is the BBB as a therapeutic target including increasing the uptake of systemically delivered therapeutics across the BBB, enhancing clearance of potential neurotoxic compounds via the BBB, and preventing BBB dysfunction. Finally, a need for novel biomarkers of BBB dysfunction is addressed.
MeSH term(s)	Humans ; Blood-Brain Barrier ; Endothelial Cells ; Aging ; Alzheimer Disease ; Cerebral Amyloid Angiopathy
Language	English
Publishing date	2023-02-27
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	80381-9
ISSN	1524-4628 ; 0039-2499 ; 0749-7954
ISSN (online)	1524-4628
ISSN	0039-2499 ; 0749-7954
DOI	10.1161/STROKEAHA.122.040578
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Zs.A 448: Show issues

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Article: Transcriptomic Profile of Blood-Brain Barrier Remodeling in Cerebral Amyloid Angiopathy.

Situ, Muyu / Citalan-Madrid, Ali Francisco / Stamatovic, Svetlana M / Keep, Richard F / Andjelkovic, Anuska V

Frontiers in cellular neuroscience

2022 Volume 16, Page(s) 931247

Abstract: Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by amyloid β (Aβ) peptide deposition within the walls of medium to small-caliber blood vessels, cerebral microhemorrhage, and blood-brain barrier (BBB) leakage. It is commonly ... ...

Abstract	Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by amyloid β (Aβ) peptide deposition within the walls of medium to small-caliber blood vessels, cerebral microhemorrhage, and blood-brain barrier (BBB) leakage. It is commonly associated with late-stage Alzheimer's disease. BBB dysfunction is indicated as a pathological substrate for CAA progression with hyperpermeability, enhancing the extravasation of plasma components and inducing neuroinflammation, further worsening BBB injury and contributing to cognitive decline. Although significant effort has been made in defining the gene mutations and risk factors involved in microvascular alterations with vascular dementia and Alzheimer's disease, the intra- and intercellular pathogenic mechanisms responsible for vascular hyperpermeability are still largely unknown. The present study aimed to elucidate the transcriptional profile of the cerebral microvessels (BBB) in a murine model with CAA vasculopathy to define potential causes and underlying mechanisms of BBB injury. A comprehensive RNA sequencing analysis was performed of CAA vasculopathy in Tg-SwDI mice at 6 and 18 months in comparison to age-matched wildtype controls to examine how age and amyloid accumulation impact the transcriptional signature of the BBB. Results indicate that Aβ has a critical role in triggering brain endothelial cell and BBB dysfunction in CAA vasculopathy, causing an intense proinflammatory response, impairing oxidative metabolism, altering the coagulation status of brain endothelial cells, and remodeling barrier properties. The proinflammatory response includes both adaptive and innate immunity, with pronounced induction of genes that regulate macrophage/microglial activation and chemokines/adhesion molecules that support T and B cell transmigration. Age has an important impact on the effects of Aβ, increasing the BBB injury in CAA vasculopathy. However, early inflammation, particularly microglia/macrophage activation and the mediators of B lymphocytes' activities are underlying processes of BBB hyperpermeability and cerebral microbleeds in the early stage of CAA vasculopathy. These findings reveal a specific profile of the CAA-associated BBB injury that leads to a full progression of CAA.
Language	English
Publishing date	2022-06-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2022.931247
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Article ; Online: Cerebral Cavernous Malformation Pathogenesis

Chelsea M. Phillips / Svetlana M. Stamatovic / Richard F. Keep / Anuska V. Andjelkovic

International Journal of Molecular Sciences, Vol 23, Iss 5000, p

Investigating Lesion Formation and Progression with Animal Models

2022 Volume 5000

Abstract: Cerebral cavernous malformation (CCM) is a cerebromicrovascular disease that affects up to 0.5% of the population. Vessel dilation, decreased endothelial cell–cell contact, and loss of junctional complexes lead to loss of brain endothelial barrier ... ...

Abstract	Cerebral cavernous malformation (CCM) is a cerebromicrovascular disease that affects up to 0.5% of the population. Vessel dilation, decreased endothelial cell–cell contact, and loss of junctional complexes lead to loss of brain endothelial barrier integrity and hemorrhagic lesion formation. Leakage of hemorrhagic lesions results in patient symptoms and complications, including seizures, epilepsy, focal headaches, and hemorrhagic stroke. CCMs are classified as sporadic (sCCM) or familial (fCCM), associated with loss-of-function mutations in KRIT1/CCM1 , CCM2 , and PDCD10/CCM3. Identifying the CCM proteins has thrust the field forward by (1) revealing cellular processes and signaling pathways underlying fCCM pathogenesis, and (2) facilitating the development of animal models to study CCM protein function. CCM animal models range from various murine models to zebrafish models, with each model providing unique insights into CCM lesion development and progression. Additionally, these animal models serve as preclinical models to study therapeutic options for CCM treatment. This review briefly summarizes CCM disease pathology and the molecular functions of the CCM proteins, followed by an in-depth discussion of animal models used to study CCM pathogenesis and developing therapeutics.
Keywords	cerebrovascular malformation ; KRIT1 ; CCM2 ; PDCD10 ; hemorrhagic lesions ; CCM animal models ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: A novel approach to treatment of thromboembolic stroke in mice: Redirecting neutrophils toward a peripherally implanted CXCL1-soaked sponge.

Stamatovic, Svetlana M / Phillips, Chelsea M / Keep, Richard F / Andjelkovic, Anuska V

Experimental neurology

2020 Volume 330, Page(s) 113336

Abstract: Neutrophils are considered key participants in post-ischemic stroke inflammation. They are the first white blood cells to arrive in ischemic brain and their presence in the brain tissue positively correlates with post-ischemic injury severity. CXCL1 is a ...

Abstract	Neutrophils are considered key participants in post-ischemic stroke inflammation. They are the first white blood cells to arrive in ischemic brain and their presence in the brain tissue positively correlates with post-ischemic injury severity. CXCL1 is a neutrophil attractant chemokine and the present study evaluates whether redirecting neutrophil migration using a peripherally implanted CXCL1-soaked sponge can reduce brain inflammation and improve outcomes in a novel mouse model of thromboembolic (TE) stroke. TE stroke was induced by injection of a platelet-rich microemboli suspension into the internal carotid artery of adult C57BL/6 male mice. The model induced neuroinflammation that was associated with increases in multiple brain and serum cytokines/chemokines at the mRNA and protein levels, including very marked increases in CXCL1. In other groups of animals, an absorbable sterile hemostatic sponge, previously immersed in either saline (0.9%NaCl) or CXCL1, was implanted into subcutaneous pockets formed in the inguinal region on the left and right side following stroke surgery. Mice implanted with the sponge soaked with CXCL1 had significantly reduced neuroinflammation and infarct size after TE stroke compared to mice implanted with the sponge soaked with 0.9%NaCl. There was also reduced mortality and improved neurological deficits in the TE stroke + CXCL1 sponge group compared to the TE stroke +0.9%NaCl sponge group. In conclusion: redirecting bloodstream leukocytes toward a peripherally-implanted neutrophil chemokine CXCL1-soaked sponge improves outcomes in a novel mouse model of thromboembolic stroke. The present findings suggest a novel therapeutic strategy for patients with acute stroke.
MeSH term(s)	Animals ; Chemokine CXCL1/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophil Infiltration/drug effects ; Neutrophils/metabolism ; Stroke ; Surgical Sponges ; Thromboembolism
Chemical Substances	Chemokine CXCL1
Language	English
Publishing date	2020-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2020.113336
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Article ; Online: Association of ATG16L1 rs2241880 and TP53 rs1042522 with characteristics and course of diffuse large B-cell lymphoma.

Živanović, Anđelina / Stamatović, Dragana / Strelić, Nataša / Magić, Zvonko / Tarabar, Olivera / Miljanović, Olivera / Mišović, Miroslav / Đukić, Svetlana / Cikota-Aleksić, Bojana

Pathology, research and practice

2022 Volume 237, Page(s) 154033

Abstract: Background: Diffuse large B-cell lymphoma (DLBCL) represents the most frequent lymphoma in adults. Prognosis for DLBCL patients may be evaluated through the most prominent clinical/laboratory parameters or pattern of gene expression. In order to improve ...

Abstract	Background: Diffuse large B-cell lymphoma (DLBCL) represents the most frequent lymphoma in adults. Prognosis for DLBCL patients may be evaluated through the most prominent clinical/laboratory parameters or pattern of gene expression. In order to improve prognostic/prediction scores or provide new therapeutic targets, novel genetic markers are needed. This study evaluates the association of ATG16L1 rs2241880 and TP53 rs1042522 with clinical characteristics and course of DLBCL. Methods: The study included 108 DLCBL patients treated with R-CHOP. Of these, 44 patients were subjected to stem cell transplantation and 55 to radiotherapy. Genotyping was performed by TaqMan genotyping assays. Results: Amongst analyzed characteristics and prognostic scores, genotypes were associated with clinical stage (TP53 CG+CC vs GG p = 0.06), extranodal disease (ATG16L1 AG vs AA p = 0.07; AG vs GG p = 0.04), lymphocyte-to-monocyte ratio (LMR) (ATG16L1 AA vs AG+GG, p = 0.052; AA vs GG, p = 0.054) and neutrophils-to-lymphocytes ratio (NLR) (ATG16L1 AA vs AG+GG, p = 0.033; AA vs GG, p = 0.003). Analyzed genotypes didn't impact response to therapy, relapse and therapy-related complications. Considering outcome, patients with ATG16L1 AA had higher survival rate than GG carriers (p = 0.04). In all patients, duration of overall survival (OS) and relapse free survival (RFS) was not affected by analyzed genotypes. When subjected to radiotherapy, patients with ATG16L1 A allele (p = 0.05) or AA genotype (p = 0.03) had superior OS. Conclusion: Our results demonstrated the association of TP53 rs1042522 with clinical stage and ATG16L1 rs2241880 with extranodal disease, LMR and NLR. The impact of ATG16L1 genotypes on OS in patients subjected to radiotherapy, indicates significance of individual single nucleotide polymorphisms (SNPs) in particular subgroups of DLBCL.
MeSH term(s)	Adult ; Humans ; Genetic Markers ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Neoplasm Recurrence, Local/drug therapy ; Lymphoma, Large B-Cell, Diffuse/genetics ; Lymphoma, Large B-Cell, Diffuse/pathology ; Vincristine/therapeutic use ; Tumor Suppressor Protein p53/genetics ; Autophagy-Related Proteins/genetics
Chemical Substances	Genetic Markers ; Vincristine (5J49Q6B70F) ; TP53 protein, human ; Tumor Suppressor Protein p53 ; ATG16L1 protein, human ; Autophagy-Related Proteins
Language	English
Publishing date	2022-07-19
Publishing country	Germany
Document type	Journal Article
ZDB-ID	391889-0
ISSN	1618-0631 ; 0344-0338
ISSN (online)	1618-0631
ISSN	0344-0338
DOI	10.1016/j.prp.2022.154033
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Article ; Online: Modeling blood-brain barrier pathology in cerebrovascular disease in vitro: current and future paradigms.

Andjelkovic, Anuska V / Stamatovic, Svetlana M / Phillips, Chelsea M / Martinez-Revollar, Gabriela / Keep, Richard F

Fluids and barriers of the CNS

2020 Volume 17, Issue 1, Page(s) 44

Abstract: The complexity of the blood-brain barrier (BBB) and neurovascular unit (NVU) was and still is a challenge to bridge. A highly selective, restrictive and dynamic barrier, formed at the interface of blood and brain, the BBB is a "gatekeeper" and guardian ... ...

Abstract	The complexity of the blood-brain barrier (BBB) and neurovascular unit (NVU) was and still is a challenge to bridge. A highly selective, restrictive and dynamic barrier, formed at the interface of blood and brain, the BBB is a "gatekeeper" and guardian of brain homeostasis and it also acts as a "sensor" of pathological events in blood and brain. The majority of brain and cerebrovascular pathologies are associated with BBB dysfunction, where changes at the BBB can lead to or support disease development. Thus, an ultimate goal of BBB research is to develop competent and highly translational models to understand mechanisms of BBB/NVU pathology and enable discovery and development of therapeutic strategies to improve vascular health and for the efficient delivery of drugs. This review article focuses on the progress being made to model BBB injury in cerebrovascular diseases in vitro.
MeSH term(s)	Astrocytes/physiology ; Blood-Brain Barrier/immunology ; Blood-Brain Barrier/pathology ; Blood-Brain Barrier/physiopathology ; Cerebrovascular Disorders/immunology ; Cerebrovascular Disorders/pathology ; Cerebrovascular Disorders/physiopathology ; Endothelial Cells/physiology ; Humans ; In Vitro Techniques ; Models, Neurological ; Neurons/physiology ; Tight Junctions/physiology
Language	English
Publishing date	2020-07-16
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/s12987-020-00202-7
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