LIVIVO - Search results -

Search results

Result 1 - 10 of total 76

Search options

Article ; Online: Hypoxia and interleukin-1-primed mesenchymal stem/stromal cells as novel therapy for stroke.

Salaudeen, Maryam Adenike / Allan, Stuart / Pinteaux, Emmanuel

2023 Volume 37, Issue 1, Page(s) 154–166

Abstract: Promising preclinical stroke research has not yielded meaningful and significant success in clinical trials. This lack of success has prompted the need for refinement of preclinical studies with the intent to optimize the chances of clinical success. ... ...

Abstract	Promising preclinical stroke research has not yielded meaningful and significant success in clinical trials. This lack of success has prompted the need for refinement of preclinical studies with the intent to optimize the chances of clinical success. Regenerative medicine, especially using mesenchymal stem/stromal cells (MSCs), has gained popularity in the last decade for treating many disorders, including central nervous system (CNS), such as stroke. In addition to less stringent ethical constraints, the ample availability of MSCs also makes them an attractive alternative to totipotent and other pluripotent stem cells. The ability of MSCs to differentiate into neurons and other brain parenchymal and immune cells makes them a promising therapy for stroke. However, these cells also have some drawbacks that, if not addressed, will render MSCs unfit for treating ischaemic stroke. In this review, we highlighted the molecular and cellular changes that occur following an ischaemic stroke (IS) incidence and discussed the physiological properties of MSCs suitable for tackling these changes. We also went further to discuss the major drawbacks of utilizing MSCs in IS and how adequate priming using both hypoxia and interleukin-1 can optimize the beneficial properties of MSCs while eliminating these drawbacks.
MeSH term(s)	Humans ; Stroke/therapy ; Brain Ischemia/therapy ; Interleukin-1 ; Mesenchymal Stem Cells ; Hypoxia ; Ischemic Stroke ; Mesenchymal Stem Cell Transplantation
Chemical Substances	Interleukin-1
Language	English
Publishing date	2023-11-21
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	1149134-6
ISSN	1749-0774 ; 0914-7470
ISSN (online)	1749-0774
ISSN	0914-7470
DOI	10.1007/s13577-023-00997-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 3676: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: Preconditioning with interleukin-1 alpha is required for the neuroprotective properties of mesenchymal stem cells after ischemic stroke in mice.

Wong, Raymond / Smith, Craig J / Allan, Stuart M / Pinteaux, Emmanuel

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2023 Volume 43, Issue 12, Page(s) 2040–2048

Abstract: Mesenchymal stem cell (MSC) pre-conditioning with interleukin-1 alpha (IL-1ɑ) drives MSCs toward a potent anti-inflammatory phenotype. The aim of this study was to assess the therapeutic potential of intra-arterially administered IL-1ɑ preconditioned ... ...

Abstract	Mesenchymal stem cell (MSC) pre-conditioning with interleukin-1 alpha (IL-1ɑ) drives MSCs toward a potent anti-inflammatory phenotype. The aim of this study was to assess the therapeutic potential of intra-arterially administered IL-1ɑ preconditioned MSCs, after experimental cerebral ischaemia in mice. After 3 h from the start of middle cerebral artery occlusion, animals were treated with vehicle, 9.1 × 10
MeSH term(s)	Humans ; Mice ; Animals ; Ischemic Stroke/metabolism ; Interleukin-1alpha/metabolism ; Stroke ; Mesenchymal Stem Cells/metabolism ; Infarction, Middle Cerebral Artery/metabolism ; Mesenchymal Stem Cell Transplantation
Chemical Substances	Interleukin-1alpha
Language	English
Publishing date	2023-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X231197109
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1663: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Endothelial cell activation by interleukin-1 and extracellular matrix laminin-10 occurs via the YAP signalling pathway.

Thurgur, Hannah / Penny, Jeffrey / Pinteaux, Emmanuel

Journal of neuroimmunology

2022 Volume 373, Page(s) 577993

Abstract: Laminin-10 (LM-10) is a key regulator of blood-brain barrier (BBB) repair after hypoxia and inflammation. Here we investigated the signalling mechanisms regulated by LM-10 in human brain endothelial cell line hCMEC/D3 in response to interleukin(IL)-1beta( ...

Abstract	Laminin-10 (LM-10) is a key regulator of blood-brain barrier (BBB) repair after hypoxia and inflammation. Here we investigated the signalling mechanisms regulated by LM-10 in human brain endothelial cell line hCMEC/D3 in response to interleukin(IL)-1beta(β) in vitro. LM-10 promoted endothelial proliferation and repair of an endothelial monolayer after scratch injury, and upregulated IL-1β-induced ICAM-1 and VCAM-1 expression. IL-1β and LM-10 regulated YAP signalling pathway in endothelial cells leading to differential expression of YAP target genes, ctgf and serpine-1, providing evidence that the YAP signalling pathway could be a new therapeutic target for the treatment of BBB dysfunction in CNS diseases.
MeSH term(s)	Humans ; Endothelial Cells/metabolism ; Cells, Cultured ; Laminin/pharmacology ; Laminin/metabolism ; Extracellular Matrix/metabolism ; Blood-Brain Barrier/metabolism
Chemical Substances	laminin 10 ; Laminin
Language	English
Publishing date	2022-10-28
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2022.577993
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1646: 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)

Order via subito

Details ▾

Article ; Online: Microglia in the Neurovascular Unit: Blood-Brain Barrier-microglia Interactions After Central Nervous System Disorders.

Thurgur, Hannah / Pinteaux, Emmanuel

Neuroscience

2018 Volume 405, Page(s) 55–67

Abstract: Over the past few decades, microglial cells have been regarded as the main executor of inflammation after acute and chronic central nervous system (CNS) disorders, responding rapidly to exogenous stimuli during acute trauma or infections, or signals ... ...

Abstract	Over the past few decades, microglial cells have been regarded as the main executor of inflammation after acute and chronic central nervous system (CNS) disorders, responding rapidly to exogenous stimuli during acute trauma or infections, or signals released by cells undergoing cell death during conditions such as stroke, Alzheimer's disease (AD) and Parkinson's disease (PD). Barriers of the nervous system, and in particular the blood-brain barrier (BBB), play a key role in the normal physiological and cognitive functions of the brain. Being at the interface between the central and peripheral compartment, the BBB is regarded as a sensor of homeostasis, and any disruption within the brain or the systemic compartment triggers BBB dysfunction and neuroinflammation, both contributing to the pathogenesis of cerebrovascular disease. This involves a dynamic response mediated by all components of the neurovascular unit (NVU), and ongoing research suggests that BBB-microglia interaction is critical to dictate the microglial response to NVU injury. The present review aims to give an up-to-date account of the emerging critical role of BBB-microglia interactions during neuroinflammation, and how these could be targeted for the therapeutic treatment of major central inflammatory disease.
MeSH term(s)	Animals ; Blood-Brain Barrier/pathology ; Brain/metabolism ; Brain/pathology ; Cell Communication/physiology ; Central Nervous System Diseases/pathology ; Cerebrovascular Disorders/pathology ; Humans ; Inflammation/pathology ; Microglia/pathology
Language	English
Publishing date	2018-07-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2018.06.046
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1215: 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)

Order via subito

Details ▾

Article ; Online: Intracerebral Administration of a Novel Self-Assembling Peptide Hydrogel Is Safe and Supports Cell Proliferation in Experimental Intracerebral Haemorrhage.

Bolan, Faye / Dickie, Ben R / Cook, James R / Thomas, Josephine M / Pinteaux, Emmanuel / Allan, Stuart M / Saiani, Alberto / Lawrence, Catherine B

Translational stroke research

2023

Abstract: Intracerebral haemorrhage (ICH) is the deadliest form of stroke, but current treatment options are limited, meaning ICH survivors are often left with life-changing disabilities. The significant unmet clinical need and socioeconomic burden of ICH mean ... ...

Abstract	Intracerebral haemorrhage (ICH) is the deadliest form of stroke, but current treatment options are limited, meaning ICH survivors are often left with life-changing disabilities. The significant unmet clinical need and socioeconomic burden of ICH mean novel regenerative medicine approaches are gaining interest. To facilitate the regeneration of the ICH lesion, injectable biomimetic hydrogels are proposed as both scaffolds for endogenous repair and delivery platforms for pro-regenerative therapies. In this paper, the objective was to explore whether injection of a novel self-assembling peptide hydrogel (SAPH) Alpha2 was feasible, safe and could stimulate brain tissue regeneration, in a collagenase-induced ICH model in rats. Alpha2 was administered intracerebrally at 7 days post ICH and functional outcome measures, histological markers of damage and repair and RNA-sequencing were investigated for up to 8 weeks. The hydrogel Alpha2 was safe, well-tolerated and was retained in the lesion for several weeks, where it allowed infiltration of host cells. The hydrogel had a largely neutral effect on functional outcomes and expression of angiogenic and neurogenic markers but led to increased numbers of proliferating cells. RNAseq and pathway analysis showed that ICH altered genes related to inflammatory and phagocytic pathways, and these changes were also observed after administration of hydrogel. Overall, the results show that the novel hydrogel was safe when injected intracerebrally and had no negative effects on functional outcomes but increased cell proliferation. To elicit a regenerative effect, future studies could use a functionalised hydrogel or combine it with an adjunct therapy.
Language	English
Publishing date	2023-10-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2541897-X
ISSN	1868-601X ; 1868-4483
ISSN (online)	1868-601X
ISSN	1868-4483
DOI	10.1007/s12975-023-01189-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Endothelial to mesenchymal transition in the interleukin-1 pathway during aortic aneurysm formation.

Millar, Jessica K / Salmon, Morgan / Nasser, Elias / Malik, Sabeen / Kolli, Pooja / Lu, Guanyi / Pinteaux, Emmanuel / Hawkins, Robert B / Ailawadi, Gorav

The Journal of thoracic and cardiovascular surgery

2023 Volume 167, Issue 5, Page(s) e146–e158

Abstract: Objective: Endothelial to mesenchymal transition may represent a key link between inflammatory stress and endothelial dysfunction seen in aortic aneurysm disease. Endothelial to mesenchymal transition is regulated by interleukin-1β, and previous work ... ...

Abstract	Objective: Endothelial to mesenchymal transition may represent a key link between inflammatory stress and endothelial dysfunction seen in aortic aneurysm disease. Endothelial to mesenchymal transition is regulated by interleukin-1β, and previous work has demonstrated an essential role of interleukin-1 signaling in experimental aortic aneurysm models. We hypothesize that endothelial to mesenchymal transition is present in murine aortic aneurysms, and loss of interleukin-1 signaling attenuates this process. Methods: Murine aortic aneurysms were created in novel CDH5-Cre lineage tracking mice by treating the intact aorta with peri-adventitial elastase. Endothelial to mesenchymal transition transcription factors as well as endothelial and mesenchymal cell markers were analyzed via immunohistochemistry and immunofluorescence (n = 10/group). To determine the role of interleukin-1 signaling, endothelial-specific interleukin-1 receptor 1 knockout and wild-type mice (n = 10/group) were treated with elastase. Additionally, C57/BL6 mice were treated with the interleukin-1 receptor 1 antagonist Anakinra (n = 7) or vehicle (n = 8). Results: Elastase treatment yielded greater aortic dilation compared with controls (elastase 97.0% ± 34.0%; control 5.3% ± 4.8%; P < .001). Genetic deletion of interleukin-1 receptor 1 attenuated aortic dilation (control 126.7% ± 38.7%; interleukin-1 receptor 1 knockout 35.2% ± 14.7%; P < .001), as did pharmacologic inhibition of interleukin-1 receptor 1 with Anakinra (vehicle 146.3% ± 30.1%; Anakinra 63.5% ± 23.3%; P < .001). Elastase treatment resulted in upregulation of endothelial to mesenchymal transition transcription factors (Snail, Slug, Twist, ZNF) and mesenchymal cell markers (S100, alpha smooth muscle actin) and loss of endothelial cell markers (vascular endothelial cadherin, endothelial nitric oxide synthase, von Willebrand factor). These changes were attenuated by interleukin-1 receptor 1 knockout and Anakinra treatment. Conclusions: Endothelial to mesenchymal transition occurs in aortic aneurysm disease and is attenuated by loss of interleukin-1 signaling. Endothelial dysfunction through endothelial to mesenchymal transition represents a new and novel pathway in understanding aortic aneurysm disease and may be a potential target for future treatment.
MeSH term(s)	Mice ; Animals ; Interleukin 1 Receptor Antagonist Protein/pharmacology ; Mice, Knockout ; Aortic Aneurysm ; Receptors, Interleukin-1/genetics ; Aortic Diseases ; Interleukin-1beta ; Pancreatic Elastase ; Transcription Factors ; Aortic Aneurysm, Abdominal/chemically induced ; Aortic Aneurysm, Abdominal/genetics ; Disease Models, Animal ; Mice, Inbred C57BL
Chemical Substances	Interleukin 1 Receptor Antagonist Protein ; Receptors, Interleukin-1 ; Interleukin-1beta ; Pancreatic Elastase (EC 3.4.21.36) ; Transcription Factors
Language	English
Publishing date	2023-11-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	3104-5
ISSN	1097-685X ; 0022-5223
ISSN (online)	1097-685X
ISSN	0022-5223
DOI	10.1016/j.jtcvs.2023.11.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uk I Zs.104: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Selective deletion of interleukin-1 alpha in microglia regulates neuronal responses and neurorepair processes after experimental ischemic stroke.

Lemarchand, Eloise / Grayston, Alba / Wong, Raymond / Rogers, Miyako / Ouvrier, Blake / Llewellyn, Benjamin / Webb, Freddie / Lénárt, Nikolett / Denes, Adam / Brough, David / Allan, Stuart M / Bix, Gregory / Pinteaux, Emmanuel

bioRxiv : the preprint server for biology

2024

Abstract: Inflammation is a key contributor to stroke pathogenesis and drives exacerbated brain damage leading to poor outcome. Interleukin-1 (IL-1) is an important regulator of post-stroke inflammation, and blocking its actions is beneficial in pre-clinical ... ...

Abstract	Inflammation is a key contributor to stroke pathogenesis and drives exacerbated brain damage leading to poor outcome. Interleukin-1 (IL-1) is an important regulator of post-stroke inflammation, and blocking its actions is beneficial in pre-clinical stroke models and safe in the clinical setting. IL-1α and IL-1β are the two major IL-1 type 1 receptor (IL-1R1) agonists from the IL-1 family. The distinct roles of both isoforms, and particularly that of IL-1α, remain largely unknown. Here we show that IL-1α and IL-1β have different spatio-temporal expression profiles in the brain after experimental stroke, with early microglial IL-1α expression (4 h) and delayed IL-1β expression in infiltrated neutrophils and a small microglial subset (24-72 h). We examined the specific contribution of microglial-derived IL-1α in experimental permanent and transient ischemic stroke through cell-specific tamoxifen-inducible Cre-loxP-mediated recombination. Microglial IL-1α deletion did not influence acute brain damage, cerebral blood flow, IL-1β expression, neutrophil infiltration, microglial nor endothelial activation after ischemic stroke. However, microglial IL-1α knock out (KO) mice showed reduced peri-infarct vessel density and reactive astrogliosis at 14 days post-stroke, alongside a worse functional recovery. RNA sequencing analysis and subsequent pathway analysis on ipsilateral/contralateral cortex 4 h after stroke revealed a downregulation of the neuronal CREB signaling pathway in microglial IL-1α KO compared to WT mice. Our study identifies for the first time a critical role for microglial IL-1α on neuronal activity, neurorepair and functional recovery after stroke, highlighting the importance of targeting specific IL-1 mechanisms in brain injury to develop more effective therapies.
Language	English
Publishing date	2024-03-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.16.580635
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: Neurogenesis After Stroke: A Therapeutic Perspective.

Rahman, Abir A / Amruta, Narayanappa / Pinteaux, Emmanuel / Bix, Gregory J

Translational stroke research

2020 Volume 12, Issue 1, Page(s) 1–14

Abstract: Stroke is a major cause of death and disability worldwide. Yet therapeutic strategies available to treat stroke are very limited. There is an urgent need to develop novel therapeutics that can effectively facilitate functional recovery. The injury that ... ...

Abstract	Stroke is a major cause of death and disability worldwide. Yet therapeutic strategies available to treat stroke are very limited. There is an urgent need to develop novel therapeutics that can effectively facilitate functional recovery. The injury that results from stroke is known to induce neurogenesis in penumbra of the infarct region. There is considerable interest in harnessing this response for therapeutic purposes. This review summarizes what is currently known about stroke-induced neurogenesis and the factors that have been identified to regulate it. Additionally, some key studies in this field have been highlighted and their implications on future of stroke therapy have been discussed. There is a complex interplay between neuroinflammation and neurogenesis that dictates stroke outcome and possibly recovery. This highlights the need for a better understanding of the neuroinflammatory process and how it affects neurogenesis, as well as the need to identify new mechanisms and potential modulators. Neuroinflammatory processes and their impact on post-stroke repair have therefore also been discussed.
MeSH term(s)	Animals ; Brain/cytology ; Brain/pathology ; Brain/physiology ; Brain Ischemia/pathology ; Brain Ischemia/therapy ; Humans ; Neurogenesis/drug effects ; Neurogenesis/physiology ; Neuroprotective Agents/administration & dosage ; Recovery of Function/physiology ; Stem Cell Transplantation/trends ; Stroke/pathology ; Stroke/therapy
Chemical Substances	Neuroprotective Agents
Language	English
Publishing date	2020-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2541897-X
ISSN	1868-601X ; 1868-4483
ISSN (online)	1868-601X
ISSN	1868-4483
DOI	10.1007/s12975-020-00841-w
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Neuroinflammation and fibrosis in stroke: The good, the bad and the ugly.

Amruta, Narayanappa / Rahman, Abir A / Pinteaux, Emmanuel / Bix, Gregory

Journal of neuroimmunology

2020 Volume 346, Page(s) 577318

Abstract: Stroke is the leading cause of death and the main cause of disability in surviving patients. The detrimental interaction between immune cells, glial cells, and matrix components in stroke pathology results in persistent inflammation that progresses to ... ...

Abstract	Stroke is the leading cause of death and the main cause of disability in surviving patients. The detrimental interaction between immune cells, glial cells, and matrix components in stroke pathology results in persistent inflammation that progresses to fibrosis. A substantial effort is being directed toward understanding the exact neuroinflammatory events that take place as a result of stroke. The initiation of a potent cytokine response, along with immune cell activation and infiltration in the ischemic core, has massive acute deleterious effects, generally exacerbated by comorbid inflammatory conditions. There is secondary neuroinflammation that promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. This highlights the need for a better understanding of the neuroinflammatory and fibrotic processes, as well as the need to identify new mechanisms and potential modulators. In this review, we summarize several aspects of stroke-induced inflammation, fibrosis, and include a discussion of cytokine inhibitors/inducers, immune cells, and fibro-inflammation signaling inhibitors in order to identify new pharmacological means of intervention.
Language	English
Publishing date	2020-07-09
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2020.577318
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1646: 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)

Order via subito

Details ▾

Article: Regenerative Medicine Therapies for Targeting Neuroinflammation After Stroke.

Rajkovic, Olivera / Potjewyd, Geoffrey / Pinteaux, Emmanuel

Frontiers in neurology

2018 Volume 9, Page(s) 734

Abstract: Inflammation is a major pathological event following ischemic stroke that contributes to secondary brain tissue damage leading to poor functional recovery. Following the initial ischemic insult, post-stroke inflammatory damage is driven by initiation of ... ...

Abstract	Inflammation is a major pathological event following ischemic stroke that contributes to secondary brain tissue damage leading to poor functional recovery. Following the initial ischemic insult, post-stroke inflammatory damage is driven by initiation of a central and peripheral innate immune response and disruption of the blood-brain barrier (BBB), both of which are triggered by the release of pro-inflammatory cytokines and infiltration of circulating immune cells. Stroke therapies are limited to early cerebral blood flow reperfusion, and whilst current strategies aim at targeting neurodegeneration and/or neuroinflammation, innovative research in the field of regenerative medicine aims at developing effective treatments that target both the acute and chronic phase of inflammation. Anti-inflammatory regenerative strategies include the use of nanoparticles and hydrogels, proposed as therapeutic agents and as a delivery vehicle for encapsulated therapeutic biological factors, anti-inflammatory drugs, stem cells, and gene therapies. Biomaterial strategies-through nanoparticles and hydrogels-enable the administration of treatments that can more effectively cross the BBB when injected systemically, can be injected directly into the brain, and can be 3D-bioprinted to create bespoke implants within the site of ischemic injury. In this review, these emerging regenerative and anti-inflammatory approaches will be discussed in relation to ischemic stroke, with a perspective on the future of stroke therapies.
Language	English
Publishing date	2018-09-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2018.00734
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito