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Article ; Online: Measurement of Uninterrupted Cerebral Blood Flow by Laser Speckle Contrast Imaging (LSCI) During the Mouse Middle Cerebral Artery Occlusion Model by an Inverted LSCI Setup.

Hong, Sung-Ha / Doan, Andrea / Marrelli, Sean P

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

2023 Volume 2616, Page(s) 83–96

Abstract: Laser speckle contrast imaging (LSCI) offers the ability to measure relative cerebral blood flow (CBF) through the intact skull in mice. LSCI can be used to measure changes in cortical CBF in the middle cerebral artery occlusion/reperfusion (MCAo/R) ... ...

Abstract	Laser speckle contrast imaging (LSCI) offers the ability to measure relative cerebral blood flow (CBF) through the intact skull in mice. LSCI can be used to measure changes in cortical CBF in the middle cerebral artery occlusion/reperfusion (MCAo/R) stroke model. However, because conventional LSCI approaches are designed to image from above, uninterrupted measurement of CBF during the MCAo/R procedure is not possible due to the need to repeatedly reposition the mouse between prone and supine positions. We present a modified method to perform LSCI measurement from beneath the surgical preparation, thus allowing uninterrupted measurement of relative CBF from baseline through re-introduction of blood flow. We provide a 3D printable imaging platform and corresponding head frame, as well as methods to improve skull clarity in young and aged mice.
MeSH term(s)	Mice ; Animals ; Infarction, Middle Cerebral Artery/diagnostic imaging ; Laser Speckle Contrast Imaging ; Stroke ; Hemodynamics ; Cerebrovascular Circulation/physiology ; Laser-Doppler Flowmetry/methods
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2926-0_9
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Article ; Online: CD13 facilitates immune cell migration and aggravates acute injury but promotes chronic post-stroke recovery.

Nguyen, Justin N / Mohan, Eric C / Pandya, Gargee / Ali, Uzma / Tan, Chunfeng / Kofler, Julia K / Shapiro, Linda / Marrelli, Sean P / Chauhan, Anjali

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 232

Abstract: Introduction: Acute stroke leads to the activation of myeloid cells. These cells express adhesion molecules and transmigrate to the brain, thereby aggravating injury. Chronically after stroke, repair processes, including angiogenesis, are activated and ... ...

Abstract	Introduction: Acute stroke leads to the activation of myeloid cells. These cells express adhesion molecules and transmigrate to the brain, thereby aggravating injury. Chronically after stroke, repair processes, including angiogenesis, are activated and enhance post-stroke recovery. Activated myeloid cells express CD13, which facilitates their migration into the site of injury. However, angiogenic blood vessels which play a role in recovery also express CD13. Overall, the specific contribution of CD13 to acute and chronic stroke outcomes is unknown. Methods: CD13 expression was estimated in both mice and humans after the ischemic stroke. Young (8-12 weeks) male wild-type and global CD13 knockout (KO) mice were used for this study. Mice underwent 60 min of middle cerebral artery occlusion (MCAO) followed by reperfusion. For acute studies, the mice were euthanized at either 24- or 72 h post-stroke. For chronic studies, the Y-maze, Barnes maze, and the open field were performed on day 7 and day 28 post-stroke. Mice were euthanized at day 30 post-stroke and the brains were collected for assessment of inflammation, white matter injury, tissue loss, and angiogenesis. Flow cytometry was performed on days 3 and 7 post-stroke to quantify infiltrated monocytes and neutrophils and CXCL12/CXCR4 signaling. Results: Brain CD13 expression and infiltrated CD13 Conclusions: CD13 is involved in the trans-migration of monocytes and neutrophils after stroke, and acutely, led to decreased infarct size and improved behavioral outcomes. However, loss of CD13 led to reductions in post-stroke angiogenesis by reducing CXCL12/CXCR4 signaling.
MeSH term(s)	Humans ; Male ; Animals ; Mice ; Stroke/metabolism ; Brain/metabolism ; Infarction, Middle Cerebral Artery/metabolism ; Ischemic Stroke/metabolism ; Mice, Knockout ; Cell Movement ; Mice, Inbred C57BL ; Brain Ischemia/metabolism
Language	English
Publishing date	2023-10-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02918-3
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Article ; Online: Neutrophils and Neutrophil Extracellular Traps Cause Vascular Occlusion and Delayed Cerebral Ischemia After Subarachnoid Hemorrhage in Mice.

Zeineddine, Hussein A / Hong, Sung-Ha / Peesh, Pedram / Dienel, Ari / Torres, Kiara / Thankamani Pandit, Peeyush / Matsumura, Kanako / Huang, Shuning / Li, Wen / Chauhan, Anjali / Hagan, John P / Marrelli, Sean P / McCullough, Louise D / Blackburn, Spiros L / Aronowski, Jaroslaw / McBride, Devin W

Arteriosclerosis, thrombosis, and vascular biology

2024 Volume 44, Issue 3, Page(s) 635–652

Abstract: Background: After subarachnoid hemorrhage (SAH), neutrophils are deleterious and contribute to poor outcomes. Neutrophils can produce neutrophil extracellular traps (NETs) after ischemic stroke. Our hypothesis was that, after SAH, neutrophils contribute ...

Abstract	Background: After subarachnoid hemorrhage (SAH), neutrophils are deleterious and contribute to poor outcomes. Neutrophils can produce neutrophil extracellular traps (NETs) after ischemic stroke. Our hypothesis was that, after SAH, neutrophils contribute to delayed cerebral ischemia (DCI) and worse outcomes via cerebrovascular occlusion by NETs. Methods: SAH was induced via endovascular perforation, and SAH mice were given either a neutrophil-depleting antibody, a PAD4 (peptidylarginine deiminase 4) inhibitor (to prevent NETosis), DNAse-I (to degrade NETs), or a vehicle control. Mice underwent daily neurological assessment until day 7 and then euthanized for quantification of intravascular brain NETs (iNETs). Subsets of mice were used to quantify neutrophil infiltration, NETosis potential, iNETs, cerebral perfusion, and infarction. In addition, NET markers were assessed in the blood of aneurysmal SAH patients. Results: In mice, SAH led to brain neutrophil infiltration within 24 hours, induced a pro-NETosis phenotype selectively in skull neutrophils, and caused a significant increase in iNETs by day 1, which persisted until at least day 7. Neutrophil depletion significantly reduced iNETs, improving cerebral perfusion, leading to less neurological deficits and less incidence of DCI (16% versus 51.9%). Similarly, PAD4 inhibition reduced iNETs, improved neurological outcome, and reduced incidence of DCI (5% versus 30%), whereas degrading NETs marginally improved outcomes. Patients with aneurysmal SAH who developed DCI had elevated markers of NETs compared with non-DCI patients. Conclusions: After SAH, skull-derived neutrophils are primed for NETosis, and there are persistent brain iNETs, which correlated with delayed deficits. The findings from this study suggest that, after SAH, neutrophils and NETosis are therapeutic targets, which can prevent vascular occlusion by NETs in the brain, thereby lessening the risk of DCI. Finally, NET markers may be biomarkers, which can predict which patients with aneurysmal SAH are at risk for developing DCI.
MeSH term(s)	Humans ; Mice ; Animals ; Subarachnoid Hemorrhage/complications ; Neutrophils/metabolism ; Extracellular Traps ; Brain Ischemia/etiology ; Brain Ischemia/prevention & control ; Cerebrovascular Disorders/complications
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.123.320224
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Article ; Online: Clinical significance and potential role of trimethylamine N-oxide in neurological and neuropsychiatric disorders.

Mudimela, Sowjanya / Vishwanath, Narahari Koppa / Pillai, Anilkumar / Morales, Rodrigo / Marrelli, Sean P / Barichello, Tatiana / Giridharan, Vijayasree V

Drug discovery today

2022 Volume 27, Issue 11, Page(s) 103334

Abstract: In the past three decades, research on the gut microbiome and its metabolites, such as trimethylamines (TMA), trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), branched-chain amino acids (BCAAs), bile acids, tryptophan and indole ... ...

Abstract	In the past three decades, research on the gut microbiome and its metabolites, such as trimethylamines (TMA), trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), branched-chain amino acids (BCAAs), bile acids, tryptophan and indole derivatives, has attracted the attention of many scientists and industrialists. Among these metabolites, TMAO is produced from dietary choline, phosphatidylcholine, carnitine,andbetaine. TMAO and other gut metabolites, such as TMA and SCFAs, reach the brain by crossing the blood-brain barrier (BBB) and are involved in brain development, neurogenesis, and behavior. Gut-microbiota composition is influenced by diet, lifestyle, antibiotics, and age. Several studies have confirmed that altered TMAO levels contribute to metabolic, vascular, psychiatric, and neurodegenerative disorders. This review focuses on how altered TMAO levels impact oxidative stress, microglial activation, and the apoptosis of neurons, and may lead to neuroinflammation, which can subsequently result in the development of psychiatric, cognitive, and behavioral disorders.
Language	English
Publishing date	2022-08-23
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2022.08.002
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Article ; Online: Increased Expression of Interferon-Induced Transmembrane 3 (IFITM3) in Stroke and Other Inflammatory Conditions in the Brain.

Harmon, Elisabeth / Doan, Andrea / Bautista-Garrido, Jesus / Jung, Joo Eun / Marrelli, Sean P / Kim, Gab Seok

International journal of molecular sciences

2022 Volume 23, Issue 16

Abstract: Microglia, the resident innate immune cells of the brain, become more highly reactive with aging and diseased conditions. In collaboration with other cell types in brains, microglia can contribute both to worsened outcome following stroke or other ... ...

Abstract	Microglia, the resident innate immune cells of the brain, become more highly reactive with aging and diseased conditions. In collaboration with other cell types in brains, microglia can contribute both to worsened outcome following stroke or other neurodegenerative diseases and to the recovery process by changing their phenotype toward reparative microglia. Recently, IFITM3 (a member of the "interferon-inducible transmembrane" family) has been revealed as a molecular mediator between amyloid pathology and neuroinflammation. Expression of IFITM3 in glial cells, especially microglia following stroke, is not well described. Here, we present evidence that ischemic stroke causes an increase in IFITM3 expression along with increased microglial activation marker genes in aged brains. To further validate the induction of IFITM3 in post-stroke brains, primary microglia and microglial-like cells were exposed to a variety of inflammatory conditions, which significantly induced IFITM3 as well as other inflammatory markers. These findings suggest the critical role of IFITM3 in inducing inflammation. Our findings on the expression of IFITM3 in microglia and in aged brains following stroke could establish the basic foundations for the role of IFITM3 in a variety of neurodegenerative diseases, particularly those that are prevalent or enhanced in the aged brain.
MeSH term(s)	Biomarkers/metabolism ; Brain/metabolism ; Humans ; Interferons/metabolism ; Membrane Proteins/metabolism ; Microglia/metabolism ; Neurodegenerative Diseases/metabolism ; RNA-Binding Proteins/metabolism ; Stroke/metabolism
Chemical Substances	Biomarkers ; IFITM3 protein, human ; Membrane Proteins ; RNA-Binding Proteins ; Interferons (9008-11-1)
Language	English
Publishing date	2022-08-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23168885
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Article: Astrocytic Slc4a4 regulates blood-brain barrier integrity in healthy and stroke brains via a NO-CCL2-CCR2 pathway.

Ye, Qi / Jo, Juyeon / Wang, Chih-Yen / Oh, Heavin / Choy, Tiffany J / Kim, Kyoungin / D'Alessandro, Angelo / Reshetnyak, Yana K / Jung, Sung Yun / Chen, Zheng / Marrelli, Sean P / Lee, Hyun Kyoung

bioRxiv : the preprint server for biology

2023

Abstract: Astrocytes play vital roles in blood-brain barrier (BBB) maintenance, yet how they support BBB integrity under normal or pathological conditions remains poorly defined. Recent evidence suggests pH homeostasis is a new cellular mechanism important for BBB ...

Abstract	Astrocytes play vital roles in blood-brain barrier (BBB) maintenance, yet how they support BBB integrity under normal or pathological conditions remains poorly defined. Recent evidence suggests pH homeostasis is a new cellular mechanism important for BBB integrity. In the current study, we investigated the function of an astrocyte-specific pH regulator, Slc4a4, in BBB maintenance and repair. We show that astrocytic Slc4a4 is required for normal astrocyte morphological complexity and BBB function. Multi-omics analyses identified increased astrocytic secretion of CCL2 coupled with dysregulated arginine-NO metabolism after Slc4a4 deletion. Using a model of ischemic stroke, we found that loss of Slc4a4 exacerbates BBB disruption and reactive gliosis, which were both rescued by pharmacological or genetic inhibition of the NO-CCL2 pathway
Language	English
Publishing date	2023-04-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.03.535167
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Article ; Online: Pirh2-dependent DNA damage in neurons induced by the G-quadruplex ligand pyridostatin.

Escarcega, Rocio Diaz / Patil, Abhijeet A / Moruno-Manchon, Jose F / Urayama, Akihiko / Marrelli, Sean P / Kim, Nayun / Monchaud, David / McCullough, Louise D / Tsvetkov, Andrey S

The Journal of biological chemistry

2023 Volume 299, Issue 10, Page(s) 105157

Abstract: Noncanonical base pairing between four guanines (G) within single-stranded G-rich sequences leads to formation of а G-quartet. Self-stacking of G-quartets results in a columnar four-stranded DNA structure known as the G-quadruplex (G4 or G4-DNA). In ... ...

Abstract	Noncanonical base pairing between four guanines (G) within single-stranded G-rich sequences leads to formation of а G-quartet. Self-stacking of G-quartets results in a columnar four-stranded DNA structure known as the G-quadruplex (G4 or G4-DNA). In cancer cells, G4-DNA regulates multiple DNA-dependent processes, including transcription, replication, and telomere function. How G4s function in neurons is poorly understood. Here, we performed a genome-wide gene expression analysis (RNA-Seq) to identify genes modulated by a G4-DNA ligand, pyridostatin (PDS), in primary cultured neurons. PDS promotes stabilization of G4 structures, thus allowing us to define genes directly or indirectly responsive to G4 regulation. We found that 901 genes were differentially expressed in neurons treated with PDS out of a total of 18,745 genes with measured expression. Of these, 505 genes were downregulated and 396 genes were upregulated and included gene networks regulating p53 signaling, the immune response, learning and memory, and cellular senescence. Within the p53 network, the E3 ubiquitin ligase Pirh2 (Rchy1), a modulator of DNA damage responses, was upregulated by PDS. Ectopically overexpressing Pirh2 promoted the formation of DNA double-strand breaks, suggesting a new DNA damage mechanism in neurons that is regulated by G4 stabilization. Pirh2 downregulated DDX21, an RNA helicase that unfolds G4-RNA and R-loops. Finally, we demonstrated that Pirh2 increased G4-DNA levels in the neuronal nucleolus. Our data reveal the genes that are responsive to PDS treatment and suggest similar transcriptional regulation by endogenous G4-DNA ligands. They also connect G4-dependent regulation of transcription and DNA damage mechanisms in neuronal cells.
Language	English
Publishing date	2023-08-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.105157
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Article ; Online: Systemic Administration of the TRPV3 Ion Channel Agonist Carvacrol Induces Hypothermia in Conscious Rodents.

Feketa, Viktor V / Marrelli, Sean P

PloS one

2015 Volume 10, Issue 11, Page(s) e0141994

Abstract: Therapeutic hypothermia is a promising new strategy for neuroprotection. However, the methods for safe and effective hypothermia induction in conscious patients are lacking. The current study explored the Transient Receptor Potential Vanilloid 3 (TRPV3) ... ...

Abstract	Therapeutic hypothermia is a promising new strategy for neuroprotection. However, the methods for safe and effective hypothermia induction in conscious patients are lacking. The current study explored the Transient Receptor Potential Vanilloid 3 (TRPV3) channel activation by the agonist carvacrol as a potential hypothermic strategy. It was found that carvacrol lowers core temperature after intraperitoneal and intravenous administration in mice and rats. However, the hypothermic effect at safe doses was modest, while higher intravenous doses of carvacrol induced a pronounced drop in blood pressure and substantial toxicity. Experiments on the mechanism of the hypothermic effect in mice revealed that it was associated with a decrease in whole-body heat generation, but not with a change in cold-seeking behaviors. In addition, the hypothermic effect was lost at cold ambient temperature. Our findings suggest that although TRPV3 agonism induces hypothermia in rodents, it may have a limited potential as a novel pharmacological method for induction of hypothermia in conscious patients due to suboptimal effectiveness and high toxicity.
MeSH term(s)	Animals ; Blood Pressure/drug effects ; Blood Pressure/physiology ; Body Temperature Regulation/drug effects ; Body Temperature Regulation/physiology ; Cymenes ; Dose-Response Relationship, Drug ; Hypothermia, Induced ; Male ; Mice ; Monoterpenes/adverse effects ; Monoterpenes/pharmacology ; Rats ; Rats, Sprague-Dawley ; TRPV Cation Channels/agonists ; TRPV Cation Channels/metabolism
Chemical Substances	Cymenes ; Monoterpenes ; TRPV Cation Channels ; TRPV3 protein, rat ; Trpv3 protein, mouse ; carvacrol (9B1J4V995Q)
Language	English
Publishing date	2015-11-03
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.0141994
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Article: Induction of therapeutic hypothermia by pharmacological modulation of temperature-sensitive TRP channels: theoretical framework and practical considerations.

Feketa, Viktor V / Marrelli, Sean P

Temperature (Austin, Tex.)

2015 Volume 2, Issue 2, Page(s) 244–257

Abstract: Therapeutic hypothermia has emerged as a remarkably effective method of neuroprotection from ischemia and is being increasingly used in clinics. Accordingly, it is also a subject of considerable attention from a basic scientific research perspective. One ...

Abstract	Therapeutic hypothermia has emerged as a remarkably effective method of neuroprotection from ischemia and is being increasingly used in clinics. Accordingly, it is also a subject of considerable attention from a basic scientific research perspective. One of the fundamental problems, with which current studies are concerned, is the optimal method of inducing hypothermia. This review seeks to provide a broad theoretical framework for approaching this problem, and to discuss how a novel promising strategy of pharmacological modulation of the thermosensitive ion channels fits into this framework. Various physical, anatomical, physiological and molecular aspects of thermoregulation, which provide the foundation for this text, have been comprehensively reviewed and will not be discussed exhaustively here. Instead, the first part of the current review, which may be helpful for a broader readership outside of thermoregulation research, will build on this existing knowledge to outline possible opportunities and research directions aimed at controlling body temperature. The second part, aimed at a more specialist audience, will highlight the conceptual advantages and practical limitations of novel molecular agents targeting thermosensitive Transient Receptor Potential (TRP) channels in achieving this goal. Two particularly promising members of this channel family, namely TRP melastatin 8 (TRPM8) and TRP vanilloid 1 (TRPV1), will be discussed in greater detail.
Language	English
Publishing date	2015-04-27
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2332-8940
ISSN	2332-8940
DOI	10.1080/23328940.2015.1024383
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Article ; Online: Increased Expression of Interferon-Induced Transmembrane 3 (IFITM3) in Stroke and Other Inflammatory Conditions in the Brain

Elisabeth Harmon / Andrea Doan / Jesus Bautista-Garrido / Joo Eun Jung / Sean P. Marrelli / Gab Seok Kim

International Journal of Molecular Sciences, Vol 23, Iss 16, p

2022 Volume 8885

Abstract	Microglia, the resident innate immune cells of the brain, become more highly reactive with aging and diseased conditions. In collaboration with other cell types in brains, microglia can contribute both to worsened outcome following stroke or other neurodegenerative diseases and to the recovery process by changing their phenotype toward reparative microglia. Recently, IFITM3 (a member of the “interferon-inducible transmembrane” family) has been revealed as a molecular mediator between amyloid pathology and neuroinflammation. Expression of IFITM3 in glial cells, especially microglia following stroke, is not well described. Here, we present evidence that ischemic stroke causes an increase in IFITM3 expression along with increased microglial activation marker genes in aged brains. To further validate the induction of IFITM3 in post-stroke brains, primary microglia and microglial-like cells were exposed to a variety of inflammatory conditions, which significantly induced IFITM3 as well as other inflammatory markers. These findings suggest the critical role of IFITM3 in inducing inflammation. Our findings on the expression of IFITM3 in microglia and in aged brains following stroke could establish the basic foundations for the role of IFITM3 in a variety of neurodegenerative diseases, particularly those that are prevalent or enhanced in the aged brain.
Keywords	stroke ; gliosis ; IFITM3 ; microglia ; interferon ; aging ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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