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Article: A rapid review of differences in cerebrospinal neurofilament light levels in clinical subtypes of progressive multiple sclerosis.

Desu, Haritha L / Sawicka, Katherine M / Wuerch, Emily / Kitchin, Vanessa / Quandt, Jacqueline A

2024 Volume 15, Page(s) 1382468

Abstract: Background: Multiple sclerosis (MS) is divided into three clinical phenotypes: relapsing-remitting MS (RRMS), secondary progressive MS (SPMS), and primary progressive MS (PPMS). It is unknown to what extent SPMS and PPMS pathophysiology share ... ...

Abstract	Background: Multiple sclerosis (MS) is divided into three clinical phenotypes: relapsing-remitting MS (RRMS), secondary progressive MS (SPMS), and primary progressive MS (PPMS). It is unknown to what extent SPMS and PPMS pathophysiology share inflammatory or neurodegenerative pathological processes. Cerebrospinal (CSF) neurofilament light (NfL) has been broadly studied in different MS phenotypes and is a candidate biomarker for comparing MS subtypes. Research question: Are CSF NfL levels different among clinical subtypes of progressive MS? Methods: A search strategy identifying original research investigating fluid neurodegenerative biomarkers in progressive forms of MS between 2010 and 2022 was applied to Medline. Identified articles underwent title and abstract screen and full text review against pre-specified criteria. Data abstraction was limited to studies that measured NfL levels in the CSF. Reported statistical comparisons of NfL levels between clinical phenotypes were abstracted qualitatively. Results: 18 studies that focused on investigating direct comparisons of CSF NfL from people with MS were included in the final report. We found NfL levels were typically reported to be higher in relapsing and progressive MS compared to healthy controls. Notably, higher NfL levels were not clearly associated with progressive MS subtypes when compared to relapsing MS, and there was no observed difference in NfL levels between PPMS and SPMS in articles that separately assessed these phenotypes. Conclusion: CSF NfL levels distinguish individuals with MS from healthy controls but do not differentiate MS subtypes. Broad biological phenotyping is needed to overcome limitations of current clinical phenotyping and improve biomarker translatability to decision-making in the clinic.
Language	English
Publishing date	2024-04-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2024.1382468
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Article ; Online: Enhanced expression of complement and microglial-specific genes prior to clinical progression in the MOG-experimental autoimmune encephalomyelitis model of multiple sclerosis.

Becquart, Pierre / Vilariño-Güell, Carles / Quandt, Jacqueline A

Brain research bulletin

2020 Volume 165, Page(s) 63–69

Abstract: Understanding the biological changes responsible for failures in repair and the development of progressive MS is paramount for therapeutic intervention. In a well characterized experimental autoimmune encephalomyelitis (EAE) model of MS the clinical ... ...

Abstract	Understanding the biological changes responsible for failures in repair and the development of progressive MS is paramount for therapeutic intervention. In a well characterized experimental autoimmune encephalomyelitis (EAE) model of MS the clinical phenotype features an acute attack with partial recovery followed by a chronic or progressive disease phase. Neuropathology-focused gene expression profiles were generated from spinal cord, hindbrain and forebrain of mice 25 days after the induction of EAE, the time when recovery plateaus and transitions to a chronic or worsening phase. Differences in gene expression were most pronounced in the spinal cord of EAE mice compared to sham-immunized animals, with a subset of genes also found to be differentially expressed in the hindbrain and the forebrain, albeit with smaller fold-changes in expression. Our data suggests that changes in complement components, chemoattractant cytokines and especially enrichment in microglial cells may be the primary drivers of processes that limit recovery in EAE.
MeSH term(s)	Animals ; Complement System Proteins/genetics ; Complement System Proteins/metabolism ; Disease Progression ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Female ; Gene Expression Profiling ; Mice ; Microglia/metabolism ; Myelin-Oligodendrocyte Glycoprotein ; Prosencephalon/metabolism ; Spinal Cord/metabolism
Chemical Substances	Myelin-Oligodendrocyte Glycoprotein ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2020-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	197620-5
ISSN	1873-2747 ; 0361-9230
ISSN (online)	1873-2747
ISSN	0361-9230
DOI	10.1016/j.brainresbull.2020.09.010
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Article ; Online: Oligodendrocyte ARNT2 expression is altered in models of MS.

Becquart, Pierre / Johnston, Jake / Vilariño-Güell, Carles / Quandt, Jacqueline A

Neurology(R) neuroimmunology & neuroinflammation

2020 Volume 7, Issue 4

Abstract: Objective: We examined expression of aryl hydrocarbon receptor nuclear translocator 2 (ARNT2), a basic-loop-helix transcription factor implicated in neuronal development and axonal health, in oligodendrocyte (OL) cultures and over the course of chronic ... ...

Abstract	Objective: We examined expression of aryl hydrocarbon receptor nuclear translocator 2 (ARNT2), a basic-loop-helix transcription factor implicated in neuronal development and axonal health, in oligodendrocyte (OL) cultures and over the course of chronic experimental autoimmune encephalomyelitis (EAE), the murine model of multiple sclerosis (MS). Methods: We assessed OL ARNT2 expression in EAE compared with sham-immunized controls and also in OL primary cultures and over the course of dibutyryl cyclic adenosine monophosphate (dbcAMP)-mediated maturation of the immortalized Oli-neu cell line. We also tested the functional role of ARNT2 in influencing OL characteristics using small interfering RNA (siRNA). Results: ARNT2 is localized to Olig2 Conclusion: The analysis of ARNT2 expression in OLs demonstrates that OL ARNT2 expression is altered in EAE and during OL maturation. Findings point to ARNT2 as an important mediator of OL viability and differentiation and warrant further characterization as a target for intervention in demyelinating disorders such as MS.
MeSH term(s)	Animals ; Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Line ; Cells, Cultured ; Cerebral Cortex/metabolism ; Embryo, Mammalian ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Female ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/metabolism ; Oligodendrocyte Precursor Cells/metabolism ; Oligodendroglia/metabolism
Chemical Substances	Arnt2 protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; Aryl Hydrocarbon Receptor Nuclear Translocator (138391-32-9)
Language	English
Publishing date	2020-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000000745
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Article: Mucosal Administration of E-selectin Limits Disability in Models of Multiple Sclerosis.

Quandt, Jacqueline A / Becquart, Pierre / Kamma, Emily / Hallenbeck, John

Frontiers in molecular neuroscience

2019 Volume 12, Page(s) 190

Abstract: E-selectin plays an important role in mediating the rolling of leukocytes along and thus, the subsequent extravasation across activated endothelial cells comprising the microvasculature of the blood brain barrier (BBB). In multiple sclerosis (MS) and ... ...

Abstract	E-selectin plays an important role in mediating the rolling of leukocytes along and thus, the subsequent extravasation across activated endothelial cells comprising the microvasculature of the blood brain barrier (BBB). In multiple sclerosis (MS) and other inflammatory disorders of the central nervous system (CNS), the microvasculature is altered and immune cells infiltrate the brain and spinal cord contributing to damage, demyelination and ultimately disability. While mucosal administration is typically used to affect lymphocyte hyporesponsiveness or tolerance to suspect autoantigens, intranasal administration to E-selectin has previously been shown to protect against CNS inflammatory insults. We characterized the potential for mucosal administration of E-selectin to modulate CNS autoimmunity in the experimental autoimmune encephalomyelitis (EAE) model of MS. Intranasally administered E-selectin reduced swelling by as much as 50% in delayed-type hypersensitivity reactions compared to ovalbumin-tolerized controls. Intranasal E-selectin delivery prior to disease induction with myelin oligodendrocyte glycoprotein (MOG)
Language	English
Publishing date	2019-08-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2019.00190
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Article ; Online: High yield primary microglial cultures using granulocyte macrophage-colony stimulating factor from embryonic murine cerebral cortical tissue.

Yu, Adam C / Neil, Sarah E / Quandt, Jacqueline A

Journal of neuroimmunology

2017 Volume 307, Page(s) 53–62

Abstract: Background: Microglia play vital roles in neurotrophic support and modulating immune or inflammatory responses to pathogens or damage/stressors during disease. This study describes the ability to establish large numbers of microglia from embryonic ... ...

Abstract	Background: Microglia play vital roles in neurotrophic support and modulating immune or inflammatory responses to pathogens or damage/stressors during disease. This study describes the ability to establish large numbers of microglia from embryonic tissues with the addition of granulocyte-macrophage stimulating factor (GM-CSF) and characterizes their similarities to adult microglia examined ex vivo as well as their responses to inflammatory mediators. Method: Microglia were seeded from a primary embryonic mixed cortical suspension with the addition of GM-CSF. Microglial expression of CD45, CD11b, CD11c, MHC class I and II, CD40, CD80, and CD86 was analyzed by flow cytometry and compared to those isolated using different culture methods and to the BV-2 cell line. GM-CSF microglia immunoreactivity and cytokine production was examined in response to lipopolysaccharide (LPS) and interferon-γ (IFN-γ). Results: Our results demonstrate GM-CSF addition during microglial culture yields higher cell numbers with greater purity than conventionally cultured primary microglia. We found that the expression of immune markers by GM-CSF microglia more closely resemble adult microglia than other methods or an immortalized BV-2 cell line. Primary differences amongst the different groups were reflected in their levels of CD39, CD86 and MHC class I expression. GM-CSF microglia produce CCL2, tumor necrosis factor-α, IL-6 and IL-10 following exposure to LPS and alter costimulatory marker expression in response to LPS or IFN-γ. Notably, GM-CSF microglia were often more responsive than the commonly used BV-2 cell line which produced negligible IL-10. Conclusion: GM-CSF cultured microglia closely model the phenotype of adult microglia examined ex vivo. GM-CSF microglia are robust in their responses to inflammatory stimuli, altering immune markers including Iba-1 and expressing an array of cytokines characteristic of both pro-inflammatory and reparative processes. Consequently, the addition of GM-CSF for the culturing of primary microglia serves as a valuable method to increase the potential for studying microglial function ex vivo.
MeSH term(s)	Animals ; Calcium-Binding Proteins/metabolism ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; Cytokines/metabolism ; Cytokines/pharmacology ; Embryo, Mammalian ; Flow Cytometry ; Gene Expression Regulation/drug effects ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Lipopolysaccharides/pharmacology ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/metabolism ; Microglia/drug effects ; Microglia/physiology ; Time Factors
Chemical Substances	Aif1 protein, mouse ; Calcium-Binding Proteins ; Cytokines ; Lipopolysaccharides ; Microfilament Proteins ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2017-04-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2017.03.018
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Zs.A 1646: Show issues

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Article ; Online: Elevated levels of serum CD5 antigen-like protein distinguish secondary progressive multiple sclerosis from other disease subtypes.

Kamma, Emily / Becquart, Pierre / Traboulsee, Anthony / Schabas, Alice / Vavasour, Irene M / Laule, Cornelia / Vilariño-Güell, Carles / Quandt, Jacqueline A

Multiple sclerosis and related disorders

2021 Volume 56, Page(s) 103269

Abstract: CD5 antigen-like (CD5L) protein is a macrophage-secreted protein with roles in immunomodulation and lipid homeostasis. We compared serum CD5L levels in healthy controls to individuals diagnosed with clinically isolated syndrome, relapsing remitting (RR), ...

Abstract	CD5 antigen-like (CD5L) protein is a macrophage-secreted protein with roles in immunomodulation and lipid homeostasis. We compared serum CD5L levels in healthy controls to individuals diagnosed with clinically isolated syndrome, relapsing remitting (RR), secondary progressive (SP), and primary progressive (PP) multiple sclerosis (MS). CD5L was increased in SPMS relative to controls, RRMS, and PPMS. SPMS CD5L was associated with longer disease duration independent of age, sex, or disease severity. The positive relationship between CD5L and disease duration in SPMS suggests a chronic peripheral inflammatory profile compared to other subtypes, particularly PPMS, warranting investigation of functional roles for CD5L in MS.
MeSH term(s)	CD5 Antigens ; Humans ; Inflammation ; Multiple Sclerosis/diagnosis ; Multiple Sclerosis, Chronic Progressive/diagnosis ; Multiple Sclerosis, Relapsing-Remitting
Chemical Substances	CD5 Antigens
Language	English
Publishing date	2021-09-20
Publishing country	Netherlands
Document type	Letter
ZDB-ID	2645330-7
ISSN	2211-0356 ; 2211-0348
ISSN (online)	2211-0356
ISSN	2211-0348
DOI	10.1016/j.msard.2021.103269
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Article ; Online: Expression of CD1d by astrocytes corresponds with relative activity in multiple sclerosis lesions.

Muir, Fraser G W / Samadi-Bahrami, Zahra / Moore, George R Wayne / Quandt, Jacqueline A

Brain pathology (Zurich, Switzerland)

2019 Volume 30, Issue 1, Page(s) 26–35

Abstract: The CD1 protein family present lipid antigens to the immune system. CD1d has been observed in the CNS of MS patients, yet no studies have quantitatively characterized this expression and related it to inflammatory demyelinative activity in MS plaques. In ...

Abstract	The CD1 protein family present lipid antigens to the immune system. CD1d has been observed in the CNS of MS patients, yet no studies have quantitatively characterized this expression and related it to inflammatory demyelinative activity in MS plaques. In this study, we set out to localize and quantify the presence of CD1d expression by astrocytes in MS brain tissue lesions. Formalin-fixed, paraffin-embedded MS and control brain tissues were examined. Lesions were classified as active, chronic active or chronic silent. Using immunofluorescence, the density of CD1d-positive cells was determined in active lesions, chronic active lesion edges and chronic active lesion centers. The percentage of CD1d-positive cells that were GFAP-positive was also determined in each of these regions. CD1d immunoreactivity was significantly increased in MS compared to control tissue, was significantly more prevalent in areas of active demyelination, and colocalized with GFAP-positive reactive astrocytes. Increases of CD1d immunoreactivity in the CNS of MS patients being greatest in areas of active demyelination and localized to GFAP-positive astrocytes lend support to the hypothesis of a lipid-targeted autoimmune process contributing to the pathogenesis of MS.
MeSH term(s)	Adult ; Antigens, CD1d/genetics ; Antigens, CD1d/metabolism ; Astrocytes/metabolism ; Brain/pathology ; Demyelinating Diseases/pathology ; Female ; Humans ; Male ; Middle Aged ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology
Chemical Substances	Antigens, CD1d ; CD1D protein, human
Language	English
Publishing date	2019-06-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.12733
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Zs.A 3585: Show issues

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Article ; Online: Genetic analysis of nucleotide-binding leucine-rich repeat (NLR) receptors in multiple sclerosis.

Popplewell, Lisa F / Encarnacion, Mary / Bernales, Cecily Q / Sadovnick, A Dessa / Traboulsee, Anthony L / Quandt, Jacqueline A / Vilariño-Güell, Carles

Immunogenetics

2020 Volume 72, Issue 6-7, Page(s) 381–385

Abstract: Genetic and functional analyses of the inflammasome suggest a role for this multiprotein complex in the biological mechanisms leading to the onset and progression of multiple sclerosis (MS). Nucleotide-binding, leucine-rich repeat (NLR) receptors trigger ...

Abstract	Genetic and functional analyses of the inflammasome suggest a role for this multiprotein complex in the biological mechanisms leading to the onset and progression of multiple sclerosis (MS). Nucleotide-binding, leucine-rich repeat (NLR) receptors trigger the activation and assembly of specific inflammasomes in response to danger signals. Mining exome sequencing data from 326 MS patients identified 17 rare missense or nonsense variants in NLR family pyrin domain containing 1 (NLRP1), NLRP3, NLRP6, NLRP7 and NLR family CARD domain containing 4 (NLRC4). Genotyping these variants in 2503 MS cases and 1076 healthy controls did not result in statistically significant differences between groups, and segregation analysis within MS families was largely unsupportive of co-segregation of these variants with disease. However, the identification of MS patients harboring rare homozygote variants in NLRP1 (p.Ile601Phe and p.Ser1387Ile), a variant in NLRP3 (p.Leu832Ile) resulting in the substitution of a critical amino acid for the formation of its leucine-rich repeat domain, and several MS patients with NLRC4 variants (p.Arg310Ter and p.Glu600Ter) causing protein truncations suggest that rare protein-altering variants in inflammasome-activating NLR receptors may contribute to MS risk.
MeSH term(s)	CARD Signaling Adaptor Proteins/genetics ; Female ; Humans ; Inflammasomes/genetics ; Male ; Multiple Sclerosis/genetics ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology ; Mutation ; Pedigree
Chemical Substances	CARD Signaling Adaptor Proteins ; Inflammasomes
Language	English
Publishing date	2020-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186560-2
ISSN	1432-1211 ; 0093-7711
ISSN (online)	1432-1211
ISSN	0093-7711
DOI	10.1007/s00251-020-01170-w
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Zs.A 1052: Show issues

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Article ; Online: Dolutegravir-containing HIV therapy reversibly alters mitochondrial health and morphology in cultured human fibroblasts and peripheral blood mononuclear cells.

Ajaykumar, Abhinav / Caloren, Loïc C / Povshedna, Tetiana / Hsieh, Anthony Y Y / Zakaria, Aya / Cai, Renying / Smith, Marie-Soleil R / Thompson, Connor A H / Becquart, Pierre / Uday, Prakruti / Pattanshetti, Rutuja / Quandt, Jacqueline A / Wong, Judy M Y / Côté, Hélène C F

AIDS (London, England)

2022 Volume 37, Issue 1, Page(s) 19–32

Abstract: Objectives: Given the success of combination antiretroviral therapy (cART) in treating HIV viremia, drug toxicity remains an area of interest in HIV research. Despite newer integrase strand transfer inhibitors (InSTIs), such as dolutegravir (DTG) and ... ...

Abstract	Objectives: Given the success of combination antiretroviral therapy (cART) in treating HIV viremia, drug toxicity remains an area of interest in HIV research. Despite newer integrase strand transfer inhibitors (InSTIs), such as dolutegravir (DTG) and raltegravir (RAL), having excellent clinical tolerance, there is emerging evidence of off-target effects and toxicities. Although limited in number, recent reports have highlighted the vulnerability of mitochondria to these toxicities. The aim of the present study is to quantify changes in cellular and mitochondrial health following exposure to current cART regimens at pharmacological concentrations. A secondary objective is to determine whether any cART-associated toxicities would be modulated by human telomerase reverse transcriptase (hTERT). Methods: We longitudinally evaluated markers of cellular (cell count, apoptosis), and mitochondrial health [mitochondrial reactive oxygen species (mtROS), membrane potential (MMP) and mass (mtMass)] by flow cytometry in WI-38 human fibroblast with differing hTERT expression/localization and peripheral blood mononuclear cells. This was done after 9 days of exposure to, and 6 days following the removal of, seven current cART regimens, including three that contained DTG. Mitochondrial morphology was assessed by florescence microscopy and quantified using a recently developed deep learning-based pipeline. Results: Exposure to DTG-containing regimens increased apoptosis, mtROS, mtMass, induced fragmented mitochondrial networks compared with non-DTG-containing regimens, including a RAL-based combination. These effects were unmodulated by telomerase expression. All effects were fully reversible following removal of drug pressure. Conclusion: Taken together, our observations indicate that DTG-containing regimens negatively impact cellular and mitochondrial health and may be more toxic to mitochondria, even among the generally well tolerated InSTI-based cART.
MeSH term(s)	Humans ; Leukocytes, Mononuclear ; HIV Infections/drug therapy ; Immune Tolerance ; Fibroblasts
Language	English
Publishing date	2022-08-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0000000000003369
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Zs.A 2228: Show issues

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Article ; Online: SPARC expression by cerebral microvascular endothelial cells in vitro and its influence on blood-brain barrier properties.

Alkabie, Samir / Basivireddy, Jayasree / Zhou, Lixin / Roskams, Jane / Rieckmann, Peter / Quandt, Jacqueline A

Journal of neuroinflammation

2016 Volume 13, Issue 1, Page(s) 225

Abstract: Background: SPARC (secreted protein acidic and rich in cysteine) is a nonstructural, cell-matrix modulating protein involved in angiogenesis and endothelial barrier function, yet its potential role in cerebrovascular development, inflammation, and ... ...

Abstract	Background: SPARC (secreted protein acidic and rich in cysteine) is a nonstructural, cell-matrix modulating protein involved in angiogenesis and endothelial barrier function, yet its potential role in cerebrovascular development, inflammation, and repair in the central nervous system (CNS) remains undetermined. Methods: This study examines SPARC expression in cultured human cerebral microvascular endothelial cells (hCMEC/D3)-an in vitro model of the blood-brain barrier (BBB)-as they transition between proliferative and barrier phenotypes and encounter pro-inflammatory stimuli. SPARC protein levels were quantified by Western blotting and immunocytochemistry and messenger RNA (mRNA) by RT-PCR. Results: Constitutive SPARC expression by proliferating hCMEC/D3s is reduced as cells mature and establish a confluent monolayer. SPARC expression positively correlated with the proliferation marker Ki-67 suggesting a role for SPARC in cerebrovascular development. The pro-inflammatory molecules tumor necrosis factor-α (TNF-α) and endotoxin lipopolysaccharide (LPS) increased SPARC expression in cerebral endothelia. Interferon gamma (IFN-γ) abrogated SPARC induction observed with TNF-α alone. Barrier function assays show recombinant human (rh)-SPARC increased paracellular permeability and decreased transendothelial electrical resistance (TEER). This was paralleled by reduced zonula occludens-1 (ZO-1) and occludin expression in hCMEC/D3s exposed to rh-SPARC (1-10 μg/ml) compared with cells in media containing a physiological dose of SPARC. Conclusions: Together, these findings define a role for SPARC in influencing cerebral microvascular properties and function during development and inflammation at the BBB such that it may mediate processes of CNS inflammation and repair.
MeSH term(s)	Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Cell Proliferation/drug effects ; Cell Proliferation/physiology ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Circulation/physiology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Gene Expression ; Humans ; Microvessels/drug effects ; Microvessels/metabolism ; Osteonectin/biosynthesis ; Osteonectin/genetics ; Osteonectin/pharmacology
Chemical Substances	Osteonectin ; SPARC protein, human
Language	English
Publishing date	2016-08-31
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-016-0657-9
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