ArticleJournal of neuroinflammation2016
SPARC expression by cerebral microvascular endothelial cells in vitro and its influence on blood-brain barrier properties.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 63 citations in OpenAlex.
- Mesenchymal stromal cells and neuroinflammation: a multimodal approach to neuroprotection and future therapeutic horizons.Translational neurodegeneration · 2026Review
- The Tumor-to-Endothelial Transfer of FTO Promotes Vascular Remodeling and Metastasis in Nasopharyngeal Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chaperone-mediated autophagy sustains pericyte stemness necessary for brain tissue homeostasis.Journal of advanced research · 2026Article
- The missing link: TNF-α as a unifying mechanism in methamphetamine-induced neuronal dysfunction and blood-brain barrier compromise.Journal of neuroimmunology · 2025Review
- Cell- and sex-specificity in the transcriptomic response of the hippocampal neurovascular unit to obesity.Communications biology · 2025Article
- Exploring the Role of SPARC in Atherosclerosis: Mechanisms and Potential Implications.Current atherosclerosis reports · 2025Review
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Insights into the mechanism of reversible blood-brain barrier opening via second near-infrared region excited gold nanorods photothermal effect: Regulation of the tight junction protein occludin.Smart molecules : open access · 2025Article
- Truncated NTRK2 is induced in CAP1 endothelial cells during mouse lung injury-repair.iScience · 2025Article
- Elevated SPARC Disrupts the Intestinal Barrier Integrity in Crohn's Disease by Interacting with OTUD4 and Activating the MYD88/NF-κB Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of endothelial cell-related gene COL1A1 in prostate cancer diagnosis and immunotherapy: insights from machine learning and single-cell analysis.Biology direct · 2025Article
- Dysregulated Genes and Signaling Pathways in the Formation and Rupture of Intracranial Aneurysm.Translational stroke research · 2024Article
- spVC for the detection and interpretation of spatial gene expression variation.Genome biology · 2024Article
- Space Flight Enhances Stress Pathways in Human Neural Stem Cells.Biomolecules · 2024Article
- Endothelial CellArteriosclerosis, thrombosis, and vascular biology · 2023Article
- Plasma SPARC Elevation in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Endothelial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Article
- The Notch signaling-regulated angiogenesis in rheumatoid arthritis: pathogenic mechanisms and therapeutic potentials.Frontiers in immunology · 2023Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSPARC (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.
methodsThis 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.
resultsConstitutive 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.
conclusionsTogether, 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.