Evidence map›Paper›PMID 34068511›Full record

ArticleNanomaterials (Basel, Switzerland)2021

Anti-Inflammatory Effect and Cellular Uptake Mechanism of Carbon Nanodots in in Human Microvascular Endothelial Cells.

Sarah Belperain, Zi Yae Kang, Andrew Dunphy, Brandon Priebe, Norman H L Chiu, Zhenquan Jia

Open access · goldAbstract read
In one paragraph

Article in Nanomaterials (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Carbon Dots for the Treatment of Inflammatory Diseases: An Appraisal ofOxidative medicine and cellular longevity · 2023
    Review
  4. Article
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Sarah BelperainDepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.
Zi Yae KangDepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.
Andrew DunphyDepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.
Brandon PriebeDepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.ORCID 0000-0002-4791-282X
Norman H L ChiuDepartment of Chemistry and Biochemistry, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.
Zhenquan JiaDepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.ORCID 0000-0002-5187-1549
University of North Carolina at Greensboro · US

Funding

Novel Carbon Nanodots against Vascular InflammationR15HL129212 · NHLBI · UNIVERSITY OF NORTH CAROLINA GREENSBORO · PI JIA, ZHENQUAN · 2016 to 2016
$455k
Novel carbon nanodots for modulation of OxLDL mediated inflammation and inhibition of atherosclerosisR15HL150664 · NHLBI · UNIVERSITY OF NORTH CAROLINA GREENSBORO · PI JIA, ZHENQUAN · 2020 to 2020
$447k
NHLBI NIH HHS R15 HL129212NHLBI NIH HHS R15 HL150664NIH HHS 1R15HL129212-01A1 and 1R15HL150664-01A1
6 · The paper itself

Abstract

Cardiovascular disease (CVD) has become an increasingly important topic in the field of medical research due to the steadily increasing rates of mortality caused by this disease. With recent advancements in nanotechnology, a push for new, novel treatments for CVD utilizing these new materials has begun. Carbon Nanodots (CNDs), are a new form of nanoparticles that have been coveted due to the green synthesis method, biocompatibility, fluorescent capabilities and potential anti-antioxidant properties. With much research pouring into CNDs being used as bioimaging and drug delivery tools, few studies have been completed on their anti-inflammatory potential, especially in the cardiovascular system. CVD begins initially by endothelial cell inflammation. The cause of this inflammation can come from many sources; one being tumor necrosis factor (TNF-α), which can not only trigger inflammation but prolong its existence by causing a storm of pro-inflammatory cytokines. This study investigated the ability of CNDs to attenuate TNF-α induced inflammation in human microvascular endothelial cells (HMEC-1). Results show that CNDs at non-cytotoxic concentrations reduce the expression of pro-inflammatory genes, mainly Interleukin-8 (IL-8), and interleukin 1 beta (IL-1β). The uptake of CNDs by HMEC-1s was examined. Results from the studies involving channel blockers and endocytosis disruptors suggest that uptake takes place by endocytosis. These findings provide insights on the interaction CNDs and endothelial cells undergoing TNF-α induced cellular inflammation.

Indexed as

carbon nanodotstumor necrosis factor-alphavascular inflammation

Identifiers

PMID34068511
PMCPMC8151002
OpenAlexW3162683889

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.