Evidence map›Paper›PMID 39512370›Full record

ArticleFrontiers in cardiovascular medicine2024

Gene expression profiles of precursor cells identify compounds that reduce NRP1 surface expression in macrophages: Implication for drug repositioning for COVID-19.

Akira Iwata, Sarvesh Chelvanambi, Takaharu Asano, Mary Whelan, Yuto Nakamura, Elena Aikawa, Yusuke Sasaki, Masanori Aikawa

Abstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

8 authors.

Akira Iwata *Center for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Sarvesh Chelvanambi *Center for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Takaharu AsanoCenter for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Mary WhelanCenter for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Yuto NakamuraCenter for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Elena AikawaCenter for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Yusuke SasakiCenter for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Masanori AikawaCenter for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.

Funding

Pro-inflammatory activation of human macrophages regulated by lncRNAsR01HL149302 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, MASANORI · 2019 to 2022
$2.9M
PARP9 and PARP14 in atherosclerosisR01HL126901 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, MASANORI · 2016 to 2019
$2.4M
Nef in impaired efferocytosis: a novel mechanism for vascular disease in HIVR01HL174066 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI Elena Aikawa, Masanori Aikawa · 2024 to 2026
$2.2M
NHLBI NIH HHS R01 HL126901NHLBI NIH HHS R01 HL149302NHLBI NIH HHS R01 HL174066
6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) is transitioning from a pandemic to an endemic phase through recurring mutations. Initial efforts focused on developing strategies to mitigate infection of lung epithelial cells which are the primary targets of the SARS-CoV-2 virus using the affinity of the spike protein to human ACE2 receptor. SARS-CoV-2, however, infects additional cell types present in the lung such as macrophages through the alternate entry receptor Neuropilin 1 (NRP1). Developing novel therapeutic strategies to prevent SARS-CoV-2 infection of cells crucial for immunosurveillance could thus be integral to treat post-acute sequelae of COVID-19 (PASC). Since traditional drug development process takes a long time, it is imperative to establish new strategies that can be rapidly deployed to combat the dynamic nature of COVID-19 evolution and to contribute to prevention of future pandemics. We obtained the gene expression profiles of THP-1 monocytes from L1000-based Connectivity Map using CLUE, cloud- based software platform for the analysis of perturbational datasets to identify compounds that could reduce the expression level of NRP1. Out of 33,590 compounds, we analyzed the profiles of 45 compounds for their ability to reduce NRP1 expression. We selected the top five small molecule inhibitors predicted to decrease the expression of NRP1 for validation studies. All five selected compounds showed low cytotoxicity at tested doses and their ability to reduce NRP1 surface expression was evaluated in THP-1 monocytes, THP-1-derived macrophage like cells and human peripheral blood mononuclear cell (PBMC)-derived primary macrophages. Five compounds with the largest predicted reduction of NRP1 expression decreased macrophage NRP1 surface expression measured using flow cytometry and fluorescent microscopy assays in both cell line and primary macrophages. Using our computational approach, we identified 45 compounds that could potentially decrease NRP1 surface expression in macrophages based on their effect on THP-1 monocytes. Validation studies showed that such an approach can help to identify compounds for drug repositioning in target cells that are absent in the L1000 database. Our proposed approach can be applicable for the rapid compound exploration to combat novel cell types that SARS-CoV-2 targets for infection and could provide molecular bases for the development of new drugs.

Indexed as

COVID-19drug developmentdrug screeninggene expression profilingL1000-based Connectivity MapmacrophageNeuropilin 1SARS-CoV-2

Identifiers

PMID39512370
PMCPMC11541348

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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.