Evidence map›Paper›PMID 35028455›Full record

ArticleHeliyon2022

Production of NOS2 and inflammatory cytokines is reduced by selected protein kinase inhibitors with partial repolarization of HL-60 derived and human blood macrophages.

Gábor Bögel, József Murányi, Bálint Szokol, Zoltán Kukor, István Móra, Tamás Kardon, László Őrfi, András Hrabák

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In one paragraph

Article in Heliyon, 2022. 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
–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

5 citing papers in PubMed.

  1. Review
  2. Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  3. Pharmaceutics · 2025
    Article
  4. LINC01119 encapsulated by cancer-associated adipocytes-derived exosomes promotes M2 polarization of macrophages to induce immune escape in ovarian cancer in a 3D co-culture cell-based model.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  5. Review
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.

Gábor BögelDepartment of Molecular Biology, Institute of Biochemistry and Molecular Biology, Semmelweis University, Budapest, H-1094, Tűzoltó u. 37-43, Hungary.
József MurányiDepartment of Molecular Biology, Institute of Biochemistry and Molecular Biology, Semmelweis University, Budapest, H-1094, Tűzoltó u. 37-43, Hungary.
Bálint SzokolVichem Chemie Research Ltd., Veszprém, H-8200, Viola u. 2., Hungary.
Zoltán KukorDepartment of Molecular Biology, Institute of Biochemistry and Molecular Biology, Semmelweis University, Budapest, H-1094, Tűzoltó u. 37-43, Hungary.
István MóraDepartment of Molecular Biology, Institute of Biochemistry and Molecular Biology, Semmelweis University, Budapest, H-1094, Tűzoltó u. 37-43, Hungary.
Tamás KardonDepartment of Molecular Biology, Institute of Biochemistry and Molecular Biology, Semmelweis University, Budapest, H-1094, Tűzoltó u. 37-43, Hungary.
László ŐrfiVichem Chemie Research Ltd., Veszprém, H-8200, Viola u. 2., Hungary.
András HrabákDepartment of Molecular Biology, Institute of Biochemistry and Molecular Biology, Semmelweis University, Budapest, H-1094, Tűzoltó u. 37-43, Hungary.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

JAK/STAT pathway plays a well-known role in macrophage polarization, but other signaling routes may also be involved. The aim of this study was to identify new signaling pathways and repolarize macrophages by selected protein kinase inhibitors. HL-60 derived macrophages were chosen as model cells and human blood macrophages were used for comparison. M1 and M2 polarization of HL60 derived and human blood macrophages was promoted by LPS + IFNγ (LIF) and IL-4 treatments, respectively. In HL-60 derived macrophages, M1 polarization was mediated by Erk1/2 and p38 phosphorylation, while HSP27 phosphorylation was involved in M2 polarization. The inhibition of both MAPK and JAK/STAT pathways reduced the expression of NOS2, IP-10 and TNFα, IL-8 production was decreased by the inhibition of AMPK and PKD, the upstream kinase of HSP27. HSP27 phosphorylation was inhibited by NB 142, a PKD inhibitor. The expression of CD80 (M1 marker) was reduced by MAPK and JAK/STAT inhibitors, without increasing CD206 (M2 marker). On the other hand, CD206 was reduced by PKD and AMPK inhibitors, without increasing CD80 marker. Phagocytic capacity of HL-60 derived macrophages was higher in M1 macrophages and decreased by trametinib and a p38 inhibitor, while in human blood macrophages, where AT 9283, a JAK/STAT inhibitor also caused a significant decrease in M1 polarized macrophages, no difference was observed between M1 and M2 macrophages. Our results suggest that the repolarization of macrophages cannot be achieved by inhibiting their signaling pathways; nevertheless, the expression of certain polarization markers was decreased, therefore a "depolarization" could be observed both in M1 and M2 polarized cells. Selected protein kinase inhibitors of M1 polarization, decreasing NOS 2 and inflammatory cytokines may be potential candidates for therapeutical trials against inflammatory diseases.

Indexed as

Inflammatory cytokinesKinase inhibitorsM1-M2 polarization signalingMacrophageNitric oxide synthase 2

Identifiers

PMID35028455
PMCPMC8741463

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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.