Evidence map›Paper›PMID 35216073›Full record

ArticleInternational journal of molecular sciences2022

Alpha 1 Antitrypsin Regulates Trophoblast Syncytialization and Inflammatory Factor Expression.

Kanoko Yoshida, Aruto Yano, Kazuya Kusama, Gen Ishikawa, Kazuhiro Tamura

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Therapeutic Targeting of the Proteolytic Enzymes.International journal of molecular sciences · 2022
    Article
  9. Human Chorionic Villous Differentiation and Placental Development.International journal of molecular sciences · 2022
    Review
  10. 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

5 authors at 2 institutions in 1 country.

Kanoko YoshidaDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan.
Aruto YanoDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan.
Kazuya KusamaDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan.ORCID 0000-0002-9120-0475
Gen IshikawaDepartment of Obstetrics, Miyagi Children's Hospital, Sendai 989-3126, Japan.
Kazuhiro TamuraDepartment of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan.ORCID 0000-0003-3351-895X
Tokyo University of Pharmacy and Life Sciences · JPMiyagi Children's Hospital · JP

Funding

Japan Society for the Promotion of Science 20H03133
6 · The paper itself

Abstract

The serine protease inhibitor alpha1-antitrypsin (A1AT) may possess protective functions of impaired organs in a manner independent of its protease inhibitor activity. A1AT expression has been shown to fluctuate in patients with pregnancy-induced hypertension, which suggests that A1AT may play a role in the syncytialization of villous trophoblasts. A1AT expression was knocked down in primary trophoblasts. RNA was extracted from these cells and subjected to RNA-sequencing analysis to determine the levels of expression of markers of syncytialization and inflammation. In addition, A1AT protein was localized in trophoblastic cells in placental tissues. Knockdown of A1AT upregulated the expression of FOSL1 and markers of syncytialization, as well as cell fusion, whereas overexpression of A1AT had the opposite effects. FOSL1 overexpression stimulated syncytialization, similar to the effects of A1AT knock down. Inhibitors of p38MAPK and JNK reduce the expression of inflammatory factors, whereas a p38MAPK inhibitor suppressed FOSL1 expression. Collectively, these findings indicated A1AT may negatively regulate inflammatory responses by controlling the activation of p38MAPK and JNK, and that p38MAPK mediates trophoblast syncytialization by altering FOSL1 expression. Therefore, a dysfunction in A1AT could be responsible for abnormal placental formation and pregnancy-associated disorders.

Indexed as

alpha 1-AntitrypsinBiomarkersCell LineFemaleHumansInflammationInflammation MediatorsPlacentaPregnancyTrophoblastsalpha 1-AntitrypsinBiomarkersInflammation Mediatorsalpha-1-antitrypsin (A1AT)AP-1 transcription factor subunit (FOSL1)FOS like 1inflammatory factorsyncytializationtrophoblasts

Identifiers

PMID35216073
PMCPMC8879717
OpenAlexW4210955220

What OpenQuestion holds

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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 OpenQuestion graph.