Evidence map›Paper›PMID 33821330›Full record

ArticleCellular and molecular neurobiology2022

Prolactin Attenuates Neuroinflammation in LPS-Activated SIM-A9 Microglial Cells by Inhibiting NF-κB Pathways Via ERK1/2.

Preethi Jayakumar, Carlos G Martínez-Moreno, Mary Y Lorenson, Ameae M Walker, Teresa Morales

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Traumatic brain injury and prolactin.Reviews in endocrine & metabolic disorders · 2024
    Review
  8. Article
  9. Article
  10. Effects of Fucoidans on Activated Retinal Microglia.International journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. 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

5 authors at 2 institutions in 2 countries.

Preethi JayakumarDepartamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico.ORCID http://orcid.org/0000-0002-4961-6370
Carlos G Martínez-MorenoDepartamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico.ORCID http://orcid.org/0000-0002-6868-3413
Mary Y LorensonDepartment of Biomedical Sciences, University of California, Riverside, CA, USA.ORCID http://orcid.org/0000-0003-3934-5893
Ameae M WalkerDepartment of Biomedical Sciences, University of California, Riverside, CA, USA.ORCID http://orcid.org/0000-0002-7614-7450
Teresa MoralesDepartamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico. marter@unam.mx.ORCID http://orcid.org/0000-0003-1539-2070
Universidad Nacional Autónoma de México · MXUniversity of California, Riverside · US

Funding

CONACYT 285004CONACYT A1S8948UNAM-DGAPA-PAPIIT IN201817, IN207018, IN208419UNAM-DGAPA-PAPIIT IN204718University of California Institute for Mexico and the United States CN18-43
6 · The paper itself

Abstract

Prolactin (PRL) is a pleiotropic hormone with multiple functions in several tissues and organs, including the brain. PRL decreases lesion-induced microgliosis and modifies gene expression related to microglial functions in the hippocampus, thereby providing a possible mechanism through which it might participate in neuroimmune modulatory responses and prevent neuronal cell damage. However, the direct contribution of microglial cells to PRL-mediated neuroprotection is still unclear and no studies have yet documented whether PRL can directly activate cellular pathways in microglial cells. The aim of this study is to elucidate in vitro actions of PRL on the immortalized SIM-A9 microglia cell line in basal and LPS-stimulated conditions. PRL alone induced a time-dependent extracellular signal-regulated kinase 1/2 (ERK1/2) activation. Pretreatment with PRL attenuated LPS (200 ng/ml) stimulated pro-inflammatory markers: nitric oxide (NO) levels, inducible nitric oxide synthase (iNOS), interleukins (IL)-6, -1β and tumor necrosis factor (TNF-α) expression at 20 nM dosage. PRL suppressed LPS-induced nuclear factor (NF)-κappaB (NF-κB) p65 subunit phosphorylation and its upstream p-ERK1/2 activity. In conclusion, PRL exhibits anti-inflammatory effects in LPS-stimulated SIM-A9 microglia by downregulating pro-inflammatory mediators corresponding to suppression of LPS-activated ERK1/2 and NF-κB phosphorylation.

Indexed as

MicrogliaNF-kappa BAnti-Inflammatory AgentsHumansInterleukin-6LipopolysaccharidesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 3Neuroinflammatory DiseasesNitric OxideNitric Oxide Synthase Type IIProlactinTumor Necrosis Factor-alphaAnti-Inflammatory AgentsInterleukin-6LipopolysaccharidesMitogen-Activated Protein Kinase 3NF-kappa BNitric OxideNitric Oxide Synthase Type IIProlactinTumor Necrosis Factor-alphaCell signalingCytokinesMicrogliaPRLSIM-A9

Identifiers

PMID33821330
PMCPMC11421592
OpenAlexW3140169954

What OpenQuestion holds

Textmetadata
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.