Evidence map›Paper›PMID 36140432›Full record

ArticleBiomedicines2022

Stress Hormone Corticosterone Controls Metabolic Mitochondrial Performance and Inflammatory Signaling of In Vitro Cultured Sertoli Cells.

Ana M Silva, Carina T Ribeiro, Raquel L Bernardino, Ivana Jarak, Rui A Carvalho, M A Pereira-Sampaio, Diogo B de Souza, Marco G Alves, Pedro F Oliveira

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

9 authors at 4 institutions in 2 countries.

Ana M SilvaDepartment of Anatomy and Unit for Multidisciplinary Research in Biomedicine (UMIB), School of Medicine and Biomedical Sciences (ICBAS), University of Porto, 4050-313 Porto, Portugal.ORCID 0000-0001-7172-4266
Carina T RibeiroDepartment of Anatomy and Unit for Multidisciplinary Research in Biomedicine (UMIB), School of Medicine and Biomedical Sciences (ICBAS), University of Porto, 4050-313 Porto, Portugal.
Raquel L BernardinoDepartment of Anatomy and Unit for Multidisciplinary Research in Biomedicine (UMIB), School of Medicine and Biomedical Sciences (ICBAS), University of Porto, 4050-313 Porto, Portugal.ORCID 0000-0002-1941-6634
Ivana JarakDepartment of Anatomy and Unit for Multidisciplinary Research in Biomedicine (UMIB), School of Medicine and Biomedical Sciences (ICBAS), University of Porto, 4050-313 Porto, Portugal.
Rui A CarvalhoDepartment of Life Sciences, Faculty of Sciences and Technology, University of Coimbra, 3030-790 Coimbra, Portugal.
M A Pereira-SampaioUrogenital Research Unit, Rio De Janeiro State University, Rio De Janeiro 20551-030, Brazil.ORCID 0000-0003-2574-7058
Diogo B de SouzaUrogenital Research Unit, Rio De Janeiro State University, Rio De Janeiro 20551-030, Brazil.ORCID 0000-0003-3456-5029
Marco G AlvesDepartment of Anatomy and Unit for Multidisciplinary Research in Biomedicine (UMIB), School of Medicine and Biomedical Sciences (ICBAS), University of Porto, 4050-313 Porto, Portugal.ORCID 0000-0001-7635-783X
Pedro F OliveiraLAQV-REQUIMTE and Department of Chemistry, University of Aveiro, 3810-193 Aveiro, Portugal.ORCID 0000-0002-4989-5699
Universidade do Porto · PTUniversidade do Estado do Rio de Janeiro · BRRede de Química e Tecnologia · PTUniversity of Coimbra · PT

Funding

Coordenação de Aperfeicoamento de Pessoal de Nível Superior N/AFundação para a Ciência e Tecnologia LA/P/0064/2020Fundação para a Ciência e Tecnologia UIDB/00215/2020Fundação para a Ciência e Tecnologia UIDB/50006/2020Fundação para a Ciência e Tecnologia UIDP/00215/2020
6 · The paper itself

Abstract

Stress, as a physiological response, is a major factor that affects several processes, including reproductive functions. The main hormonal players of stress are cortisol (humans) and corticosterone (rodents). Sertoli cells (SCs), as key contributors for the testicular homeostasis maintenance, are extensively challenged by different hormones, with glucocorticoid corticosterone being the signaling modulator that may impact these cells at different levels. We aimed to characterize how corticosterone modulates SCs energy balance, putting the mitochondrial performance and signaling output in perspective as the cells can disperse to the surroundings. TM4 mouse SCs were cultured in the absence and presence of corticosterone (in nM: 20, 200, and 2000). Cells were assessed for extracellular metabolic fluxes, mitochondrial performance (cell respirometry, mitochondrial potential, and mitochondrial complex expressions and activities), and the expression of androgen and corticosteroid receptors, as well as interleukine-6 (IL-6) and glutathione content. Corticosterone presented a biphasic impact on the extracellular fluxes of metabolites. Low sub-physiological corticosterone stimulated the glycolytic activity of SCs. Still, no alterations were perceived for lactate and alanine production. However, the lactate/alanine ratio was decreased in a dose-dependent mode, opposite to the mitochondrial complex II activity rise and concurrent with the decrease of IL-6 expression levels. Our results suggest that corticosterone finely tuned the energetic profile of mouse SCs, with sub-physiological concentrations promoting glycolytic expenditure, without translating into cell redox power and mitochondrial respiratory chain performance. Corticosterone deeply impacted the expression of the pro-inflammatory IL-6, which may alter cell-to-cell communication in the testis, in the last instance and impact of the spermatogenic performance.

Indexed as

corticosteroneinterleukine-6male fertilitymetabolismmitochondriaSertoli cellstress

Identifiers

PMID36140432
PMCPMC9496023
OpenAlexW4296526413

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.