Cited by 71Cell Adhesion Molecules ResearchChemokine receptors and signalingAdipokines, Inflammation, and Metabolic Diseases

Prolactin stimulates integrin-mediated adhesion of circulating mononuclear cells to endothelial cells

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Montes de Oca, Pável, Macotela, Yazmín, Nava, Gabriel, López-Barrera, Fernando, de la Escalera, Gonzalo Martínez, Clapp, Carmen·2005·Laboratory Investigation

Abstract

Attachment of leukocytes to endothelial cells is an essential step for the extravasation and recruitment of cells at sites of inflammation. The pituitary hormone prolactin (PRL) is involved in the inflammatory process. Here, we show that treatment with PRL of human peripheral blood mononuclear cells (PBMC) stimulates their adhesion to human umbilical vein endothelial cells (HUVEC) activated by interleukin-1beta. Stimulation of adhesion by PRL is mediated via integrins leukocyte functional antigen-1 (LFA-1) and very late antigen-4 (VLA-4), because immunoneutralization of both integrins prevents PRL action. Also, PRL promotes the adhesion of PBMC to immobilized intercellular adhesion molecule-1 and fibronectin, ligands for LFA-1 and VLA-4, respectively. Stimulation of integrin-mediated cell adhesion by PRL may involve the activation of chemokine receptors, because PRL upregulates the expression of the G-protein-coupled chemokine receptor CXCR3 in PBMC, and pertussis toxin, a specific G-protein inhibitor, blocks PRL stimulation of PBMC adhesion to HUVEC. In addition, PRL stimulates tyrosine phosphorylation pathways leading to leukocyte adhesion. PRL triggered the tyrosine phosphorylation of Janus kinase-2, of signal transducer and activator of transcription-3 and 5, and of the focal adhesion protein paxillin. Furthermore, genistein, a tyrosine kinase inhibitor, blocked PRL-stimulated adhesion of PBMC and Jurkat T-cells to HUVEC. These results suggest that PRL promotes integrin-mediated leukocyte adhesion to endothelial cells via chemokine receptors and tyrosine phosphorylation signaling pathways.

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Crossref · 10.1038/labinvest.3700256

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  • In chronic hepatitis C virus infection, more than 50% of patients report fatigue, daytime sleepiness, and poor sleep quality.

    “Sleep disturbances are also commonly observed in chronic infection with the hepatitis C virus (HCV), with more than 50% of patients reporting fatigue, daytime sleepiness, and poor sleep quality (reviewed in Ref. 388).”

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References 61 · Cited by 71

Research works printed but not linked: 4

  1. Dorshkind K, Horseman ND. Anterior pituitary hor- mones, stress, and immune system homeostasis. Bioessays 2001;23:288-294.
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Authors
Montes de Oca, P., Macotela, Y., Nava, G., López-Barrera, F., de la Escalera, G. M., & Clapp, C.
Affiliations
Universidad Nacional Autónoma de México (MX)
Corresponding author
Clapp, Carmen
Venue
Laboratory Investigation
Publisher
Elsevier BV
Published
2005-05
Volume
85
Issue
5
Pages
633-642
ISSN
0023-6837 (ISSN-L)
OpenAlex
W2026931893
Cited by
71
References
61
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2023: 6 · 2022: 6 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 5 · 2017: 4 · 2016: 4 · 2015: 2 · 2014: 4 · 2013: 5 · 2012: 2
FWCI
1.79
Type
journal article
Language
en
Open access
Locations
  • Laboratory Investigation (publishedVersion)
  • PubMed (publishedVersion)
Funders
Universidad Nacional Autónoma de México
Topics
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
prolactin, leukocyte adhesion, integrins, LFA-1, VLA-4, mononuclear cells, endothelial cells, CXCR3, chemokine receptors, tyrosine phosphorylation, JAK/STAT signaling, paxillin, IL-1β, inflammation, genistein, pertussis toxin
MeSH terms
Adult, Cell Adhesion, Dose-Response Relationship, Drug, Endothelium, Vascular, Humans, Leukocytes, Mononuclear, Male, Middle Aged, Phosphorylation, Prolactin, RNA, Messenger, Tyrosine, Up-Regulation, Integrins, Jurkat Cells, Receptors, Chemokine, Genistein, Receptors, CXCR3

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