Cited by 38Rheumatoid Arthritis Research and TherapiesNatural Compounds in Disease TreatmentCytokine Signaling Pathways and Interactions

The role of the prolactin/vasoinhibin axis in rheumatoid arthritis: An integrative overview

Open access
Clapp, Carmen, Adán, Norma, Ledesma-Colunga, María G., Solís-Gutiérrez, Mariana, Triebel, Jakob, Martínez de la Escalera, Gonzalo·2016·Cellular and Molecular Life Sciences

Abstract

Rheumatoid arthritis (RA) is a chronic, autoimmune, inflammatory disease destroying articular cartilage and bone. The female preponderance and the influence of reproductive states in RA have long linked this disease to sexually dimorphic, reproductive hormones such as prolactin (PRL). PRL has immune-enhancing properties and increases in the circulation of some patients with RA. However, PRL also suppresses the immune system, stimulates the formation and survival of joint tissues, acquires antiangiogenic properties upon its cleavage to vasoinhibins, and protects against joint destruction and inflammation in the adjuvant-induced model of RA. This review addresses risk factors for RA linked to PRL, the effects of PRL and vasoinhibins on joint tissues, blood vessels, and immune cells, and the clinical and experimental data associating PRL with RA. This information provides important insights into the pathophysiology of RA and highlights protective actions of the PRL/vasoinhibin axis that could lead to therapeutic benefits.

Integrity signals

Registry

Crossref · 10.1007/s00018-016-2187-0

Cites

273 of 273 references verified0 citation errors · 0 not checkable

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  • Other inflammation-related genes dysregulated in hEDS/HSD include SPON2 up-regulated and PRLR decreased.

    “Other inflammation-related genes dysregulated in hEDS/HSD include SPON2, up-regulated in patients’ cells, which encodes an ECM protein with multifunctional properties in the innate immune system and inflammatory cell recruitment [152,153,154], and PRLR, showing a decreased expression in hEDS/HSD cells, which encode the prolactin receptor implicated in inflammatory responses and immune cells”
  • PRLR encodes the prolactin receptor implicated in inflammatory responses and immune cell regulation.

    “Other inflammation-related genes dysregulated in hEDS/HSD include SPON2, up-regulated in patients’ cells, which encodes an ECM protein with multifunctional properties in the innate immune system and inflammatory cell recruitment [152,153,154], and PRLR, showing a decreased expression in hEDS/HSD cells, which encode the prolactin receptor implicated in inflammatory responses and immune cells”

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Authors
Clapp, C., Adán, N., Ledesma-Colunga, M. G., Solís-Gutiérrez, M., Triebel, J., & Martínez de la Escalera, G.
Affiliations
  • Universidad Nacional Autónoma de México (MX)
  • Paracelsus Medizinische Privatuniversität (DE)
Corresponding author
Clapp, Carmen
Venue
Cellular and Molecular Life Sciences
Published
2016-03-29
Volume
73
Issue
15
Pages
2929-2948
ISSN
  • 1420-682X (ISSN-L)
  • 1420-9071
OpenAlex
W2321665593
Cited by
38
References
272
Citations by year
2026: 5 · 2025: 2 · 2024: 6 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 8 · 2018: 1 · 2017: 3 · 2016: 1
FWCI
0.68
Type
journal article
Language
en
Open access
Locations
  • Cellular and Molecular Life Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Dirección General Asuntos del Personal Académico, Universidad Nacional Autónoma de México (MX) (IN201315)
Topics
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
  • Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords
rheumatoid arthritis, prolactin, vasoinhibin, sex differences, reproductive hormones, immune regulation, antiangiogenic activity, joint destruction, risk factors, therapeutic target
MeSH terms
Animals, Arthritis, Rheumatoid, Cartilage, Articular, Female, Humans, Immune Tolerance, Immunity, Cellular, Inflammation, Joints, Male, Prolactin, Reproduction, Sex Factors, Stress, Physiological, Stress, Psychological, Angiogenesis Inhibitors

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