Cytokine-like effects of prolactin in human mononuclear and polymorphonuclear leukocytes

Dogusan, Zeynep; Hooghe, Robert; Verdood, Peggy; Hooghe‐Peters, Elisabeth L.

doi:10.1016/s0165-5728(01)00420-9

Cited by 68 publications

(35 citation statements)

References 32 publications

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“…For instance, PRL stimulates inducible NO synthase production, Ig release, and cytokine expression in human leukocytes (7)(8)(9)(10). Furthermore, PRL has anti-apoptotic properties that have been demonstrated in the Nb2 rat lymphoma (11) and in dexamethasone-treated thymocytes (12).…”

mentioning

confidence: 97%

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Gerlo¹,

Verdood²,

Gellersen

et al. 2004

The Journal of Immunology

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We previously reported that prolactin gene expression in the T-leukemic cell line Jurkat is stimulated by PGE2 and that cAMP acts synergistically with Ca2+ or protein kinase C on the activation of the upstream prolactin promoter. Using the transcription inhibitor actinomycin D, we now show that PGE2-induced prolactin expression requires de novo prolactin mRNA synthesis and that PGE2 does not influence prolactin mRNA stability. Furthermore, PGE2-induced prolactin expression was inhibited by protein kinase inhibitor fragment 14–22 and BAPTA-AM, which respectively, inhibit protein kinase A- and Ca2+-mediated signaling cascades. Using specific PGE2 receptor agonists and antagonists, we show that PGE2 induces prolactin expression through engagement of E-prostanoid (EP) 3 and EP4 receptors. We also found that PGE2 induces an increase in intracellular cAMP concentration as well as intracellular calcium concentration via EP4 and EP3 receptors, respectively. In transient transfections, 3000 bp flanking the leukocyte prolactin promoter conferred a weak induction of the luciferase reporter gene by PGE2 and cAMP, whereas cAMP in synergy with ionomycin strongly activated the promoter. Mutation of a C/EBP responsive element at −214 partially abolished the response of the leukocyte prolactin promoter to PGE2, cAMP, and ionomycin plus cAMP.

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confidence: 97%

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Gerlo¹,

Verdood²,

Gellersen

et al. 2004

The Journal of Immunology

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“…A handful of other genes has been studied to understand PRL-mediated differentiative functions and cell survival responses. Interestingly, a recent study shows fine differences in PRL signaling in different populations of blood leukocytes (Dogusan et al, 2001). PRL activates Stat5 and SOCS3 in peripheral blood mononuclear cells, while PRL activates Stat1 and SOCS2 in human granulocytes.…”

Section: Discussionmentioning

confidence: 99%

“…This interpretation is supported by in vitro studies showing PRL's protective effect in preventing glucocorticoid-induced lymphocyte cell death (apoptosis) (LaVoie and Witorsch, 1995; and by in vivo studies showing that PRL improves macrophage and splenocyte functions following trauma-hemorrhage and infections . A concerted effort by many laboratories is underway to evaluate the immunomodulatory activities of PRL in the context of stress, trauma, injury, inflammation, infection, and various autoimmune diseases (Matera et al, 2000;Richards and Murphy, 2000;Dorshkind and Horseman, 2001;Hooghe et al, 2001). …”

Section: Discussionmentioning

confidence: 99%

“…PRL stimulates IRF-1 gene expression in normal rat leukocytes derived from the bone marrow and spleen (Dogusan et al, 2000) and in human granulocytes (Dogusan et al, 2001). In rat Nb2 T cells, PRL stimulates IRF-1 gene transcription in a distinct manner over the cell cycle, with a transient but PRL-R and turn off signaling at the receptor level in a negative-feedback loop (Naka et al, 1999;Tam et al, 2001).…”

Section: B Positive Signaling To Irf-1mentioning

confidence: 99%

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Senior Author Correspondence Information

2002

Recent Progress in Hormone Research

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In mammals, sex is determined by the presence or absence of a single gene on the Y chromosome, Sry. Sry, a member of the high mobility group family of transcription factors, is required to initiate male-specific pathways and repress female-specific pathways. Expression of Sry in the gonad, beginning at 10.5 days postcoitum, leads to the differentiation of the somatic supporting cell precursors as Sertoli cells. These cells direct the other cells of the gonad into their respective lineages. Currently, no direct targets of Sry are known. A number of cellular pathways initiated by Sry are required for testis development. These include the proliferation of pre-Sertoli cells and commitment to the Sertoli lineage, migration of cells from the adjacent mesonephros, and formation of a male-specific vasculature. Work is underway to identify genes controlling these processes. These genes will then be linked to Sry.

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“…Several reports have shown that prolactin (PRL) can stimulate T cells, B cells, natural killer cells, macrophages, neutrophils, and dendritic cells (Kooijman et al 1996, Dogusan et al 2001, Matera et al 2001. Leukocytes produce PRL as an autocrine or a paracrine factor influencing cytokine production (Dimitrov et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Impaired mammary gland T cell population during early lactation in hypoprolactinemic lactation-deficient rats

Mackern-Oberti¹,

Valdéz²,

Vargas–Roig³

et al. 2013

Reproduction

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Mammary stroma is composed of various cell types, including migratory leukocytes. Although mammary antibody-secreting cells have been extensively studied, reports focusing on mammary T cells are scarce. It is thought that the recruitment mechanism of leukocytes to the mammary gland (MG) is controlled by pregnancy-and lactation-specific stimuli. But whether prolactin (PRL) modulates the T-cell population in MG is still unknown. Our aim was to study the relationship between PRL levels and T and B cells during early lactation (L2, day 2 post partum) and mid-lactation (L12, day 12 of lactation). In order to investigate whether PRL is associated with homing events to MG, female Sprague Dawley (SD) and SD-derived desmoglein 4 K/K hairless (phenotype with lactation deficit, OFA hr/hr) rats were killed during estrus, pregnancy, and post partum, and blood, MG, and corpora lutea were obtained to perform fluorescent-activated cell sorting (FACS), real-time PCR, and histological and RIA studies. Serum PRL levels were lower in OFA hr/hr rats than in SD rats during early lactation. MG of OFA hr/hr rats showed less secretory material compared with SD rats. FACS analysis showed lower percentage of MG CD3C cells in OFA hr/hr rats compared with SD rats on L2 and L12. OFA hr/hr rats showed higher absolute numbers of circulating CD3C cells compared with SD rats on L2 but not on L12. These results show that T-cell population in MG is affected in early lactating OFA hr/hr rats and strongly suggest that serum PRL levels may be involved in the homing events to MG, probably helping antibody-secreting cells and protecting the gland during lactation development.

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Cytokine-like effects of prolactin in human mononuclear and polymorphonuclear leukocytes

Cited by 68 publications

References 32 publications

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Senior Author Correspondence Information

Impaired mammary gland T cell population during early lactation in hypoprolactinemic lactation-deficient rats

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