Neuroendocrine dopaminergic regulation of prolactin release in systemic lupus                 erythematosus: a possible role of lymphocyte-derived prolactin

Méndez, Isabel García; Alcocer‐Varela, Jorge; Parra, Adalberto; Lava-Zavala, A; Cruz, Daniel; Alarcón‐Segovia, Donato; Larrea, Fernando

doi:10.1191/0961203304lu487oa

Cited by 26 publications

(21 citation statements)

References 43 publications

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“…In support of this hypothesis, we found a significant decreased of PRL concentrations following treatment with immunosuppressive drugs (Vera-Lastra et al 2003), SLE lymphocytes synthesize PRL and have alterations in the CREB family proteins, which participate in lymphocyte PRL gene expression (Gutierrez et al 1995;Larrea et al 1997;Montgomery 2001) and a functionally significant polymorphism is over expressed in SLE lymphocytes (Stevens et al 2001). Lymphocyte-derived PRL might contribute to alter the functional activity of the hypothalamic dopaminergic system in SLE attempting to maintain serum PRL within a physiological range (Mendez et al 2004). These evidences provide a potential explanation for the increased PRL release by SLE lymphocytes.…”

Section: Human Studiesmentioning

confidence: 78%

Immune‐Neuroendocrine Interactions and Autoimmune Diseases

Jara

Navarro

Medina

et al. 2006

Journal of Immunology Research

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The relationship between immune-neuroendocrine system is firmly established. The messengers of this connection are hormones, neuropeptides, neurotransmitters and cytokines. The immune-neuroendocrine system have the capacity to synthesize and release these molecules, which, in turn, can stimulate or suppress the activity of immune or neuroendocrine cells by binding to receptors. In fact, hormones, neuropeptides and neurotransmitters participate in innate and adaptive immune response.Autoimmune rheumatic diseases (ARD) are characterized by aberrant production of pro-inflammatory cytokines, which are a potent activator of the HPA axis. In consequence, high levels of pro-inflammatory hormones such as estrogens and prolactin, and low levels of glucocorticoids, an anti-inflammatory hormone, have been described in the active phase of ARD. In addition, high levels of pro-inflammatory hormones and cytokines have also been frequently detected in organ involvement of patients with ARD, suggesting an abnormal local neuroendocrine immune interaction. There is evidence that hormonal changes may appear before the symptomatic phase of the disease. Therefore, it is possible that a pro-inflammatory hormone favors the rupture of tolerance, which is a key feature of autoimmune diseases. The interactions between the immune-neuroendocrine system have a major impact on our understanding of the pathogenic mechanisms, diagnosis and therapy of ARD.

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Section: Human Studiesmentioning

confidence: 78%

Immune‐Neuroendocrine Interactions and Autoimmune Diseases

Jara

Navarro

Medina

et al. 2006

Journal of Immunology Research

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“…A number of painful conditions, known to be more prevalent in women, have been associated with high circulating PRL levels, such as cluster headaches (Waldenlind and Gustafsson, 1987;Talkad et al, 2004), migraines (Silberstein and Merriam, 1993), systemic lupus erythematosous (Walker, 2001;Mendez et al, 2004;Soto et al, 2004), rheumatic arthritis (Chikanza et al, 1993;D'Ambrosia, 2005), and breast pain (mastodynia) (Theunissen et al, 2005). Bromocriptine, a dopamine agonist and inhibitory of pituitary PRL release, has been clinically used to treat these conditions (Kullander and Svanberg, 1979;Walker, 2001;Talkad et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Prolactin Modulates TRPV1 in Female Rat Trigeminal Sensory Neurons

et al. 2006

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Sex dependency in pain perception is well documented and is thought to be attributable to the effect of reproductive hormones on nociceptive processing. In the present study, we evaluated whether estradiol alters gene transcription in the trigeminal ganglia (TG) of ovariectomized rats (OVX). These experiments demonstrated a dramatic (40-fold) upregulation of prolactin (PRL) expression in TG by 17-␤-estradiol (E2). PRL expression was restricted to TG neurons and was highly overlapped with transient potential receptor vanilloid type 1 (TRPV1) (ϳ90%) in TG. Additionally, PRL is released from neurons during stimulation. Both forms of PRL receptors (PRLRs), short and long, were also present in TG neurons. Moreover, expression of the long PRLRs was under control of estradiol. We next evaluated the novel hypothesis that PRL acts as a neuromodulator of sensory neurons. PRL pretreatment significantly enhanced capsaicin-evoked inward currents, calcium influx, and immunoreactive calcitonin gene-related peptide release from cultured TG neurons. This PRL modulation of capsaicin responses was abolished by withdrawal of E2 from TG cultures. Biochemical analysis demonstrated that PRL increased (Ͼ50%) phosphorylation levels of TRPV1 in TG. In a behavioral test, PRL pretreatment significantly potentiated capsaicin-evoked nocifensive behavior in female rats at proestrous and in OVX rats after E2 treatment. The in vivo potentiating effect of PRL on capsaicin responses was also dependent on E2. Collectively, these data demonstrate that PRL is a novel modulator of sensory neurons tightly regulated by E2. These findings are consistent with the hypothesis that PRL could contribute to the development of certain pain disorders, possibly including those modulated by estrogen.

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“…Lymphocytes in active SLE have increased production of PRL. Impaired hypothalamic function has been associated with HPRL in SLE [40,41].…”

Section: Prolactin and Systemic Lupus Erythematosusmentioning

confidence: 99%

Prolactin and Autoimmunity

Jara

Medina

Saavedra

et al. 2009

Clinic Rev Allerg Immunol

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The relationship between prolactin and the immune system has been demonstrated in the last two decades, opening new windows in the field of the immunoendocrinology. Prolactin has an important role in the innate and adaptive immune response. Increased prolactin levels have been described in autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, Sjögren syndrome, and systemic sclerosis among others. Hyperprolactinemia is associated with active disease and organ involvement in systemic lupus erythematosus. Therefore, prolactin is an integral member of the immunoneuroendocrinology network and seems to have a role in pathogenesis of autoimmune diseases. Few controlled studies of dopamine agonist treatment in humans with autoimmune disease have been conducted only in systemic lupus erythematosus patients, which support the potential efficacy of such agents even during pregnancy and postpartum. Further studies are necessary to elucidate the mechanisms by which prolactin affects autoimmune disease activity, increase the inflammatory mechanism, and determine the role of anti-prolactinemic drugs to regulate the immune/inflammatory process.

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Neuroendocrine dopaminergic regulation of prolactin release in systemic lupus erythematosus: a possible role of lymphocyte-derived prolactin

Cited by 26 publications

References 43 publications

Immune‐Neuroendocrine Interactions and Autoimmune Diseases

Immune‐Neuroendocrine Interactions and Autoimmune Diseases

Prolactin Modulates TRPV1 in Female Rat Trigeminal Sensory Neurons

Prolactin and Autoimmunity

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