Immunomodulatory role of decidual prolactin on the human fetal membranes and placenta

Flores-Espinosa, Pilar; Méndez, Isabel García; Irles, Claudine; Olmos-Ortíz, Andrea; Helguera-Repetto, Addy Cecilia; Mancilla-Herrera, Ismael; Ortuño-Sahagún, Daniel; Goffin, Vincent; Zaga‐Clavellina, Veronica

doi:10.3389/fimmu.2023.1212736

Cited by 10 publications

(3 citation statements)

References 120 publications

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“…2 Dopamine and thyrotropin-releasing hormone secreted by the hypothalamus are the main PRL regulator. 3 Additionally, other hypothalamic and intrapituitary factors and hormones from peripheral organs, mainly estradiol, are also involved in regulating PRL synthesis, secretion and action. 4 As a significant PRL inhibitor, Dopamine agonists can effectively suppress PRL synthesis and secretion.…”

Section: Introductionmentioning

confidence: 99%

Neuregulin 4 (Nrg4) cooperates with melatonin to regulate the PRL expression via ErbB4/Erk signaling pathway as a potential prolactin (PRL) regulator

Lin,

Ou,

Dai

et al. 2024

J of Cellular Biochemistry

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Neuregulin‐4 (Nrg4) and melatonin play vital roles in endocrine diseases. However, there is little discussion about the function and potential mechanism of Nrg4 and melatonin in prolactin (PRL) regulation. The human normal pituitary data from Gene Expression Profiling Interactive Analysis (GEPIA) database was used to explore the correlation between NRG4 and PRL. The expression and correlation of NRG4 and PRL were determined by Immunofluorescence staining (IF) and human normal pituitary tissue microarray. Western Blot (WB) was used to detect the expression of PRL, p‐ErbB2/3/4, ErbB2/3/4, p‐Erk1/2, Erk1/2, p‐Akt and Akt in PRL‐secreting pituitary GH3 and RC‐4B/C cells treated by Nrg4, Nrg4‐small interfering RNA, Erk1/2 inhibitor FR180204 and melatonin. The expression of NRG4 was significantly positively correlated with that of PRL in the GEPIA database and normal human pituitary tissues. Nrg4 significantly increased the expression and secretion of PRL and p‐Erk1/2 expression in GH3 cells and RC‐4B/C cells. Inhibition of Nrg4 significantly inhibited PRL expression. The increased levels of p‐Erk1/2 and PRL induced by Nrg4 were abolished significantly in response to FR180204 in GH3 and RC‐4B/C cells. Additionally, Melatonin promotes the expression of Nrg4, p‐ErbB4, p‐Erk1/2, and PRL and can further promote the expression of p‐Erk1/2 and PRL in combination with Nrg4. Further investigation into the function of Nrg4 and melatonin on PRL expression and secretion may provide new clues to advance the clinical control of prolactinomas and hyperprolactinemia.

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Section: Introductionmentioning

confidence: 99%

Neuregulin 4 (Nrg4) cooperates with melatonin to regulate the PRL expression via ErbB4/Erk signaling pathway as a potential prolactin (PRL) regulator

Lin,

Ou,

Dai

et al. 2024

J of Cellular Biochemistry

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“…After many years of intensive research, it is now known that PRL has a wide range of other diverse functions in the body [7][8][9][10], influencing not only the reproductive system [9][10][11][12][13][14][15] but also growth and development [16], metabolism [17][18][19][20], electrolyte transport [21], the integumentary system [22,23], behavior [24], the immune system [25][26][27], and carcinogenesis [28][29][30]. PRL exerts these versatile actions by acting on its receptor (PRLR), which is an archetype member of the class I cytokine receptor family [31][32][33].…”

Section: Introductionmentioning

confidence: 99%

“…Figure 4.A simplified overview of the diverse functions of the prolactin receptor (PRLR) signaling through endocrine and autocrine prolactin (PRL) binding in normal and pathological conditions (marked with yellow arrows, respectively) related to the functioning of the hypothalamic-pituitarygonadal (HPG) axis[7,44,46,[80][81][82][83], growth and development[84][85][86][87][88][89][90][91][92], metabolism[17,20,33,[93][94][95][96][97][98][99][100][101][102][103][104][105], electrolyte transport[106][107][108][109], behavior[24,[110][111][112][113] and immune system[25][26][27]33]. ↑-increase, ↓-decrease, APC-antigen-presenting cells, BAT-brown adipose tissue, GDM-gestational diabetes mellitus, GnRH-gonadotropin-releasing hormone (gonadoliberin), NAFLD-non-alcoholic fatty liver disease, P4-progesterone.…”

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confidence: 99%

Current Insights in Prolactin Signaling and Ovulatory Function

Szukiewicz

2024

IJMS

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Prolactin (PRL) is a pleiotropic hormone released from lactotrophic cells of the anterior pituitary gland that also originates from extrapituitary sources and plays an important role in regulating lactation in mammals, as well as other actions. Acting in an endocrine and paracrine/autocrine manner, PRL regulates the hypothalamic–pituitary–ovarian axis, thus influencing the maturation of ovarian follicles and ovulation. This review provides a detailed discussion of the current knowledge on the role of PRL in the context of ovulation and ovulatory disorders, particularly with regard to hyperprolactinemia, which is one of the most common causes of infertility in women. Much attention has been given to the PRL structure and the PRL receptor (PRLR), as well as the diverse functions of PRLR signaling under normal and pathological conditions. The hormonal regulation of the menstrual cycle in connection with folliculogenesis and ovulation, as well as the current classifications of ovulation disorders, are also described. Finally, the state of knowledge regarding the importance of TIDA (tuberoinfundibular dopamine), KNDγ (kisspeptin/neurokinin B/dynorphin), and GnRH (gonadotropin-releasing hormone) neurons in PRL- and kisspeptin (KP)-dependent regulation of the hypothalamic–pituitary–gonadal (HPG) axis in women is reviewed. Based on this review, a rationale for influencing PRL signaling pathways in therapeutic activities accompanying ovulation disorders is presented.

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PGRMC2 and HLA-G regulate immune homeostasis in a microphysiological model of human maternal-fetal membrane interface

Lintao,

Richardson,

Kammala

et al. 2024

Commun Biol

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Chorion trophoblasts (CTCs) and immune cell-enriched decidua (DECs) comprise the maternal-fetal membrane interface called the chorio-decidual interface (CDi) which constantly gets exposed to maternal stressors without leading to labor activation. This study explored how CTCs act as a barrier at CDi. The roles of human leukocyte antigen (HLA)-G and progesterone receptor membrane component 2 (PGRMC2) in mediating immune homeostasis were also investigated. The CDi was recreated in a two-chamber microfluidic device (CDi-on-chip) with an outer chamber of primary DECs and immune cell line-derived innate immune cells and an inner chamber of wild-type or PGRMC2 or HLA-G knockout immortalized CTCs. To mimic maternal insults, DECs were treated with lipopolysaccharide, poly(I:C), or oxidative stress inducer cigarette smoke extract. Expression levels of inflammation and immunity genes via targeted RNA sequencing, production of soluble mediators, and immune cell migration into CTCs were determined. In CDi-on-chip, decidua and immune cells became inflammatory in response to insults while CTCs were refractory, highlighting their barrier function. HLA-G and PGRMC2 are found to be vital to immune homeostasis at the CDi, with PGRMC2 serving as an upstream regulator of inflammation, HLA-G expression, and mesenchymal-epithelial transition, and HLA-G serving as a frontline immunomodulatory molecule, thus preventing fetal membrane compromise.Labor is an inflammatory process at the maternal-fetal interface characterized by leukocyte activation, migration, and recruitment, and a shift to a pro-inflammatory microenvironment 1 , leading to childbirth. Premature activation of these processes can lead to spontaneous preterm birth, a major complication of pregnancy with no known treatment 2 . The activation signals pathologically come from maternal exposure to various risk factors such as diet, environment, and lifestyle activities, and interact at the two

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Immunomodulatory role of decidual prolactin on the human fetal membranes and placenta

Cited by 10 publications

References 120 publications

Neuregulin 4 (Nrg4) cooperates with melatonin to regulate the PRL expression via ErbB4/Erk signaling pathway as a potential prolactin (PRL) regulator

Neuregulin 4 (Nrg4) cooperates with melatonin to regulate the PRL expression via ErbB4/Erk signaling pathway as a potential prolactin (PRL) regulator

Current Insights in Prolactin Signaling and Ovulatory Function

PGRMC2 and HLA-G regulate immune homeostasis in a microphysiological model of human maternal-fetal membrane interface

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