Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We found that prolactin is taken up by mast cells residing in prolactin-dependent, 7,12-dimethylbenzanthracene-induced rat mammary tumors. Light and electron microscopic immunocytochemistry showed that mast cells concentrate prolactin in their cytoplasmic granules. No prolactin was found on mast cell surface membranes or in their nuclei. In primary cultures of tumor cells, mast cells were found mainly in the periphery of dome structures and these cells concentrated prolactin. When purified rat peritoneal mast cells were incubated with 125I-labeled prolactin, uptake was time, energy, and temperature dependent. Seventy % of accumulated prolactin was released intact from cytoplasmic granules by C48/80-induced degranulation. A mouse mastocytoma cell line also took up and released prolactin. These cells contained prolactin receptors (Kd = 4.5 nM) as determined in whole cells (approximately 3150 sites/cell) and in crude membranes (approximately 180 fmol/mg protein). We conclude that mast cells might significantly influence mammary tumor growth by accumulating and releasing prolactin within tumor tissue.
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PMID:Prolactin binding and localization in rat mammary tumor mast cells. 328 35

The protein hormone prolactin was isolated from sea whale hypophysis and its amino acid sequence was partially characterized. The hormone was hydrolyzed by BrCN and trypsin, the products of hydrolysis were separated and purified by gel filtration on Sephadex G-50, G-100 and G-25, by ion-exchange chromatography on CM-cellulose and on Dowex 50 x 8 and by partition paper chromatography. The structure of the obtained peptides was determined by the Edman method and by carboxypeptidase A hydrolysis. The partial amino acid sequence of sea whale prolactin making up to 75% of the hormone molecule was established.
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PMID:[Isolation and partial characterization of the amino acid sequence of sea whale prolactin]. 708 86

The influence of mast cell activation on the secretion of prolactin has been studied in rats receiving lysophosphatidylserine, a natural occurring phospholipid with secretagogue activity in these cells. After the i.v. injection of lysophosphatidylserine (10 mg/kg) a plasma prolactin peak correlates with an increased blood histamine level. Following the secretory event, which is inhibited by the H1 anti-histamine tripelenamine, plasma prolactin level drops below the basal line. Repeated lysophosphatidylserine administrations induce mast cell desensitisation, thus reducing also the pituitary response. Under these conditions a decrease in prolactin basal level is still observed, although the pituitary stores of this hormone are preserved. Control tests in vitro with lysophosphatidylserine, show that the diacyl lysophosphatidylserine derivative amplifies the inhibitory effect of dopamine on prolactin secretion from isolated pituitaries. The data suggests that lysophosphatidylserine induces prolactin secretion through mast cell activation. After this event, the reacylation of this phospholipid into lysophosphatidylserine in the pituitary membrane may enhance the inhibitory control by dopamine.
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PMID:Mast cell--pituitary interaction: modulation by serine phospholipids. 1563 84

Like few other organs, the skin is continuously exposed to multiple exogenous and endogenous stressors. Superimposed on this is the impact of psychological stress on skin physiology and pathology. Here, we review the "brain-skin connection," which may underlie inflammatory skin diseases triggered or aggravated by stress, and we summarize relevant general principles of skin neuroimmunology and neuroendocrinology. Specifically, we portray the skin and its appendages as both a prominent target of key stress mediators (such as corticotropin-releasing hormone, ACTH, cortisol, catecholamines, prolactin, substance P, and nerve growth factor) and a potent source of these prototypic, immunomodulatory mediators of the stress responses. We delineate current views on the role of mast cell-dependent neurogenic skin inflammation and discuss the available evidence that the skin has established a fully functional peripheral equivalent of the hypothalamic-pituitary-adrenal axis as an independent, local stress response system. To cope with stress-induced oxidative damage, the skin and hair follicles also express melatonin, probably the most potent neuroendocrine antioxidant. Lastly, we outline major, as-yet unmet challenges in cutaneous stress research, particularly in the study of the cross-talk between peripheral and systemic responses to psychological stress and in the identification of promising molecular targets for therapeutic stress intervention.
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PMID:Neuroimmunology of stress: skin takes center stage. 1684 9

It has been demonstrated that mammary gland involution after lactation is initiated by accumulation of milk in alveoli after weaning. Here, we report that involution is also dependent on mammary GnRH expression that is suppressed by PRL during lactation. Reduction of plasma prolactin (PRL) by the withdrawal of suckling stimuli increased GnRH and annexin A5 (ANXA5) expression in the mammary tissues after lactation with augmentation of epithelial apoptosis. Intramammary injection of a GnRH antagonist suppressed ANXA5 expression and apoptosis of epithelial cells after forcible weaning at midlactation, whereas local administration of GnRH agonist (GnRHa) caused apoptosis of epithelial cells with ANXA5 augmentation in lactating rats. The latter treatment also decreased mammary weight, milk production, and casein accumulation. Mammary mast cells were strongly immunopositive for GnRH and the number increased in the mammary tissues after weaning. GnRHa was shown to be a chemoattractant for mast cells by mammary local administration of GnRHa and Boyden chamber assay. PRL suppressed the mammary expression of both ANXA5 and GnRH mRNA. It also decreased mast cell numbers in the gland after lactation. These results are the first to demonstrate that GnRH, synthesized locally in the mammary tissues, is required for mammary involution after lactation. GnRH is also suggested to introduce mast cells into the regressing mammary gland and would be in favor of tissue remodeling. The suppression of these processes by PRL is a novel physiological function of PRL.
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PMID:Prolactin Suppression of Gonadotropin-Releasing Hormone Initiation of Mammary Gland Involution in Female Rats. 2717 71