In vivo activation of macrophages by prolactin from young and aging mice

Chen, Yifang; Johnson, Arthur G.

doi:10.1016/0192-0561(93)90029-x

Cited by 32 publications

(1 citation statement)

References 16 publications

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“…Increased catecholamines stimulate melatonin biosynthesis or activate its receptors on skin resulting in a decrease in melanin biosynthesis. Moreover, increased levels of catecholamines, DA, estrogen, and prolactin ( 62 ) result in hyper-production of H 2 O 2 that leads to either induction of immune response against melanocytes (depigmentation) or inhibition of BH 2 reductase and BH 4 cofactor (reduced pigmentation). In addition, stress-induced cortisol hypersecretion is inhibited by feedback regulation of CRF, POMC, ACTH, and MSH related to abnormally low pigmentation of skin and/or the changes of CRF effects on NF-κB immune response, resulting in melanocyte destruction (Figure 7 ).…”

Section: Discussionmentioning

confidence: 99%

Neural and Endocrinal Pathobiochemistry of Vitiligo: Comparative Study for a Hypothesized Mechanism

El-Sayed¹,

El-Ghany²,

Mohamed³

2018

Front. Endocrinol.

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The etiology of vitiligo is still unclear. The aim is to investigate a neural and hormonal etio-pathology of vitiligo. Sixty acrofacial vitiligo patients were divided into two subgroups as active vitiligo patients group (AVPs; n = 35) and stable vitiligo patients group (SVP; n = 25). Forty healthy subjects without any systemic or dermatological disease were used as controls. Blood samples were collected, and the samples were used for measurement of free triiodothyronine (fT3), free thyroxine (fT4), thyroid-stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH), cortisol, estrogen, testosterone, melatonin, and prolactin levels by ELISA, while norepinephrine (NE), epinephrine (Epi), dopamine (DA), homo-vanillic acid (HVA), serotonin, and 5-hydroxyindoleacetic acid (5-HIAA) by high-pressure liquid chromatography. The current results showed a significant increase in plasma levels of Epi, NE, DA, HVA, serotonin, 5-HIAA, melatonin, and in serum level of TSH and prolactin either in SVP or AVP groups than the control group and in AVP than SVP group. The serum levels of fT3 and fT4 were significantly decreased either in SVP or AVP groups than the control group. A significant increase in estradiol levels was observed in females within AVP than females in either SVP or control groups. There was a significant increase in serum level of cortisol in AVP than either SVP or control group. There was a significant decrease in serum level of ACTH in either AVP or SVP than control and in AVP than SVP group. In conclusion, there are some neural and endocrine markers that play a pivotal role in pathogenesis and/or consequences of vitiligo. The abnormally disturbed levels of theses markers lead to melanocyte destruction and/or depigmentation.

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Section: Discussionmentioning

confidence: 99%

Neural and Endocrinal Pathobiochemistry of Vitiligo: Comparative Study for a Hypothesized Mechanism

El-Sayed¹,

El-Ghany²,

Mohamed³

2018

Front. Endocrinol.

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Pituitary Control of Proliferation and Differentiation of Leydig Cells and Their Putative Precursors in Immature Hypophysectomized Rat Testis

DOMBROWICZ,

SENTE,

REITER

et al. 1996

Journal of Andrology

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The objective of this study was to determine the effects of pituitary hormones (luteinizing hormone [LH], follicle‐stimulating hormone [FSH], growth hormone [GH], and prolactin [PRL]) on interstitial cell proliferation and differentiation in the testis of immature hypophysectomized rats. Macrophages, Leydig cells, precursor mesenchymal cells, endothelial lymphatic cells, and myoid cells were studied. Our experimental approach was aimed at determining whether changes in a cellular subpopulation observed after pituitary hormone treatments were the result of division of existing cells in the population, of differentiation of interstitial precursor cells, or both. In this context, it must be stressed that our data reflected the effects of hormones to prevent the decline of cells due to hypophysectomy rather than their recovery. Macrophage proliferation was taken into account because macrophages closely resemble Leydig cells and are known to proliferate after hormonal treatment. A double‐labeling procedure (acid phosphatase and anti‐bromo‐deoxyuridine [anti‐BUdR]) revealed that LH, FSH, and PRL increased the number of testicular macrophages 105‐, 104‐, and 103‐fold, respectively, in hypophysectomized rats compared to hypophy‐sectomized control animals. BUdR incorporation in testicular macrophages was greater after PRL treatment than after LH and FSH supplementation. In contrast, we were unable to demonstrate any effect of rat GH on the macrophage population. Light microscopic analysis of plastic embedded sections of treated rat testis revealed that LH increased the numbers of Leydig, precursor mesenchymal, and myoid cells 6‐, 4‐, and 1.3‐fold, respectively. LH also stimulated BUdR incorporation into all interstitial cell types. PRL administration increased both the number of Leydig and precursor mesenchymal cells (each 3‐fold) but decreased the number of endothelial lymphatic cells (1.5‐fold) when compared to the control animals. In contrast, FSH did not increase the number and proliferation of Leydig cells but exerted a slight proliferative effect on the other interstitial cell populations. In GH‐treated rats, the number of precursor mesenchymal cells increased two fold above the control rats. GH also exerted slight proliferative effects on both precursor mesenchymal and myoid cells. Immunohistochemical studies of steroidogenic enzymes in the testicular interstitium of treated rats demonstrated the presence of steroidogenic enzymes, not only in Leydig and precursor mesenchymal cells, but also in some (1%‐2%) endothelial lymphatic cells and myoid cells. This may indicate that both of these cell types are also constitutively equipped to perform steroidogenesis or that they are precursor cells undergoing differentiation. Taken together, changes in the number of Leydig cells in our animal model appeared more likely to be dependent on the transformation of pre‐cursor cells than on division of preexisting mature Leydig cells.

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