Locally secreted histamine may regulate the development of ovarian follicles by apoptosis

Inflammation Research -     

Increased permeability of human amnion to calcium ions in chorioamnionitis is related to histamine H1-receptor overexpression within amniotic epithelial cells

Inflammation Research -     

Influence of histamine on the process of human trophoblast differentiation

Inflammation Research - .     

Does histamine influence differentiation of trophoblast in preeclampsia?

Inflammation Research -     

Mast cell-derived interleukin-8 may be involved in the ovarian mechanisms of follicle growth and ovulation

Inflammation Research -     

Histamine H4 receptors in human placenta in diabetes-complicated pregnancy

Inflammation Research -     

Angiotensin II (Ang II) evoked secretion of the human placental lactogen (HPL) in intrauterine growth retardation: examination of the relationship with Ang II receptor type 1 (AT1) expression

Angiotensin II (Ang II) and its hemodynamic effects on placental vasculature mediated via Ang II receptor type 1 (AT1) may play significant role in intrauterine growth retardation (IUGR). Placental lactogen (HPL) production directly reflects placental function. We compared influence of Ang II on HPL production in normal and IUGR-complicated pregnancies and correlated this phenomenon with AT1 expression. Basal and Ang II-evoked HPL secretion was examined in perfused placental lobules using ELISA. After immunostaining of placental sections, AT1 expression was estimated using quantitative morphometry. Ang II increased HPL secretion. Ang II-evoked increase in HPL concentration in the perfusion fluid was 27.36+/-6.4 (%, +/-SEM) lower in IUGR (p<0.05) compared to normal-course pregnancies. AT1 expression was significantly decreased in IUGR and was 78.12+/-8.2 (%, +/-SEM) of the mean value of controls. Demonstrating that Ang II-evoked secretion of HPL in preeclampsia-free IUGR is decreased and correlates with down-regulated expression of AT1, we present a new approach to the pathophysiology of IUGR.     

Histamine influence on apoptosis in trophoblast cell cultures

Introduction

It has been demonstrated that histamine plays an important role in the pathogenesis of preeclampsia. Histamine regulates the process of differentiation of trophoblast cells; it also acts as a growth factor in malignant melanoma cells, and prevents monocytic apoptosis. Trophoblast research has shown that in preeclampsia placentas, trophoblast apoptosis is significantly increased.

Aim of the study

The aim of our study was to demonstrate the influence of histamine on the process of apoptosis in human trophoblast cell cultures.

Materials and methods

Placentas were obtained after vaginal delivery. Tissue samples were excised from placentas and, with the use of modified Kliman’s method, trophoblast cell cultures were established. The cultures were incubated with dexamethasone as an apoptosis inducer 48 hours prior to apoptosis detection assays. Along with dexamethasone, selected cell cultures were incubated with histamine (1 μmol/l) or histamine (1 μmol/l) and terfenadine (from 1 to 5 μmol/l), a H₁ receptor antagonist. For apoptotic activity detection, and quantitative analysis, we used an ELISA assay. M30‐Apoptosense ELISA Kit is based on the M30 monoclonal antibody that binds only the caspase‐cleaved cytokeratin 18 formed during apoptosis in trophoblast cells.

Results

Our investigation showed significantly (p < 0.05) increased apoptotic activity in cultures incubated with dexamethasone, histamine and terfenadine (% of reference value, ±SEM): up to 113.1 ± 4.33%. Cell cultures incubated with dexamethasone and histamine only showed significantly lower apoptotic activity 90.2 ± 5.17%. We suggest that histamine may inhibit apoptotic activity in trophoblast cell cultures via H₁ receptor. Thus histamine may regulate the process of trophoblast differentiation (via integrin aV‐b3 expression, as we previously suggested), and influence cell turnover in the placenta.

     

Mast cells, histamine and development of the placental vascular network in pregnancies complicated by preeclampsia and intrauterine growth retardation

Importance of angiogenesis in proper development of placenta is unquestioned. Abnormalities in vascular development are typical for complications of pregnancy: intrauterine growth retardation (IUGR) and preeclampsia (PE). As mast cells are involved in new vessels sprouting and development we tried to disclose if they can be involved in etiology or pathogenesis of IUGR and/or PE. MATERIAL AND METHODS: Placentas from PE-complicated pregnancies (n=11), IUGR-complicated pregnancies (n=10), and from healthy women--controls (n=13) were obtained after cesarean sections. Histamine concentration was measured and immunohistochemical staining for mast cell tryptase was performed. Microscopic slides of placental tissue were analyzed with morphometric software. RESULTS: We disclosed increased histamine concentration in PE group--227.3 +/- 17.7 (in ng of histamine per 1 g of tissue) and decreased concentration in IUGR group 114.3 +/- 13.5 vs control--178.1+/- 18.9. Histamine concentration corresponded with density of mast cells in examined groups: PE group--8.32 cells/mm2 +/- 1.3, IUGR--3.07 +/- 1.05 and control--5.14 +/- 1.2. The mean area of mast cells identified in PE as well as in IUGR group was smaller than the mean area of mast cells in controls. V/EVT index was decreased in PE and IUGR group in comparison to controls, respectively: 0.15 +/- 0.018; 0.12 +/- 0.014; 0.23 +/- 0.029. CONCLUSIONS: We suggest that differences in mast cells density and corresponding differences in histamine concentration are associated with pathogenesis of PE and IUGR or are consequence of primary cause.     

Increased production of β-defensin 3 (hBD-3) by human amniotic epithelial cells (HAEC) after activation of toll-like receptor 4 in chorioamnionitis

Inflammation Research -