Percentage Of Prolactin Cells Research Articles

Structural and Functional Changes in Prolactin Endocrinocytes of the Anterior Pituitary Gland in the Process of Reparative Osteogenesis of Long Tubular Bones

The aim of the study is to investigate the numerical composition and dynamics of structural and functional changes in prolactin cells of the anterior pituitary gland during reparative regeneration of long tubular bones.Material and methods. The study included 40 Wistar rats. A transverse fracture of the middle third of the tibial shaft was simulated in the animals of the experimental group. Cells of the fracture area and the distal part of the adenohypophysis were studied using methods of light microscopy, immunohistochemistry and morphometry on the 1st, 3rd, 7th, 14th, 21st, 28th, 44th and 61st days.Results. The study results demonstrated that in male rats of the control group, the percentage of prolactin cells in the adenohypophysis was 7.26±0.51%. During the fracture healing of the long tubular bone in rats, there were 2 stages of stress activation of the compensatory-adaptive potencies of the prolactin endocrinocyte adenohypophysis cluster with related changes in their structures: on the 1st–3rd days (the bone fracture effect on the body with the development of post-traumatic acute inflammation) and on the 14th–21st days (peak of chondroclast lytic activity with massive chondrolysis of cartilaginous callus).Conclusion. Thus, the importance of prolactin as a stress mediator and the need for its participation in the regulation of stress metabolic changes are evidenced. At the same time, it becomes clear that with a pronounced acute stress effect; in this study it is represented by an open fracture, even the onset of a stress response can be manifested by a maladjustment of the lactotropic activity of the adenohypophysis, which is accompanied by an early "depletion" of its structural and functional reserves and a breakdown of compensatory-adaptive potencies right on the 1st day.

Differential involvement of insulin-like growth factor-I and estrogen on prolactin cells in the mouse anterior pituitary

Estrogen and insulin-like growth factor-I (IGF-I) stimulate prolactin (PRL) production, release and proliferation of PRL-producing cells (PRL cells) in the anterior pituitary. PRL cells in adult estrogen receptor alpha (ERalpha) knockout (alphaERKO) mice and IGF-I knockout (IGF-IKO) mice are decreased considerably in number. To investigate a correlation between 17beta-estradiol (E2) and IGF-I on PRL production, IGF-I wild-type (WT) or IGF-IKO mice were ovariectomized at day 8 and the number of PRL cells was examined at days 20 and 60. Although PRL cell number at day 20 and WT or IGF-IKO mice ovariectomized at day 8 was similar to that in intact WT or IGF-IKO mice, PRL cells in adult WT or IGF-IKO mice ovariectomized at day 8 were significantly decreased as compared with those in intact WT or IGF-IKO mice. Therefore, estrogen is essential for PRL cell differentiation between days 20 and 60, regardless of IGF-I. While PRL cells in WT ovariectomized mice increased from days 20 to 60, those in IGF-IKO ovariectomized mice did not increase, suggesting that IGF-I modified PRL cell differentiation after day 20. ICI 182,780 (anti-estrogen) treatment canceled an increase of PRL cells in 30-day-old ovariectomized WT mice, indicating that the presence of ERalpha is important. The number of PRL cells in alphaERKO mice was similar to that in WT mice at day 20; however, PRL cells in alphaERKO mice at day 60 were not increased in number from day 20, supporting the idea that estrogen is essential for PRL cell differentiation after day 20. Finally, the percentage of PRL cells in IGF-IKO mice was decreased as compared with that in WT mice at day 20; therefore, IGF-I affects PRL cells before day 20. In conclusion, PRL cell differentiation is differently regulated by E2 and IGF-I depending on the age.

The role of IGF1 on the differentiation of prolactin secreting cells in the mouse anterior pituitary

IGF1 knockout (IGF1KO) mice show a reduced number of prolactin (PRL) producing cells (PRL cells); however, the role of IGF1 in PRL cell proliferation and differentiation in immature mice is unclear. In this study, ontogenic changes in the percentages of PRL cells, GH producing cells (GH cells), and 5-bromo-2'-deoxyuridine (BrdU)-labeled cells in the anterior pituitary of male IGF1KO mice during the postnatal period were investigated. The percentage of PRL cells in IGF1KO mice was significantly lower at day 20 compared with that in wild-type (WT) mice, while GH cells in IGF1KO mice were significantly increased from day 10. From days 5 to 20, the percentage of BrdU-labeled cells in WT and IGF1KO mice was similar. PRL cells and GH cells are thought to originate from the same progenitor cells, therefore, PRL cells in IGF1KO mice are not able to differentiate because progenitor cells have already committed to be GH cells. However, IGF1, 17beta-estradiol (E(2)), epidermal growth factor (EGF), or IGF1 plus E(2) treatments increased the PRL cell number in the pituitaries in vitro of 10-day-old WT and IGF1KO mice. This fact suggests that these factors are involved in PRL cell proliferation and differentiation. In addition, the increase of PRL cells in IGF1KO mice stimulated by E(2) or EGF was less than that of WT mice. Thus, IGF1 plays a crucial role in PRL cell proliferation and differentiation in mouse pituitaries by regulating the differentiation of progenitor cells and mediating the actions of E(2) and EGF.

Cellular basis for elevated prolactin secretion during incubation behavior in Bantam chickens: analysis by reverse hemolytic plaque assay.

Incubation behavior in birds is characterized by elevated serum prolactin (PRL) levels. The objective of this study was to determine the cellular basis for increased PRL secretion. Incubation behavior of Bantam hens was induced by allowing the hens to accumulate their eggs. In experiment 1, hens were allowed to accumulate their eggs in floor pens for 0, 2, 12, or 24 days (Day 0, Day 2, Day 12, and Day 24 hens, respectively). Anterior pituitaries were dissociated into individual cells with trypsin, and the resulting cells were then subjected to reverse hemolytic plaque assays for PRL. The percentage of PRL-secreting cells and serum PRL levels were higher in Day 24 hens than in the other groups (p < 0.05; n = 3 separate trials). In experiment 2, hens were allowed to accumulate their eggs for 2, 14, 18, or 24 days (Day 2, Day 14, Day 18, and Day 24 hens, respectively). The percentage of PRL-secreting cells and levels of serum PRL were greater in Day 18 and Day 24 hens than in Day 2 hens (p < 0.05; n = 4). Results from Day 14 hens were intermediate and different (p < 0.05) from those from both Day 2 and Day 18 groups. Data indicate that an increase in the proportion of PRL secretors occurred between 14 and 18 days after hens began to accumulate their eggs. The area of plaques formed by lactotrophs from Day 14 and Day 18 hens was also increased (p < 0.05). In experiment 3, hens were allowed to accumulate their eggs for 0 and 24 days (Day 0 and Day 24 hens, respectively). Their anterior pituitaries were dissected into cephalic, middle, and caudal regions, and the percentage of PRL cells were analyzed in each region separately. The percentage of PRL secretors was increased (p < 0.05) in Day 24 compared to Day 0 hens in both the cephalic and middle regions of the anterior pituitary but not in the caudal portion. We conclude that increased PRL secretion during incubation behavior involves the recruitment of additional pituitary cells into the PRL-secreting population and an increase in the capacity of these cells to secrete hormone (p < 0.05). Furthermore, this increase in PRL-secreting cells is localized to the cephalic and middle regions of the anterior pituitary.

Effects of Estrogen on the Human Pituitary: A Clinicopathologic Study

Pituitary glands obtained at autopsy of 67 men treated with diethylstilbestrol were examined for diffuse and nodular lactotrophic hyperplasia as well as prolactin cell tumorlets or adenomas. A control group consisted of 42 untreated patients with prostatic carcinoma and 209 other elderly men. Diffuse and nodular lactotrophic hyperplasia and the percentage of prolactin cells were greater in treated patients, but these differences were not statistically significant. The higher frequency of prolactin cell adenomas among treated patients (19%) than among control subjects (11%) also lacked statistical significance. An apparent low frequency of occurrence of adenoma in control patients with prostatic carcinoma remains unexplained. No correlation was noted between tumor number, size, morphologic features, or immunoreactivity and such factors as dose of estrogen therapy, associated diseases, ultimate cause of death, or patient age. A correlation was noted, however, between duration of estrogen therapy and the total number of pituitary adenomas, including those composed of prolactin cells. Relative proportions of other types of adenoma were similar within the study and control groups. We conclude that estrogen medication cannot be considered a major risk factor in the cause of prolactin-producing adenomas in older men.

Estradiol induces a shift in cultured cells that release prolactin or growth hormone.

The process by which estradiol induces an increase in the percentage of prolactin cells in the rat pituitary requires clarification. In this study the effect of estradiol treatment on growth hormone and prolactin cells in monolayer cultures of male rat pituitaries was assessed by use of reverse hemolytic plaque assays. Treatment of cultures with 17 beta-estradiol (10 nM) for 6 days elevated significantly (P less than 0.01) the percentage of all cells in culture that released prolactin without affecting the percentage of growth hormone secretors. However, by sequentially assaying single cells for growth hormone and prolactin, we found that estradiol caused a marked increase (P less than 0.01) in the proportion of individual cells that released both growth hormone and prolactin and a commensurate decrease in the proportion that released growth hormone alone. These results demonstrate that estradiol acts directly on cultures of male pituitary cells to shift the proportions of cells that released growth hormone, prolactin, or both hormones and indicate that estradiol may convert cells that release only growth hormone to those that release both growth hormone and prolactin.

Age-related changes in prolactin cell percentage and serum prolactin levels in intact and neonatally gonadectomized male and female rats.

Electron microscopically the percentages of various pituitary cell types were calculated at 30 and 90 days of age. Prolactin cell percentage was more at 90 days of age than at 30 days in both intact male and female rats. No sexual difference was observed in the percentage of prolactin cells at 30 days of age, but at 90 days female pituitaries contained more numerous prolactin cells than males ones. Neonatal ovariectomy did not affect the prolactin cell percentage at 30 days of age, while it lowered the percentage at 90 days. Neonatal orchidectomy did not affect the prolactin cell percentage at both 30 and 90 days of age. Mitotic prolactin cells were more frequently observed in intact female rats at estrus than in intact male rats at 90 days of age. These results shown the presence of the sexual difference in the proliferation of prolactin cells. Serum prolactin levels increased with age in intact male and female rats. In neonatally gonadectomized male and female rats the serum prolactin levels failed to increase at 60 and 90 days of age. In general conclusion, the changes in serum prolactin levels are in line with the changes in prolactin cell population during postnatal development.