ライフサイエンスコーパス: lactotroph

1 increase in the galanin mRNA content of the lactotroph.

2 tin expression and as a growth factor to the lactotroph.

3 ically for postnatal proliferation of somato/lactotrophs.

4 mbrane of secretory vesicles of isolated rat lactotrophs.

5 le with signals observed in somatotrophs and lactotrophs.

6 at occur during secretion from rat pituitary lactotrophs.

7 ocytic and endocytic events in rat pituitary lactotrophs.

8 duced prolactin secretion from rat pituitary lactotrophs.

9 ctive under the normal resting potentials of lactotrophs (-35 to -45 mV).

10 In rat pituitary lactotrophs, a component of thyrotropin-releasing hormon

11 Released from the stomach, it stimulates lactotroph and corticotroph secretion, increases appetit

12 ould be recapitulated in vitro in GH3 somato/lactotroph and LbetaT2 gonadotroph cell lines; knockdown

13 ole in the specification of the somatotroph, lactotroph and thyrotroph lineages and in the activation

14 d in Pact(-/-) mice with a greater impact on lactotrophs and a lesser impact on thyrotrophs.

15 independent thyrotrophs, and, interestingly, lactotrophs and gonadotrophs were less affected.

16 red calcium signaling in a majority (85%) of lactotrophs and prolactin release in mixed pituitary cel

17 capacity to promote calcium influx, whereas lactotrophs and somatotrophs fired plateau-bursting acti

18 tion and dramatically reduces the numbers of lactotrophs and somatotrophs in the pituitary.

19 d calcium influx triggered secretion only in lactotrophs and somatotrophs.

20 T(A) receptors through the G(i/o) pathway in lactotrophs and the subsequent activation of inward rect

21 tor required for development of somatotroph, lactotroph, and thyrotroph cell lineages and regulation

22 PRL by not only stimulating PRL release from lactotrophs, but also by inhibiting the activity of all

23 ation of wild-type female and male Drd2(-/-) lactotrophs, but had no effect on female Drd2(-/-) lacto

24 demonstrated potentiation of secretion from lactotrophs by cAMP- and PKC-dependent pathways.

25 We conclude that PRL inhibits lactotrophs by two distinct mechanisms: (a) indirectly b

26 rmal, but prolactin content, mRNA levels and lactotroph cell numbers were also slightly reduced, prob

27 ion and proliferation of prolactin-producing lactotroph cells by activating lactotroph dopamine D2 re

28 pamine receptors (both forms) are present on lactotroph cells coupled to the inhibition of adenylyl c

29 its GHRH-induced proliferation of GH3 somato/lactotroph cells with restored expression of GHRH recept

30 ation of TRH receptors expressed in GHFT pre-lactotroph cells.

31 min, only occasional exocytosis from type I lactotrophs (characterised by large polymorphic secretor

32 e number of exocytotic profiles from type II lactotrophs (characterized by smaller, spherical granule

33 ing in decreased concentrations of NO in the lactotrophs, consequent decreased cGMP formation, and re

34 om elevated DA levels that down-regulate the lactotroph D2 DA receptors and depress hypothalamic grow

35 tin-producing lactotroph cells by activating lactotroph dopamine D2 receptors (D2Rs).

36 Rat somatotrophs and lactotrophs exhibit spontaneous bursting and have high b

37 These data suggest lactotrophs from the AL-IZ are responsible for the chang

38 sible dopamine-independent effects of PRL on lactotroph function.

39 these peptides in neuroendocrine control of lactotroph function.

40 When pituitary lactotroph granules undergo exocytosis in the presence o

41 the role of galanin in prolactin release and lactotroph growth we now report the generation of mice c

42 In quiescent pituitary lactotrophs, however, endothelin-1 (ET-1) induced rapid

43 perprolactinemia and developed anterior lobe lactotroph hyperplasia without evidence of adenomatous t

44 hanism for the induction and perpetuation of lactotroph hyperplasia, involving the lack of dopamine s

45 rom GTP; cGMP concentrations increase in the lactotrophs leading to inhibition of PRL release.

46 in were detected in GH3 and MMQ (somatotroph-lactotroph lineages) and TtT/GF cells, and enzyme activi

47 ng infundibular angiogenesis and diminishing lactotroph (LT) VEGFR2 expression, lifting reproductive

48 ss, an accurate surrogate marker of absolute lactotroph number, was increased 10.6-fold in ACI rats a

49 ce survival of the prolactin (PRL)-producing lactotroph of the anterior pituitary gland and induce de

50 ssion, and reversed EGF-mediated somatotroph-lactotroph phenotype switching.

51 eoplastic human pituitaries showed that only lactotroph (PRL) and corticotroph (ACTH) hormone-produci

52 Moreover, it makes electrically active lactotrophs quiescent and unresponsive to other calcium-

53 Pituitary hyperplasia and lactotroph replication are induced by estrogen.

54 nstrate that although rat anterior pituitary lactotrophs, somatotrophs, and gonadotrophs exhibited sp

55 posite DNA element, is required to establish lactotroph-specific PRL gene expression, thus providing

56 t mechanism regulating basal and Ras-induced lactotroph-specific rat (r) PRL promoter activity.

57 In pituitary lactotrophs, spontaneous voltage-gated Ca2+ influx is su

58 how that prolactin release from isolated rat lactotrophs stimulated by forskolin, an activator of ade

59 The focus in this study was on lactotroph subpopulation of cells.

60 rophs, but had no effect on female Drd2(-/-) lactotrophs, suggesting a downregulation or desensitizat

61 de galanin is predominantly expressed by the lactotrophs (the prolactin secreting cell type) in the r

62 ore, in spontaneously firing and depolarized lactotrophs, the Ca(2+)-mobilizing action of ET-1 was fo

63 ogation of the proliferative response of the lactotroph to high doses of estrogen, with a failure to

64 was established in both quiescent and firing lactotrophs treated overnight with pertussis toxin (PTX)

65 secreting cell line derived from a pituitary lactotroph tumor found in 17beta-estradiol-treated Fisch

66 ors (FGFs) have been implicated in pituitary lactotroph tumorigenesis; however, little is known about

67 mechanism for PRL regulation in experimental lactotroph tumors.

68 The M-like current in lactotrophs was partially sensitive to 4-aminopyridine a

69 vesicle membrane capacitance measurements of lactotrophs, where HCN channels were either augmented by

70 In pituitary lactotrophs, which normally express TRH receptors, and i