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Studies have suggested that PGF2a may play a role in K homeostasis. Urinary PGF2a, preferentially stimulated by an increased dietary K intake, has been shown to regulate Na absorption and K secretion. The purpose of this study is to determine if PGF2a regulates VUK through the FP receptor. Mice lacking the FP receptors (FP-/-) and wild type mice were fed normal chow (1.1% K, NK), a high K diet (5% K, HK), and a low K diet (0.07% K, LK). The VUK and PK during the NK diet were similar in the FP -/- (703 ± 64 mEq and 4.45 ±0.18 mEq/l, respectively) and the wild type (627 ± 67 mEq and 4.21 ± 0.11 mEq/l, respectively) mice. The FP -/- mice had a greater VUK (1918 ± 224 mEq) on the HK diet than the wild type mice (1623 ± 299 mEq). The PK during the HK diet increased in the FP-/- mice (5.23 ± 0.18 mEq/l, r< 0.001); but not in the wild type mice (4.63±0.23 mEq/l). The LK diet decreased the VUK and PK in the FP-/- (9.59 ± 1.40 µEq and 3.78 ± .26 mEq/l, respectively) and wild type (2.87 ± 0.45 µEq and 3.72 ± .41 mEq/l, respectively, r < 0.001) mice. FP-/- mice fed a LK diet exhibited a greater VUK indicating an inability to regulate K excretion. The aldosterone concentrations during NK and HK diets were greater in the FP-/- mice (354 ± 42 and 638 ± 63 rg/ml, respectively) than in the wild type mice (223 ± 45 and 401 ± 25 rg/ml, respectively). Quantitative RTPCR analysis indicated that the SGK-1 expression was lower in the FP-/-mice than in the wild type mice. The SGK-1 expression increased with the HK diet, but still remain lower in the FP-/- mice than in the wild type mice. The results of these studies lead us to conclude that the PGF2a via the FP receptor, in part, plays a role in K homeostasis. [ABSTRACT FROM AUTHOR]

Proper control of cell migration is critically important in many biologic processes, such as wound healing, immune surveillance, and development. Much progress has been made in the initiation of cell migration; however, little is known about termination and sometimes directional reversal. During active cell migration, as in wound healing, development, and immune surveillance, the integrin expression profile undergoes drastic changes. Here, we uncovered the extensive regulatory and even opposing roles of integrins in directional cell migration in electric fields (EFs), a potentially important endogenous guidance mechanism. We established cell lines that stably express specific integrins and determined their responses to applied EFs with a high throughput screen. Expression of specific integrins drove cells to migrate to the cathode or to the anode or to lose migration direction. Cells expressing αMβ2, β1, α2, αIIbβ3, and α5 migrated to the cathode, whereas cells expressing β3, α6, and α9 migrated to the anode. Cells expressing α4, αV, and α6β4 lost directional electrotaxis. Manipulation of α9 molecules, one of the molecular directional switches, suggested that the intracellular domain is critical for the directional reversal. These data revealed an unreported role for integrins in controlling stop, go, and reversal activity of directional migration of mammalian cells in EFs, which might ensure that cells reach their final destination with well-controlled speed and direction. [ABSTRACT FROM AUTHOR]

There is evidence that isoprostanes (IsoPs) can regulate sympathetic neurotransmission in bovine irides in vitro (Opere et al., Free Rad Res. 35:2001). However, the regulation of dopamine (DA) levels by IsoPs in mammalian retinae remains unclear. We examined the effect of IsoPs on endogenous DA levels in rabbit, in vivo and on K+-evoked release of exogenously applied [³H]DA release in bovine retinae, in vitro. Albino rabbits were sedated, then injected intravitreally with IsoPs. After 4 hours, animals were sacrificed and retinae isolated for measurement of DA using HPLC. Isolated bovine retinae were incubated in Krebs solution containing 150 nM of [³H]DA for 45 mins and then prepared for studies of neurotransmitter release using the Superfusion Method. In rabbit retina, 8-isoPGF2α (0.1 µM & 10µM) attenuated DA levels by 50% (p<0.05) and 52% (p<0.05) while 8-isoPGE2 (0.1 µM & 10µM) increased DA levels by 56 % (p<0.01) and 107 % (p<0.001). In isolated bovine retinae, 8-isoPGF2α (0.1 µM and 10 µM) attenuated DA release by 25% and 16% while 8-isoPGE2 inhibited the catecholamine by 25% (p<0.05) and 50% (p<0.01) respectively. The effect of both IsoPs on K+-evoked [³H]DA release was reversed by the COX enzyme inhibitor, flubiprofen (3 µM). IsoPs can regulate endogenous DA levels and the release of exogenously applied DA in mammalian retinae. PGs are involved in the inhibitory effect of IsoPs on DA release. [ABSTRACT FROM AUTHOR]

Presents an analysis of the electrical inhibition of lens epithelial cell (LEC) proliferation as an additional factor in secondary cataract. Description of cataract; Effect of electrical fields on the proliferation of LEC; Role of electrical fields on cell cycle regulators.