Catecholaminergic Regulation of Na-K-Cl Cotransport in Pigmented Ciliary Epithelium: Differences Between PE and NPE

Hochgesand, D; Dunn, Jonathan J.; Crook, Richard B.

doi:10.1006/exer.2000.0927

Cited by 14 publications

(15 citation statements)

References 37 publications

(39 reference statements)

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“…However, we cannot rule out an alternative possibility, that a second protein kinase (in addition to PKA) also participates in the kinasephosphatase loop. In this regard we found that adrenergic stimulation of Na-K-Cl cotransport was not completely blocked by PKA inhibitors (Hochgesand et al, 2001), which points to this possibility. Haas, McBrayer and Lytle (1995) concluded that a protein kinase which stimulates Na-K-Cl cotransport in canine lung epithelial cells was not one of the well known kinases, but may be a chloride-activatable protein kinase.…”

Section: Discussionmentioning

confidence: 93%

“…This strongly suggests that an enzyme exists in PE cells which functionally opposes PP1 by stimulating Na-K-Cl cotransporter activity (Cohen, 1989). This enzyme is probably PKA, since activators of PKA such as forskolin and cAMP analogues stimulate Na-K-Cl cotransport, and stimulation is blocked by PKA inhibitors (Hochgesand et al, 2001). Furthermore, pretreatment of PE cells with the PKA inhibitor PKI (14-22) partially blocked elevation of cotransport by calyculin, again suggesting a role for PKA in opposing PP1 (Table II).…”

Section: Discussionmentioning

confidence: 94%

“…PKA activation stimulates Na-K-Cl cotransport in PE cells (Hochgesand et al, 2001). To determine whether PKA functions in a regulatory loop with PP1, the PKA inhibitor PKI (14±22) (Mitchell et al, 1995) was given to cells for 10 min prior to treatment with 10 nM calyculin (Table II).…”

Section: Effect Of Protein Kinase Inhibitors On Calyculin a Stimulatimentioning

confidence: 98%

“…This increase may involve Na-K-Cl cotransport since isoproterenol stimulates both blood-to-aqueous chloride transport and Na-K-Cl cotransport in rabbit ciliary epithelium (Crook et al, 2000). Adrenergic stimulation of cotransport occurs via the cAMP pathway in cultured ciliary epithelial cells (Hochgesand, Dunn and Crook, 2001) and is rapidly reversed when the agonist is removed from the culture medium (Crook and Riese, 1996). In the rabbit, adrenergic agonists appear to evoke a coordinated regulatory response which includes stimulation of both chloride entry into the bilayer via cotransport and chloride exit into the aqueous humor via chloride channels (Crook et al, 2000).…”

Section: Introductionmentioning

confidence: 97%

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Down-regulation of Na-K-Cl Cotransport by Protein Kinase C is Mediated by Protein Phosphatase 1 in Pigmented Ciliary Epithelial Cells

Layne

Yip

Crook

2001

Experimental Eye Research

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Section: Effect Of Protein Kinase Inhibitors On Calyculin a Stimulatimentioning

confidence: 98%

Section: Introductionmentioning

confidence: 97%

See 2 more Smart Citations

Down-regulation of Na-K-Cl Cotransport by Protein Kinase C is Mediated by Protein Phosphatase 1 in Pigmented Ciliary Epithelial Cells

Layne

Yip

Crook

2001

Experimental Eye Research

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“…Unattached cells were rinsed away with calcium-magnesium-free phosphate buffered saline (CMF-PBS) and the coverslips were placed in Medium 154 supplemented with HKGS, ABAM, 1.8 mM calcium, and 10 mM HEPES, pH 7.4, in the galvanotaxis chambers previously described by Erickson and Nuccitelli [1984]. The inhibitor concentrations used in this study were chosen from their IC 50 and Ki values and comparable cell kinase inhibition studies [Hochgesand et al, 2001]. All inhibitors were added 1 h prior to placement in the electric field at the indicated concentrations.…”

Section: Cell Culturementioning

confidence: 99%

Cyclic AMP‐dependent protein kinase A plays a role in the directed migration of human keratinocytes in a DC electric field

Pullar

Isseroff

Nuccitelli

2001

Cell Motil. Cytoskeleton

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Skin wound healing requires epithelial cell migration for re-epithelialization, wound closure, and re-establishment of normal function. We believe that one of the earliest signals to initiate wound healing is the lateral electric field generated by the wound current. Normal human epidermal keratinocytes migrate towards the negative pole, representing the center of the wound, in direct currents of a physiological strength, 100 mV/mm. Virtually nothing is known about the signal transduction mechanisms used by these cells to sense the endogenous electric field. To elucidate possible protein kinase (PK) involvement in the process, PK inhibitors were utilized. Two important findings have been described. Firstly, addition of 50 nM KT5720, an inhibitor of PKA, resulted in a 53% percent reduction in the directional response of keratinocytes in the electric field, while not significantly affecting general cell motility. The reduction was dose-dependent, there was a gradual decrease in the directional response from 5 to 50 nM. Secondly, addition of 1 microM ML-7, a myosin light chain kinase inhibitor, resulted in an approximate 31% decrease in the distance the cells migrated without affecting directional migration. The PKC inhibitors GF109203X at 4 microM and H-7 at 20 microM and W-7, a CaM kinase inhibitor, did not significantly alter either directed migration or cell migration, although they all resulted in a slight reduction in directional migration. D-erythro-sphingosine at 15 microM, a PKC inhibitor, had virtually no effect on either migration distance or directed migration. These findings demonstrate that divergent kinase signaling pathways regulate general cell motility and sustained directional migration and highlight the complexity of the signal transduction mechanisms involved. The inhibitor studies described in this paper implicate a role for PKA in the regulation of the directional migratory response to applied electric fields, galvanotaxis.

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Kammerwasserdynamik

Grüb

Mielke

2004

Der Ophthalmologe

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Intraocular pressure is mainly controlled by the rate of aqueous humor production and the resistance to its outflow. Aqueous humor formation is the result of fast unidirectional secretion and slow contradirectional reabsorption. The most striking evidence of endogenous regulation of the ciliary epithelial secretion is provided by the observation of the circadian rhythm. Aqueous humor formation is mainly controlled by the interaction of inhibiting alpha(2)-adrenoreceptors and stimulating beta-adrenoceptors. The role of the central nervous system in the regulation of this process remains unclear and the precise mechanism of outflow regulation is not fully understood. The aqueous humor passes into the anterior chamber and leaves the eye by two routes: the direct outflow pathway through the trabecular meshwork or the indirect outflow pathway through the ciliary muscle. Further biochemical, biological and pharmacological investigations are necessary to determine the fundamental process of aqueous humor formation, outflow and regulation.

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Catecholaminergic Regulation of Na-K-Cl Cotransport in Pigmented Ciliary Epithelium: Differences Between PE and NPE

Cited by 14 publications

References 37 publications

Down-regulation of Na-K-Cl Cotransport by Protein Kinase C is Mediated by Protein Phosphatase 1 in Pigmented Ciliary Epithelial Cells

Down-regulation of Na-K-Cl Cotransport by Protein Kinase C is Mediated by Protein Phosphatase 1 in Pigmented Ciliary Epithelial Cells

Cyclic AMP‐dependent protein kinase A plays a role in the directed migration of human keratinocytes in a DC electric field

Kammerwasserdynamik

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