Increased sodium ion influx is necessary to initiate rat hepatocyte proliferation

Koch, Katherine S.; Leffert, Hyam L.

doi:10.1016/0092-8674(79)90364-7

Cited by 360 publications

(179 citation statements)

References 30 publications

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“…Indeed, changes in membrane polarization may play a key role in the initiation of liver growth (for review see [15,23]). Enhanced activity of the amiloxidesensitive Na' carrier was described many years ago [24] as a necessary process to initiate hepatocyte proliferation. Peptides involved in liver regeneration, like glucagon and epidermal growth factor (EGF), induce Na"- 41 s 8 Vesicles from both experimental groups, C6 and R6.…”

Section: Nem (Mm1mentioning

confidence: 99%

Up‐regulation of system A activity in the regenerating rat liver

et al. 1993

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System A activity for neutral amino acid transport, measured as the MeAIB‐sensitive Na+‐dependent l‐alanine uptake, is induced 6 h after partial hepatectomy in plasma membrane vesicles from rat livers. Other Na+‐dependent transporters, like system ASC (MeAIB‐insensitive Na+‐dependent l‐alanine transport) and the nucleoside carrier show similar inductions. Up‐regulation of system A is not explained by changes in the dissipation rate of the Na+ transmembrane gradient, as deduced from uptake measurements performed in the presence of monensin. To determine whether induced system A shared any similarity with the activity found in hepatoma cell lines, we analyzed the N‐ethylmaleimide (NEM) sensitivity of system A in both regenerating and control rat liver plasma membrane vesicles. NEM treatment was equally effective in inhibiting system A in both experimental groups. Thus, during the prereplicative phase of liver growth, a transport activity similar to basal system A is up‐regulated in liver parenchymal cells, by a stable mechanism that does not involve changes in the Na+ transmembrane gradient.

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Section: Nem (Mm1mentioning

confidence: 99%

Up‐regulation of system A activity in the regenerating rat liver

et al. 1993

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“…The assymetrical distribution of the exchanger over the hepatocyte plasma membrane indicates that it may also be involved in bile formation (see [ll]). A role for Na+/H' exchange in the control of liver regeneration and hepatocyte proliferation has also been proposed [13,14], although the nonspecific effects of amiloride on the N a + / K + ATPase and on protein synthesis [15] make the interpretation of these early results difficult.…”

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confidence: 99%

Epidermal growth factor and cyclic AMP stimulate Na⁺/H⁺ exchange in isolated rat hepatocytes

Moule

McGivan

1990

European Journal of Biochemistry

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Na+/H+ exchange in acid‐loaded isolated hepatocytes was measured using the intracellular pH indicator biscarboxyethyl‐carboxyfluorescein (BCECF) to follow intracellular pH (pHi). The rate of amiloride‐sensitive Na+‐dependent recovery from cytoplasmic‐acid‐loading was found to be increased in cells treated with epidermal growth factor (EGF), 8‐(4‐chlorophenylthio)adenosine 3′,5′‐monophosphate (ClPhScAMP) or phorbol 12‐myristate 13‐acetate (PMA). These three agents increased the rate of Na+/H+ exchange to similar extents and their effects were not additive. The stimulation was shown in all three cases to be due an alkaline shift of 0.1 in the set point pH of the Na+/H+ exchanger. Experiments measuring the uptake of 22Na+ into acid‐loaded primary hepatocyte monolayer cultures confirmed these results. EGF, ClPhScAMP and PMA significantly increased the amiloride‐inhibitable accumulation of 22Na+, thus providing further evidence that Na+/H+ exchange is stimulated by these effectors.

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“…Since Na/H exchange has been shown to be stimulated by a wide variety of mitogenic agents in many different cell types (8,9,15,16), we hypothesized that platelet-derived growth factor might stimulate Na/H exchange in VSMC. In this regard, it was found that platelet-derived growth factor 1.…”

mentioning

confidence: 99%

“…These studies demonstrate that three different VSMC mitogens can also stimulate Na/H exchange in VSMC. Since Na/H exchange has been proposed to be important in control of cell proliferation (8,9,15,16), it is important to understand how this transport system is regulated in VSMC.…”

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confidence: 99%

Effect of catecholamines on Na/H exchange in vascular smooth muscle cells.

Owen¹

1986

The Journal of Cell Biology

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Abstract. Catecholamines were found to activate Na/H exchange in a concentration-dependent manner in primary cultures of vascular smooth muscle cells (VSMC). The potency order was found to be epinephrine > norepinephrine > isoproterenol. The major pathway for catecholamine effects appeared to be via interaction with an alpha~ adrenergic receptor. In addition, it was found that alpha1 receptor-mediated Na/H exchange in VSMC was increased by angiotensin II and inhibited by 12-O-tetradecanoyl phorbol-D-acetate (TPA).Adrenergic receptors have been shown to be coupled to both adenylate cyclase and to inositol phosphate release (Leeb-Lundberg, L. M. E, S. Cotecchia, J. W. Lomasney, J. E DeBernadis, R. J. Lefkowitz, and M. G. Caron, 1985, Proc. Natl. Acad. $ci. USA, 82:5651-5655.). It was found that catecholamines increased AMP levels in the potency order isoproterenol > norepinephrine > epinephrine and the receptor involved was a beta adrenergic receptor. Since these findings did not parallel the results obtained for catecholamine stimulation of Na/H exchange, an increase in AMP levels was probably not the mechanism by which major pathway for catecholamine-stimulated Na/H exchange in VSMC (via the alpha] receptor) was activated. When the effects of catecholamines were measured on inositol phosphate release, the potency order for catecholamine stimulation was epinephrine > norepinephrine > isoproterenol, and the receptor involved was an alpha~ adrenergic receptor. In addition, angiotensin II increased and TPA inhibited catecholamine-stimulated inositol phosphate release. Since these findings paralleled the results obtained for catecholamine stimulation of Na/H exchange, inositol phosphate release may be the mechanism by which the major pathway for catecholamine-stimulated Na/H exchange in VSMC (via the alphal receptor) was activated.

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Increased sodium ion influx is necessary to initiate rat hepatocyte proliferation

Cited by 360 publications

References 30 publications

Up‐regulation of system A activity in the regenerating rat liver

Up‐regulation of system A activity in the regenerating rat liver

Epidermal growth factor and cyclic AMP stimulate Na⁺/H⁺ exchange in isolated rat hepatocytes

Effect of catecholamines on Na/H exchange in vascular smooth muscle cells.

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Increased sodium ion influx is necessary to initiate rat hepatocyte proliferation

Cited by 360 publications

References 30 publications

Up‐regulation of system A activity in the regenerating rat liver

Up‐regulation of system A activity in the regenerating rat liver

Epidermal growth factor and cyclic AMP stimulate Na+/H+ exchange in isolated rat hepatocytes

Effect of catecholamines on Na/H exchange in vascular smooth muscle cells.

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Epidermal growth factor and cyclic AMP stimulate Na⁺/H⁺ exchange in isolated rat hepatocytes