Roles of tyrosine kinase in insulin action on cell volume of fetal rat type II pneumocyte

Marunaka, Yoshinori; Shintani, Yutaka; Sugimoto, Eizo; Niisato, Naomi

doi:10.1007/s004240050171

Cited by 11 publications

(4 citation statements)

References 8 publications

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“…7A). Our previous study (Marunaka, Shintani, Sugimoto & Niisato, 1996) indicates that the bumetanide-sensitive Na+-K+-2CFcotransporter contributes to maintenance of cell volume of FDLE cells. The activity of this cotransporter may produce a higher electrochemical potential of intracellular Clthan that of extracellular Cl-.…”

Section: Discussionmentioning

confidence: 91%

Beta‐agonist‐induced activation of Na+ absorption and KCl release in rat fetal distal lung epithelium: a study of cell volume regulation

Nakahari

Marunaka²

1997

Experimental Physiology

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SUMMARYThe effects of terbutaline (a selective /?2-adrenoceptor agonist) on cell volume and ion transport in rat fetal distal lung epithelial (FDLE) cells were studied. In FDLE cells, benzamil (1 /SM) induced cell shrinkage, while cell volume was increased by 1 mm quinine or 2 mM Ba2+ but was not affected by 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB, 20juM). Terbutaline (10 nM) induced transient cell swelling, which was suppressed by benzamil, while 10 /lM terbutaline induced initial rapid cell shrinkage followed by delayed slow cell shrinkage, which was suppressed by 1 mm quinine or 20 /tM NPPB but not by 2 mM Ba2+. Application of benzamil enhanced the cell shrinkage induced by 10 /uM terbutaline. These observations suggest that: (1) benzamil-blockable Na+-permeable channels and quinine-and Ba2+-blockable K+ channels contribute to maintenance of cell volume of FDLE cells; (2) terbutaline at both 10 nm and 1O #M activates benzamilblockable Na+-permeable channels; (3) quinine-blockable K+ channels are activated by 10 /SM terbutaline; and (4) NPPB-blockable CF-channels are responsible for Cl-movement in cell volume changes induced by terbutaline. The present study demonstrates that the cellular mechanisms of volume change induced by terbutaline are closely related to activation of Na+ absorption and KCI release.

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Section: Discussionmentioning

confidence: 91%

Beta‐agonist‐induced activation of Na+ absorption and KCl release in rat fetal distal lung epithelium: a study of cell volume regulation

Nakahari

Marunaka²

1997

Experimental Physiology

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“…For example, a report (Sargeant et al 1995) suggests that insulin activates the Na + ‐K + pump by increasing the intracellular Na + concentration due to an increase in Na + influx via the bumetanide‐sensitive Na + ‐K + ‐2Cl − cotransporter. Indeed, insulin stimulates the Na + ‐K + ‐2Cl − cotransporter (Longo, 1996; Marunaka et al 1996; Marunaka et al 1999 b ). Removal of extracellular Cl − diminishes the Na + influx via the Na + ‐K + ‐2Cl − cotransporter, inhibiting the insulin action on the Na + ‐K + pump (Sargeant et al 1995).…”

Section: Discussionmentioning

confidence: 99%

Activation of the Na⁺‐K⁺ pump by hyposmolality through tyrosine kinase‐dependent Cl⁻ conductance in Xenopus renal epithelial A6 cells

Niisato

Marunaka

1999

The Journal of Physiology

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We studied the regulatory mechanism of Na+ transport by hyposmolality in renal epithelial A6 cells. Hyposmolality increased (1) Na+ absorption, which was detected as an amiloride‐sensitive short‐circuit current (INa), (2) Na+‐K+ pump activity, (3) basolateral Cl− conductance (Gb,Cl), and (4) phosphorylation of tyrosine, suggesting an increase in activity of protein tyrosine kinase (PTK). A Cl− channel blocker, 5‐nitro‐2‐(3‐phenylpropylamino)‐benzoate (NPPB), which abolished Gb,Cl, blocked the INa by inhibiting the Na+‐K+ pump without any direct effect on amiloride‐sensitive Na+ channels. Diminution of Gb,Cl by Cl− replacement with a less permeable anion, gluconate, also decreased the hyposmolality‐increased Na+‐K+ pump activity. The PTK inhibitors tyrphostin A23 and genistein induced diminution of the hyposmolality‐stimulated Gb,Cl, which was associated with attenuation of the hyposmolality‐increased Na+‐K+ pump activity. Taken together, these observations suggest that: (1) hyposmolality activates PTK; (2) the activated PTK increases Gb,Cl; and (3) the PTK‐increased Gb,Cl stimulates the Na+‐K+ pump. This PTK‐activated Gb,Cl‐mediated signalling of hyposmolality is a novel pathway for stimulation of the Na+‐K+ pump.

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“…In general, the NKCC maintains cell volume via influxes of Na + , K + , and Cl -under normal conditions. In this study, we performed the functional assay for NKCC by measuring the cell volume in these cells after treatment with furosemide [16]. Although cell shrinkage in MKN28 and MKN45 was observed after treatment with furosemide (Fig.…”

Section: Nkcc Functional Assaymentioning

confidence: 99%

Furosemide, a Blocker of Na+/K+/2Cl− Cotransporter, Diminishes Proliferation of Poorly Differentiated Human Gastric Cancer Cells by Affecting G0/G1 State

et al. 2006

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Furosemide, a blocker of Na + /K + /2Cl -cotransporter (NKCC), is often used as a diuretic to improve edema, ascites, and pleural effusion of patients with cancers. The aim of the present study was to investigate whether an NKCC blocker affects cancer cell growth. If so, we would clarify the mechanism of this action. We found that poorly differentiated gastric adenocarcinoma cells (MKN45) expressed the mRNA of NKCC1 three times higher than moderately differentiated ones (MKN28) and that the NKCC in MKN45 showed higher activity than that in MKN28. A cell proliferation assay indicates that furosemide significantly inhibited cell growth in MKN45 cells, but not in MKN28 cells. Using flow cytometrical analysis, we found that the exposure to furosemide brought MKN45 cells to spend more time at the G 0 /G 1 phase, but not MKN28 cells. Based on these observations, we indicate that furosemide diminishes cell growth by delaying the G 1 -S phase progression in poorly differentiated gastric adenocarcinoma cells, which show high expression and activity of NKCC, but not in moderately differentiated gastric adenocarcinoma cells with low expression and NKCC activity.Key words: gastric cancer cell, Na + /K + /2Cl -cotransporter (NKCC), furosemide, cell cycle, cell proliferation.In the past two decades, many researchers have reported the characteristics of ion channels/transporters in various types of cells, including cancer cells. Several types of K + , Ca 2+ , and Cl -channels have been identified in colorectal, breast, lung, and prostate cancer cells [1,2]. Some studies indicate that the transepithelial ion transport plays an important role in cell apoptosis [3,4]. Particularly, the modulation of Cl -transport via Cl -channel, K + /Cl -cotransporter (KCC), and Na + /K + /2Cl -cotransporter (NKCC) occurs in cell proliferation [5][6][7]. However, it is unknown whether NKCC affects the proliferation of cancer cells. In the treatment of patients with terminal stage cancers, however, furosemide (an NKCC blocker, a loop diuretic) is often used as a diuretic to keep urine output and to improve edema, ascites, or pleural effusion. Therefore we performed the present study to clarify the effect of furosemide on the proliferation of cancer cells.In the present study, we used two human gastric cancer cell lines, MKN28 and MKN45, which were established from moderately and poorly differentiated adenocarcinoma, respectively [8]. We determined the mRNA and functional expression levels of the NKCC and investigated the inhibitory effect of an NKCC blocker, furosemide, on the proliferation in these two cancer cell lines. We found that mRNA and the functional expression levels of NKCC were both higher in MKN45 than in MKN28 cells. Furthermore, furosemide diminished the cell proliferation, delaying the G 1 -S phase progression in MKN45 cells, but not in MKN28 cells. MATERIALS AND METHODSCell culture. The moderately differentiated human gastric adenocarcinoma cell line, MKN28, and the poorly differentiated human gastric adenocarcinoma cel...

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Roles of tyrosine kinase in insulin action on cell volume of fetal rat type II pneumocyte

Cited by 11 publications

References 8 publications

Beta‐agonist‐induced activation of Na+ absorption and KCl release in rat fetal distal lung epithelium: a study of cell volume regulation

Beta‐agonist‐induced activation of Na+ absorption and KCl release in rat fetal distal lung epithelium: a study of cell volume regulation

Activation of the Na⁺‐K⁺ pump by hyposmolality through tyrosine kinase‐dependent Cl⁻ conductance in Xenopus renal epithelial A6 cells

Furosemide, a Blocker of Na+/K+/2Cl− Cotransporter, Diminishes Proliferation of Poorly Differentiated Human Gastric Cancer Cells by Affecting G0/G1 State

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Roles of tyrosine kinase in insulin action on cell volume of fetal rat type II pneumocyte

Cited by 11 publications

References 8 publications

Beta‐agonist‐induced activation of Na+ absorption and KCl release in rat fetal distal lung epithelium: a study of cell volume regulation

Beta‐agonist‐induced activation of Na+ absorption and KCl release in rat fetal distal lung epithelium: a study of cell volume regulation

Activation of the Na+‐K+ pump by hyposmolality through tyrosine kinase‐dependent Cl− conductance in Xenopus renal epithelial A6 cells

Furosemide, a Blocker of Na+/K+/2Cl− Cotransporter, Diminishes Proliferation of Poorly Differentiated Human Gastric Cancer Cells by Affecting G0/G1 State

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Activation of the Na⁺‐K⁺ pump by hyposmolality through tyrosine kinase‐dependent Cl⁻ conductance in Xenopus renal epithelial A6 cells