Change in K+ current of HeLa cells with progression of the cell cycle studied by patch-clamp technique

Takahashi, Akira; Yamaguchi, Hisao; Miyamoto, Hiroshi

doi:10.1152/ajpcell.1993.265.2.c328

Cited by 38 publications

(25 citation statements)

References 29 publications

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“…The [Ca 2ϩ ] i oscillations translate into oscillation of the activity of Ca 2ϩ -activated K ϩ channels, and thus of V m , as shown in Ras oncogene-expressing cells (512). A variety of K ϩ channels have been implicated in the regulation of proliferation (972,1069) and cell cycle progression (1066). Accordingly, tumor cells often show enhanced K ϩ channel activity (775,1069).…”

Section: Cell Proliferationmentioning

confidence: 99%

Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,302

1,677

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The ability to control cell volume is pivotal for cell function. Cell volume perturbation elicits a wide array of signaling events, leading to protective (e.g., cytoskeletal rearrangement) and adaptive (e.g., altered expression of osmolyte transporters and heat shock proteins) measures and, in most cases, activation of volume regulatory osmolyte transport. After acute swelling, cell volume is regulated by the process of regulatory volume decrease (RVD), which involves the activation of KCl cotransport and of channels mediating K+, Cl−, and taurine efflux. Conversely, after acute shrinkage, cell volume is regulated by the process of regulatory volume increase (RVI), which is mediated primarily by Na+/H+exchange, Na+-K+-2Cl−cotransport, and Na+channels. Here, we review in detail the current knowledge regarding the molecular identity of these transport pathways and their regulation by, e.g., membrane deformation, ionic strength, Ca2+, protein kinases and phosphatases, cytoskeletal elements, GTP binding proteins, lipid mediators, and reactive oxygen species, upon changes in cell volume. We also discuss the nature of the upstream elements in volume sensing in vertebrate organisms. Importantly, cell volume impacts on a wide array of physiological processes, including transepithelial transport; cell migration, proliferation, and death; and changes in cell volume function as specific signals regulating these processes. A discussion of this issue concludes the review.

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Section: Cell Proliferationmentioning

confidence: 99%

Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,302

1,677

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“…Beyond that, K + channel meditated cell shrinkage may at some stage be important in cell proliferation [29]. K + channel activity was found to be highest in the G 1 phase and then gradually decreases to a minimum in the S phase [44]. Inhibition of K + channels has been shown to arrest cells in the G 1 phase, but did not affect the cell cycle at later stages, i.e.…”

Section: Cell Volume Regulatory K + Channelsmentioning

confidence: 99%

Cell Volume in the Regulation of Cell Proliferation and Apoptotic Cell Death

Läng¹,

Ritter²,

Gamper³

et al. 2000

Cell Physiol Biochem

228

181

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Cell proliferation must – at some time point – lead to increase of cell volume and one of the hallmarks of apoptosis is cell shrinkage. At constant extracellular osmolarity those alterations of cell volume must reflect respective changes of cellular osmolarity which are hardly possible without the participation of cell volume regulatory mechanisms. Indeed, as shown for ras oncogene expressing 3T3 fibroblasts, cell proliferation is paralleled by activation of Na⁺/H⁺ exchange and Na⁺,K⁺,2Cl^- cotransport, the major transport systems accomplishing regulatory cell volume increase. Conversely, as evident from CD95-induced apoptotic cell death, apoptosis is paralleled by inhibition of Na⁺/H⁺ exchanger and by activation of Cl^- channels and release of the organic osmolyte taurine, major components of regulatory cell volume decrease. However, ras oncogene activation leads to activation and CD95 receptor triggering to inhibition of K⁺ channels. The effects counteract the respective cell volume changes. Presumably, they serve to regulate cell membrane potential, which is decisive for Ca⁺⁺ entry through I_CRAC and the generation of cytosolic Ca⁺⁺ oscillations in proliferating cells. As a matter of fact I_CRAC is activated in ras oncogene expressing cells and inhibited in CD95-triggered cells. Activation of K⁺ channels and Na⁺/H⁺ exchanger as well as Ca⁺⁺ oscillations have been observed in a wide variety of cells upon exposure to diverse mitogenic factors. Conversely, diverse apoptotic factors have been shown to activate Cl^- channels and organic osmolyte release. Inhibition of K⁺ channels is apparently, however, not a constant phenomenon paralleling apoptosis which in some cells may even require the operation of K⁺ channels. Moreover, cell proliferation may at some point require activation of Cl^- channels. In any case, the alterations of cell volume are obviously important for the outcome, as cell shrinkage impedes cell proliferation and apoptosis can be elicited by increase of extracellular osmolarity. At this stage little is known about the interplay of cell volume regulatory mechanisms and the cellular machinery leading to mitosis or death of the cell. Thus, considerable further experimental effort is required in this exciting area of cell physiology.

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“…For this reason, the LNCaP cell line has been extensively studied and used as a model for studies of prostate cancer cell growth [6][7][8]. Control of prostate cancer cell proliferation is believed to depend on both external (hormones and growth factors) and internal signals that modify the activity of cell cycle proteins [9][10][11][12]. However, it is not clear which intracellular transduction mechanism from the cell surface to the nucleus mediates these processes.…”

Section: Introductionmentioning

confidence: 99%