Cell Volume Regulatory Ion Channels in Cell Proliferation and Cell Death

2007 ◽  
pp. 209-225 ◽  
Author(s):  
Florian Lang ◽  
Michael Föller ◽  
Karl Lang ◽  
Philipp Lang ◽  
Markus Ritter ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Cell Volume

Ion Channels and Cell Volume in Regulation of Cell Proliferation and Apoptotic Cell Death

2006 ◽  
pp. 142-160 ◽  
Author(s):  
Florian Lang ◽  
Ekaterina Shumilina ◽  
Markus Ritter ◽  
Erich Gulbins ◽  
Alexey Vereninov ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

Ion Channels, Cell Volume, Cell Proliferation and Apoptotic Cell Death

2008 ◽  
pp. 69-84 ◽  
Author(s):  
Florian Lang ◽  
Erich Gulbins ◽  
Ildiko Szabo ◽  
Alexey Vereninov ◽  
Stephan M. Huber
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Volume Cell

Ion Channels, Cell Volume, and Apoptotic Cell Death

1998 ◽  
Vol 8 (6) ◽  
pp. 285-292 ◽  
Author(s):  
F. Lang ◽  
A. Lepple-Wienhues ◽  
M. Paulmichl ◽  
I. Szabó ◽  
D. Siemen ◽  
...  
Keyword(s):  
Cell Death ◽  
Ion Channels ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals Ion Channels in Hematopoietic and Mesenchymal Stem Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Serena Pillozzi ◽  
Andrea Becchetti
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Ion Channels ◽  
Cell Volume ◽  
Cell Types ◽  
Cell Interaction ◽  
Integrin Receptors ◽  
Mesodermal Cell ◽  
Bone Marrow Niches

Hematopoietic stem cells (HSCs) reside in bone marrow niches and give rise to hematopoietic precursor cells (HPCs). These have more restricted lineage potential and eventually differentiate into specific blood cell types. Bone marrow also contains mesenchymal stromal cells (MSCs), which present multilineage differentiation potential toward mesodermal cell types. In bone marrow niches, stem cell interaction with the extracellular matrix is mediated by integrin receptors. Ion channels regulate cell proliferation and differentiation by controlling intracellular Ca2+, cell volume, release of growth factors, and so forth. Although little evidence is available about the ion channel roles in true HSCs, increasing information is available about HPCs and MSCs, which present a complex pattern of K+channel expression. K+channels cooperate with Ca2+and Cl−channels in regulating calcium entry and cell volume during mitosis. Other K+channels modulate the integrin-dependent interaction between leukemic progenitor cells and the niche stroma. These channels can also regulate leukemia cell interaction with MSCs, which also involves integrin receptors and affects the MSC-mediated protection from chemotherapy. Ligand-gated channels are also implicated in these processes. Nicotinic acetylcholine receptors regulate cell proliferation and migration in HSCs and MSCs and may be implicated in the harmful effects of smoking.

Ion Channels in Cell Proliferation and Apoptotic Cell Death

2005 ◽  
Vol 205 (3) ◽  
pp. 147-157 ◽  
Author(s):  
F. Lang ◽  
M. Föller ◽  
K.S. Lang ◽  
P.A. Lang ◽  
M. Ritter ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

Cell Volume in Cell Proliferation and Apoptotic Cell Death

1998 ◽  
pp. 158-168 ◽  
Author(s):  
F. Lang ◽  
A. Lepple-Wienhues ◽  
I. Szab� ◽  
D. Siemen ◽  
E. Gulbins
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals Ion channels and apoptosis in cancer

2014 ◽  
Vol 369 (1638) ◽  
pp. 20130104 ◽  
Author(s):  
Carl D. Bortner ◽  
John A. Cidlowski
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Cell Growth ◽  
Cancer Cells ◽  
Critical Role ◽  
Cell Number ◽  
Tumour Formation ◽  
Constant Cell ◽  
Critical Components

Humans maintain a constant cell number throughout their lifespan. This equilibrium of cell number is accomplished when cell proliferation and cell death are kept balanced, achieving a steady-state cell number. Abnormalities in cell growth or cell death can lead to an overabundance of cells known as neoplasm or tumours. While the perception of cancer is often that of an uncontrollable rate of cell growth or increased proliferation, a decrease in cell death can also lead to tumour formation. Most cells when detached from their normal tissue die. However, cancer cells evade cell death, tipping the balance to an overabundance of cell number. Therefore, overcoming this resistance to cell death is a decisive factor in the treatment of cancer. Ion channels play a critical role in cancer in regards to cell proliferation, malignant angiogenesis, migration and metastasis. Additionally, ion channels are also known to be critical components of apoptosis. In this review, we discuss the modes of cell death focusing on the ability of cancer cells to evade apoptosis. Specifically, we focus on the role ion channels play in controlling and regulating life/death decisions and how they can be used to overcome resistance to apoptosis in the treatment of cancer.

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

2000 ◽  
Vol 10 (5-6) ◽  
pp. 417-428 ◽  
Author(s):  
Florian Lang ◽  
Markus Ritter ◽  
Nikita Gamper ◽  
Stephan Huber ◽  
Sophie Fillon ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

The P-MAPA immunomodulator partially prevents apoptosis induced by Zika virus infection in THP-1 cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Morganna C. Lima ◽  
Elisa A. N. Azevedo ◽  
Clarice N. L. de Morais ◽  
Larissa I. O. de Sousa ◽  
Bruno M. Carvalho ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Virus Infection ◽  
Virus Replication ◽  
Zika Virus ◽  
Mammalian Cells ◽  
Caspase 3 ◽  
Neurological Complications ◽  
Zika Virus Infection

Background: Zika virus is an emerging arbovirus of global importance. ZIKV infection is associated with a range of neurological complications such as the Congenital Zika Syndrome and Guillain Barré Syndrome. Despite the magnitude of recent outbreaks, there is no specific therapy to prevent or to alleviate disease pathology. Objective: To investigate the role of P-MAPA immunomodulator in Zika-infected THP-1 cells. Methods: THP-1 cells were subjected at Zika virus infection (Multiplicity of Infection = 0.5) followed by treatment with P-MAPA for until 96 hours post-infection. After that, the cell death was analyzed by annexin+/ PI+ and caspase 3/ 7+ staining by flow cytometry. In addition, the virus replication and cell proliferation were accessed by RT-qPCR and Ki67 staining, respectively. Results: We demonstrate that P-MAPA in vitro treatment significantly reduces Zika virus-induced cell death and caspase-3/7 activation on THP-1 infected cells, albeit it has no role in virus replication and cell proliferation. Conclusions: Our study reveals that P-MAPA seems to be a satisfactory alternative to inhibits the effects of Zika virus infection in mammalian cells.

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