The K+ channel openers diazoxide and NS1619 induce depolarization of mitochondria and have differential effects on cell Ca2+ in CD34+ cell line KG-1a

Körper, Sixten; Nolte, Florian; Rojewski, Markus; Thiel, Eckhard; Schrezenmeier, Hubert

doi:10.1016/s0301-472x(03)00199-1

Cited by 42 publications

(39 citation statements)

References 41 publications

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“…For these reasons, the identification and characterization of ion channels expressed by CD34 + HSCs are essential prerequisites for biotechnological manipulation or physiological understanding of this cell type. However, direct investigations of ion channel function in CD34 + HSCs are rare and primarily focus on cancer cell lines (Korper et al, 2003;Pillozzi et al, 2002;Shirihai et al, 1998). One study using primary CD34 + HSCs demonstrated the inwardly rectifying K + currents but did not systemically examine the other ion channels (Shirihai et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Identification and Functional Characterization of Ion Channels in CD34+ Hematopoietic Stem Cells from Human Peripheral Blood

Park

Pang

Park

et al. 2011

Molecules and Cells

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Section: Introductionmentioning

confidence: 99%

Identification and Functional Characterization of Ion Channels in CD34+ Hematopoietic Stem Cells from Human Peripheral Blood

Park

Pang

Park

et al. 2011

Molecules and Cells

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“…At this time, we will continue to use the term gBK to promote a consistent terminology and minimize any confusion that could result as a new name to the literature. Besides, BK channels already have numerous other aliases, such as Maxi-K, hSlo, mSlo, KCNMA1, calciumdependent, or large conductance-or voltage-activated channels (15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, BK channels were found on the ER and the mitochondria (7,8), providing a plausible rationale for why these organelles are specifically targeted in paraptosis. These ion channels are also called Maxi-K, hSlo, mSlo, KCNMA1, calcium-dependent, large conductance-, or voltage-activated channels (9)(10)(11)(12)(13)(14)(15)(16)(17). The complex interaction between various ions and their respective ion channels at the invadopodia of the malignant gliomas is speculated to explain some of the invasive properties of gliomas (18)(19)(20).…”

mentioning

confidence: 99%

Glioma Big Potassium Channel Expression in Human Cancers and Possible T Cell Epitopes for Their Immunotherapy

Ge¹,

Hoa²,

Cornforth

et al. 2012

The Journal of Immunology

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Big potassium (BK) ion channels have several spliced variants. One spliced variant initially described within human glioma cells is the glioma BK (gBK) channel. This isoform consists of 34 aa inserted into the intracellular region of the basic BK ion channel. PCR primers specific for this inserted region confirmed that human glioma cell lines and freshly resected surgical tissues from glioblastoma multiforme patients strongly expressed gBK mRNA. Normal human brain tissue very weakly expressed this transcript. An Ab specific for this gBK isoform confirmed that human glioma cells displayed this protein in the cell membrane, mitochondria, Golgi, and endoplasmic reticulum. Within the gBK region, two putative epitopes (gBK1 and gBK2) are predicted to bind to the HLA-A*0201 molecule. HLA-A*0201–restricted human CTLs were generated in vitro using gBK peptide-pulsed dendritic cells. Both gBK1 and gBK2 peptide-specific CTLs killed HLA-A2+/gBK+ gliomas, but they failed to kill non-HLA-A2–expressing but gBK+ target cells in cytolytic assays. T2 cells loaded with exogenous gBK peptides, but not with the influenza M1 control peptide, were only killed by their respective CTLs. The gBK-specific CTLs also killed a variety of other HLA-A*0201+ cancer cells that possess gBK, as well as HLA-A2+ HEK cells transfected with the gBK gene. Of clinical relevance, we found that T cells derived from glioblastoma multiforme patients that were sensitized to the gBK peptide could also kill target cells expressing gBK. This study shows that peptides derived from cancer-associated ion channels maybe useful targets for T cell-mediated immunotherapy.

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“…It is an early event preceding phosphatidylserine externalization and coincides with caspase activation (22,23). We used a JC-1 dye-based assay to evaluate mitochondrial membrane potential.…”

Section: Discussionmentioning

confidence: 99%

“…This structure, in turn, recruits and activates caspase-9. Activated caspase-9 cleaves and activates executioner caspases, such as caspase-3, and eventually results in apoptosis (22,23,26). Therefore, to evaluate the effect on MW on the mitochondrion-dependent apoptosis pathway, we evaluated the release of cytochrome c and the activation of caspase-9 and caspase-3.…”

Section: Discussionmentioning

confidence: 99%

Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes

Sferra

Chen

et al. 2011

Mol Med Report

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Abstract. Millimeter wave (MW) is an electromagnetic wave with a wavelength between 1 and 10 mm and a frequency of 30-300 GHz that causes multiple biological effects, both locally and globally. MW has been widely used in clinical medicine. Although our previous work demonstrated that MW is capable of inhibiting sodium nitroprussiate (SNP)-induced apoptosis in chondrocytes, the precise mechanism of the antiapoptotic activity remains to be elucidated. The purpose of this study was to investigate the effects of MW in SNP-induced apoptotic chondrocytes. Sprague Dawley rat chondrocytes were isolated and cultured, and the cells were counted. Cell viability was evaluated using MTT assay. Cells were then treated with SNP and MW, and flow cytometry was used to detect apoptosis. Our results showed that MW treatment inhibited a SNP-induced mitochondrion-dependent pathway of apoptosis. MW treatment inhibited the loss of plasma membrane asymmetry (externalization of phosphatidylserine), collapse of mitochondrial membrane potential, and activation of caspase-9 and caspase-3. Taken together, the results indicate that MW inhibits the mitochondrion-dependent pathway of apoptosis in chondrocytes and this may, in part, explain its clinical effect in the treatment of osteoarthritis.

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The K+ channel openers diazoxide and NS1619 induce depolarization of mitochondria and have differential effects on cell Ca2+ in CD34+ cell line KG-1a

Cited by 42 publications

References 41 publications

Identification and Functional Characterization of Ion Channels in CD34+ Hematopoietic Stem Cells from Human Peripheral Blood

Identification and Functional Characterization of Ion Channels in CD34+ Hematopoietic Stem Cells from Human Peripheral Blood

Glioma Big Potassium Channel Expression in Human Cancers and Possible T Cell Epitopes for Their Immunotherapy

Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes

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