Expression of Kir 4.1 in human astrocytic tumors: Correlation with pathologic grade

Ge, Tan; Sun, Shanquan; Yuan, Dongli

doi:10.1016/j.bbrc.2008.01.014

Cited by 18 publications

(18 citation statements)

References 25 publications

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“…Thus, the localization in the nucleus observed in glioma cell lines in culture ([18]; present study) does not represent a consistent feature of human primary glial tumor. Accordingly, nuclear localization has not been reported in other studies analyzing the expression pattern of Kir4.1 in surgical specimens of both low- and high-grade astrocytomas [16,17]. However, in agreement with our observations, Warth and colleagues [16] reported a redistribution of Kir4.1 in astrocytomas (with reduced perivascular astrocyte endfeet), suggesting a compromised buffering capacity of glial tumor cells.…”

Section: Discussionsupporting

confidence: 91%

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Regulation of Kir4.1 expression in astrocytes and astrocytic tumors: a role for interleukin-1 β

Zurolo

Groot

Iyer

et al. 2012

J Neuroinflammation

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ObjectiveDecreased expression of inwardly rectifying potassium (Kir) channels in astrocytes and glioma cells may contribute to impaired K+ buffering and increased propensity for seizures. Here, we evaluated the potential effect of inflammatory molecules, such as interleukin-1β (IL-1β) on Kir4.1 mRNA and protein expression.MethodsWe investigated Kir4.1 (Kcnj10) and IL-1β mRNA expression in the temporal cortex in a rat model of temporal lobe epilepsy 24 h and 1 week after induction of status epilepticus (SE), using real-time PCR and western blot analysis. The U373 glioblastoma cell line and human fetal astrocytes were used to study the regulation of Kir4.1 expression in response to pro-inflammatory cytokines. Expression of Kir4.1 protein was also evaluated by means of immunohistochemistry in surgical specimens of patients with astrocytic tumors (n = 64), comparing the expression in tumor patients with (n = 38) and without epilepsy (n = 26).ResultsTwenty-four hours after onset of SE, Kir4.1 mRNA and protein were significantly down-regulated in temporal cortex of epileptic rats. This decrease in expression was followed by a return to control level at 1 week after SE. The transient downregulation of Kir4.1 corresponded to the time of prominent upregulation of IL-1β mRNA. Expression of Kir4.1 mRNA and protein in glial cells in culture was downregulated after exposure to IL-1β. Evaluation of Kir4.1 in tumor specimens showed a significantly lower Kir4.1 expression in the specimens of patients with epilepsy compared to patients without epilepsy. This paralleled the increased presence of activated microglial cells, as well as the increased expression of IL-1β and the cytoplasmic translocation of high mobility group box 1 (HMGB1).ConclusionsTaken together, these findings indicate that alterations in expression of Kir4.1 occurring in epilepsy-associated lesions are possibly influenced by the local inflammatory environment and in particular by the inflammatory cytokine IL-1β.

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Section: Discussionsupporting

confidence: 91%

“…Kir4.1 IR was detected around blood vessels (Figure 4A) as previously reported [16,17] and occasionally in the cytoplasm of astroglial cells. Astrocytoma WHO grade II and III, as well as GBM displayed mainly cytoplasmic staining in tumor cells (Figures 4B-F).…”

Section: Kir41 and Il-1β Expression In Human Astrocytic Tumorssupporting

confidence: 86%

Regulation of Kir4.1 expression in astrocytes and astrocytic tumors: a role for interleukin-1 β

Zurolo

Groot

Iyer

et al. 2012

J Neuroinflammation

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“…The expression of other TRP channels such as TRPM8, TRPC1, TRPC3, TRPC5, and TRPC6 has been observed in gliomas, and the expression levels of TRPM8 have been correlated with tumor progression (Bomben and Sontheimer, 2008;Tan et al, 2008;Yee, 2015). Additionally, TRP vanilloid-1 (TRPV1) is highly expressed in high-grade astrocytomas and weakly expressed in the tumor-free brain.…”

Section: Calcium Channel-associated Transientmentioning

confidence: 99%

Calcium Channels and Associated Receptors in Malignant Brain Tumor Therapy

Morrone¹,

Gehring²,

Nicoletti³

2016

Molecular Pharmacology

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Malignant brain tumors are highly lethal and aggressive. Despite recent advances in the current therapies, which include the combination of surgery and radio/chemotherapy, the average survival rate remains poor. Altered regulation of ion channels is part of the neoplastic transformation, which suggests that ion channels are involved in cancer. Distinct classes of calciumpermeable channels are abnormally expressed in cancer and are likely involved in the alterations underlying malignant growth. Specifically, cytosolic Ca 21 activity plays an important role in the regulation of cell proliferation, and Ca 21 signaling is altered in proliferating tumor cells. A series of previous studies emphasized the importance of the T-type low-voltage-gated calcium channels (VGCC) in different cancer types, including gliomas, and remarkably, pharmacologic inhibition of T-type VGCC caused antiproliferative effects and triggered apoptosis of human glioma cells. Other calcium permeable channels, such as transient receptor potential (TRP) channels, contribute to changes in Ca 21 by modulating the driving force for Ca 21 entry, and some TRP channels are required for proliferation and migration in gliomas. Furthermore, recent evidence shows that TRP channels contribute to the progression and survival of the glioblastoma patients. Likewise, the purinergic P2X7 receptor acts as a direct conduit for Ca 21 -influx and an indirect activator of voltage-gated Ca 21 -channel. Evidence also shows that P2X7 receptor activation is linked to elevated expression of inflammation promoting factors, tumor cell migration, an increase in intracellular mobilization of Ca 21 , and membrane depolarization in gliomas. Therefore, this review summarizes the recent findings on calcium channels and associated receptors as potential targets to treat malignant gliomas.

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“…The latter channel is an octameric complex resulting from the combination of four SUR subunits with four Kir (potassium inwardly rectifying) subunits, both of which exist in several isoforms (SUR1, SUR2A, and SUR2B; Kir6.1 and Kir6.2) [21]. Kir channels are also implicated in glioma cell biology [22,23]. Recently, it was reported that the SUR1 subunit associated to the transient receptor potential "melastatin" 4 (TRPM4) channel protein (forming the NC CaeATP channel) was overexpressed in glial cells under ischemic conditions [24].…”

Section: Introductionmentioning

confidence: 99%

N-Aryl-N′-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: Screening, synthesis of simplified derivatives, and structure–activity relationship analysis

Goffin

Lamoral-Theys

Tajeddine

et al. 2012

European Journal of Medicinal Chemistry

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Expression of Kir 4.1 in human astrocytic tumors: Correlation with pathologic grade

Cited by 18 publications

References 25 publications

Regulation of Kir4.1 expression in astrocytes and astrocytic tumors: a role for interleukin-1 β

Regulation of Kir4.1 expression in astrocytes and astrocytic tumors: a role for interleukin-1 β

Calcium Channels and Associated Receptors in Malignant Brain Tumor Therapy

N-Aryl-N′-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: Screening, synthesis of simplified derivatives, and structure–activity relationship analysis

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