scholarly journals Acute Oxygen Sensing in Heme Oxygenase-2 Null Mice

2006 ◽  
Vol 128 (4) ◽  
pp. 405-411 ◽  
Author(s):  
Patricia Ortega-Sáenz ◽  
Alberto Pascual ◽  
Raquel Gómez-Díaz ◽  
José López-Barneo
Keyword(s):  
Gene Expression ◽  
K Channel ◽  
Α Subunit ◽  
Organ Growth ◽  
K Channels ◽  
Channel Gene ◽  
Sensitive Organ ◽  
Stress Dependent ◽  
Acute Oxygen Sensing ◽  
O2 Sensing

Hemeoxygenase-2 (HO-2) is an antioxidant enzyme that can modulate recombinant maxi-K+ channels and has been proposed to be the acute O2 sensor in the carotid body (CB). We have tested the physiological contribution of this enzyme to O2 sensing using HO-2 null mice. HO-2 deficiency leads to a CB phenotype characterized by organ growth and alteration in the expression of stress-dependent genes, including the maxi-K+ channel α-subunit. However, sensitivity to hypoxia of CB is remarkably similar in HO-2 null animals and their control littermates. Moreover, the response to hypoxia in mouse and rat CB cells was maintained after blockade of maxi-K+ channels with iberiotoxin. Hypoxia responsiveness of the adrenal medulla (AM) (another acutely responding O2-sensitive organ) was also unaltered by HO-2 deficiency. Our data suggest that redox disregulation resulting from HO-2 deficiency affects maxi-K+ channel gene expression but it does not alter the intrinsic O2 sensitivity of CB or AM cells. Therefore, HO-2 is not a universally used acute O2 sensor.

scholarly journals Effects of Development and Thyroid Hormone on K+Currents and K+Channel Gene Expression in Rat Ventricle

1997 ◽  
Vol 504 (2) ◽  
pp. 271-286 ◽  
Author(s):  
A. D. Wickenden ◽  
R. Kaprielian ◽  
T. G. Parker ◽  
O. T. Jones ◽  
P. H. Backx
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
K Channel ◽  
Channel Gene ◽  
Rat Ventricle ◽  
K Currents

O2 sensing by recombinant TWIK-related halothane-inhibitable K+ channel-1 background K+ channels heterologously expressed in human embryonic kidney cells

Neuroscience ◽  
2005 ◽  
Vol 135 (4) ◽  
pp. 1087-1094 ◽  
Author(s):  
V.A. Campanucci ◽  
S.T. Brown ◽  
K. Hudasek ◽  
I.M. O’Kelly ◽  
C.A. Nurse ◽  
...  
Keyword(s):  
K Channel ◽  
Kidney Cells ◽  
Human Embryonic Kidney ◽  
Human Embryonic Kidney Cells ◽  
K Channels ◽  
O2 Sensing

scholarly journals A Nongenomic Mechanism for Progesterone-mediated Immunosuppression: Inhibition of K+ Channels, Ca2+ Signaling, and Gene Expression in T Lymphocytes

1998 ◽  
Vol 188 (9) ◽  
pp. 1593-1602 ◽  
Author(s):  
George R. Ehring ◽  
Hubert H. Kerschbaum ◽  
Claudia Eder ◽  
Amber L. Neben ◽  
Christopher M. Fanger ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
T Cell ◽  
T Lymphocytes ◽  
Cell Lines ◽  
K Channel ◽  
Na Channel ◽  
Activated T Cells ◽  
K Channels ◽  
Voltage Gated

The mechanism by which progesterone causes localized suppression of the immune response during pregnancy has remained elusive. Using human T lymphocytes and T cell lines, we show that progesterone, at concentrations found in the placenta, rapidly and reversibly blocks voltage-gated and calcium-activated K+ channels (KV and KCa, respectively), resulting in depolarization of the membrane potential. As a result, Ca2+ signaling and nuclear factor of activated T cells (NF-AT)-driven gene expression are inhibited. Progesterone acts distally to the initial steps of T cell receptor (TCR)-mediated signal transduction, since it blocks sustained Ca2+ signals after thapsigargin stimulation, as well as oscillatory Ca2+ signals, but not the Ca2+ transient after TCR stimulation. K+ channel blockade by progesterone is specific; other steroid hormones had little or no effect, although the progesterone antagonist RU 486 also blocked KV and KCa channels. Progesterone effectively blocked a broad spectrum of K+ channels, reducing both Kv1.3 and charybdotoxin–resistant components of KV current and KCa current in T cells, as well as blocking several cloned KV channels expressed in cell lines. Progesterone had little or no effect on a cloned voltage-gated Na+ channel, an inward rectifier K+ channel, or on lymphocyte Ca2+ and Cl− channels. We propose that direct inhibition of K+ channels in T cells by progesterone contributes to progesterone-induced immunosuppression.

Dietary K+ regulates apical membrane expression of maxi-K channels in rabbit cortical collecting duct

2005 ◽  
Vol 289 (4) ◽  
pp. F922-F932 ◽  
Author(s):  
Fadi Najjar ◽  
Hao Zhou ◽  
Tetsuji Morimoto ◽  
James B. Bruns ◽  
Hai-Sheng Li ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Collecting Duct ◽  
K Channel ◽  
Ambystoma Tigrinum ◽  
Intercalated Cells ◽  
Sk Channels ◽  
Cortical Collecting Duct ◽  
Α Subunit ◽  
K Channels ◽  
Channel Density

The cortical collecting duct (CCD) is a final site for regulation of K+ homeostasis. CCD K+ secretion is determined by the electrochemical gradient and apical permeability to K+. Conducting secretory K+ (SK/ROMK) and maxi-K channels are present in the apical membrane of the CCD, the former in principal cells and the latter in both principal and intercalated cells. Whereas SK channels mediate baseline K+ secretion, maxi-K channels appear to participate in flow-stimulated K+ secretion. Chronic dietary K+ loading enhances the CCD K+ secretory capacity due, in part, to an increase in SK channel density (Palmer et al., J Gen Physiol 104: 693–710, 1994). Long-term exposure of Ambystoma tigrinum to elevated K+ increases renal K+ excretion due to an increase in apical maxi-K channel density in their CDs (Stoner and Viggiano, J Membr Biol 162: 107–116, 1998). The purpose of the present study was to test whether K+ adaptation in the mammalian CCD is associated with upregulation of maxi-K channel expression. New Zealand White rabbits were fed a low (LK), control (CK), or high (HK) K+ diet for 10–14 days. Real-time PCR quantitation of message encoding maxi-K α- and β2–4-subunits in single CCDs from HK animals was greater than that detected in CK and LK animals ( P < 0.05); β1-subunit was not detected in any CCD sample but was present in whole kidney. Indirect immunofluorescence microscopy revealed a predominantly intracellular distribution of α-subunits in LK kidneys. In contrast, robust apical labeling was detected primarily in α-intercalated cells in HK kidneys. In summary, K+ adaptation is associated with an increase in steady-state abundance of maxi-K channel subunit-specific mRNAs and immunodetectable apical α-subunit, the latter observation consistent with redistribution from an intracellular pool to the plasma membrane.

scholarly journals Circadian Variation of Cardiac K + Channel Gene Expression

Circulation ◽  
2003 ◽  
Vol 107 (14) ◽  
pp. 1917-1922 ◽  
Author(s):  
Takeshi Yamashita ◽  
Akiko Sekiguchi ◽  
Yu-ki Iwasaki ◽  
Kouichi Sagara ◽  
Hiroyuki Iinuma ◽  
...  
Keyword(s):  
Gene Expression ◽  
Circadian Variation ◽  
K Channel ◽  
Channel Gene
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