Results: 4

1.
Fig. 1.

Fig. 1. From: Modulation of Na+-K+-ATPase cell surface abundance through structural determinants on the ?1-subunit.

Lactate dehydrogenase (LDH) released by α1- and α1-L499V-expressing opossum kidney (OK) cells exposed to ischemia followed by reperfusion. LDH release was measured as an index of cell injury in the media of α1- and α1-L499V-expressing cells after 110 min Krebs-Henseleit (KH) buffer (C, control, n = 6) or after 20 min KH/30 min substrate/coverslip-induced ischemia/60 min KH (IR60: ischemia-reperfusion 60, n = 6). Values are expressed as means ± SE. ***P < 0.001 and **P < 0.01 vs. respective controls; and #P < 0.05 vs. IR60 α1.

Sandrine V. Pierre, et al. Am J Physiol Cell Physiol. 2011 January;300(1):C42-C48.
2.
Fig. 2.

Fig. 2. From: Modulation of Na+-K+-ATPase cell surface abundance through structural determinants on the ?1-subunit.

Annexin V/propidium iodide (IP) staining in Na+-K+-ATPase α1- and α1-L499V-expressing OK cells exposed to ischemia followed by reperfusion. After treatment, fluorescent staining of Annexin V (green), PI (red), and DAPI (blue) was performed as described in methods, and cells were examined by fluorescence confocal microscopy. C, control (110 min KH); IR60, 20 min KH/30 min substrate/coverslip-induced ischemia/60 min KH. Pictures are representative of at least 10 fields observed in 3 different preparations for each condition in Na+-K+-ATPase α1- and α1-L499V-expressing OK cells. Scale bar = 25 μm.

Sandrine V. Pierre, et al. Am J Physiol Cell Physiol. 2011 January;300(1):C42-C48.
3.
Fig. 4.

Fig. 4. From: Modulation of Na+-K+-ATPase cell surface abundance through structural determinants on the ?1-subunit.

Internalization of Na+-K+-ATPase units in cells exposed to 30 min of substrate/coverslip-induced ischemia followed by 30 min of reperfusion. After treatment, assessment of the amount of endocytosed Na+-K+-ATPase α1 units and immunofluorescent staining of Na+-K+-ATPase α1 were performed as described in methods. A: endocytosed Na+-K+-ATPase. Inset, typical immunoblot of biotinylated endocytosed Na+-K+-ATPase α1 recovered by affinity purification with streptavidin. Graph depicts the pooled data relative to control represented as means ± SE (n = 4). **P < 0.01 vs. control. B: pictures are representative of 6 independent experiments for each condition. C, control (60 min without ischemia); IR30, 30 min substrate/coverslip-induced ischemia followed by 30 min of reperfusion. Scale bar = 10 μM.

Sandrine V. Pierre, et al. Am J Physiol Cell Physiol. 2011 January;300(1):C42-C48.
4.
Fig. 3.

Fig. 3. From: Modulation of Na+-K+-ATPase cell surface abundance through structural determinants on the ?1-subunit.

Surface and total expression of Na+-K+-ATPase units in α1- and α1-L499V-expressing OK cells exposed to 30 min of substrate/coverslip-induced ischemia followed by 5 min of reperfusion. A: surface expression. Top, typical immunoblot of biotinylated membrane proteins recovered by affinity purification with streptavidin. Bottom, pooled data relative to basal expression of wild-type α1 represented as means ± SE (n = 8–10). *P < 0.05 and ***P < 0.001 vs. control α1; ##P < 0.01 vs. C α1-L499V, and $$P < 0.01 vs. IR5 α1. B: total expression. Top, typical immunoblots of cell lysates probed with antibodies specific for rat α1 and actin. Bottom, pooled data relative to basal expression of wild-type α1, represented as means ± SE (n = 8–10). No significant difference was found. IR5, exposed to 30 min coverslip-induced ischemia followed by 5 min of reperfusion.

Sandrine V. Pierre, et al. Am J Physiol Cell Physiol. 2011 January;300(1):C42-C48.

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