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1.

Fig. 5. Rieske iron-sulfur protein silencing prevents, whereas rieske gene overexpression enhances, the hypoxic ROS production in isolated PASM mitochondria and cells. From: Primary role of mitochondrial Rieske iron-sulfur protein in hypoxic ROS production in pulmonary artery myocytes.

(A) Effect of Rieske iron-sulfur protein silencing on the hypoxic ROS production in isolated mitochondria from PASMCs. (B) Effect of Rieske iron-sulfur protein silencing on mitochondrial ROS production in PASMCs. (C) Effect of Rieske iron-sulfur protein overexpression on the hypoxic ROS production in isolated mitochondria from PASMCs. (D) Effect of Rieske iron-sulfur protein overexpression on mitochondrial ROS production in PASMCs.

Amit S. Korde, et al. Free Radic Biol Med. ;50(8):945-952.
2.
Fig. 4

Fig. 4. Rieske iron-sulfur protein overexpression augments the hypoxic ROS generation in complex III from PASMCs. From: Primary role of mitochondrial Rieske iron-sulfur protein in hypoxic ROS production in pulmonary artery myocytes.

(A) Western blotting images show Rieske iron-sulfur protein and GAPDH protein expression in PASMCs untransfected (control) and transfected with Rieske iron-sulfur gene or expression vector alone. Graph depicts the effect of Rieske iron-sulfur protein overexpression on its protein expression in PASMCs. (B) Effect of Rieske iron-sulfur protein overexpression on the hypoxic increase in isolated complex III activity. (C) Effect of Rieske iron-sulfur protein overexpression on the hypoxic ROS production in isolated complex III.

Amit S. Korde, et al. Free Radic Biol Med. ;50(8):945-952.
3.
Fig. 2

Fig. 2. Hypoxia significantly increases ROS production in isolated complex III from PASMCs. From: Primary role of mitochondrial Rieske iron-sulfur protein in hypoxic ROS production in pulmonary artery myocytes.

(A) Effect of hypoxia on ROS formation (H2DCF fluorescence) in isolated complex III. (B) Representative Western blots show the presence of the complex III subunit Core 1 protein, but not the complex IV subunit COX IV protein in isolated complex III samples. (C) Effect of hypoxia on isolated complex III activity, gauged by assessing the absorbance of cytochrome c reduction at 550 nm.

Amit S. Korde, et al. Free Radic Biol Med. ;50(8):945-952.
4.
Fig. 6

Fig. 6. Rieske iron-sulfur protein silencing inhibits HPV and hypoxic increase in [Ca2+]i in PASMCs. From: Primary role of mitochondrial Rieske iron-sulfur protein in hypoxic ROS production in pulmonary artery myocytes.

(A) Representative Western blots show Rieske iron-sulfur protein expression in PAs untransfected (control) and transfected with Rieske iron-sulfur protein siRNAs by reverse permeabilization. Bar graph summarizes the effect of Rieske iron-sulfur protein and scrambled siRNAs on Rieske iron-sulfur protein expression levels. (B) A representative recording illustrates hypoxic vasoconstriction in an isolated pulmonary artery. Graph shows the effect of Rieske iron-sulfur protein silencing on HPV. (C) Effect of Rieske iron-sulfur protein silencing on the hypoxic increase in [Ca2+]i in PASMCs. The Number in parenthesis indicates the number of independent experiments performed from 3 separate preparations.

Amit S. Korde, et al. Free Radic Biol Med. ;50(8):945-952.
5.

Fig. 3. Rieske iron-sulfur protein silencing blocks the hypoxic ROS production in isolated complex III from PASMCs. From: Primary role of mitochondrial Rieske iron-sulfur protein in hypoxic ROS production in pulmonary artery myocytes.

(A) Effect of siRNA-mediated Rieske iron-sulfur protein silencing on its protein expression in PASMCs. Representative Western blots illustrate Rieske iron-sulfur protein and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein expression in PASMCs untransfected (control) and transfected with Rieske iron-sulfur protein siRNAs or scrambled siRNAs. Bar graph summarizes the effect of Rieske iron-sulfur protein siRNAs on Rieske iron-sulfur protein expression levels. *P<0.05 compared with untransfected cells (control). (B) Effect of Rieske iron-sulfur protein silencing on the acute hypoxic increase in the activity of isolated complex III. *P<0.05 compared with normoxic, untransfected samples; #P<0.05 compared with hypoxic, untransfected samples. (C) Effect of Rieske iron-sulfur protein silencing on the hypoxic increase in ROS formation in isolated complex III. (D) Effect of acute hypoxia on Rieske iron-sulfur protein expression in PASMCs.

Amit S. Korde, et al. Free Radic Biol Med. ;50(8):945-952.
6.

Fig. 1. Hypoxia causes a large increase in ROS production in isolated mitochondria from PASMCs. From: Primary role of mitochondrial Rieske iron-sulfur protein in hypoxic ROS production in pulmonary artery myocytes.

(A) Representative electron microscopic image of isolated mitochondria. (B) Cytochrome c release in isolated mitochondria before and after application of Triton X-100 (1 mM) for 5 min. Numbers in parentheses mean the number of independent experiments performed. *P<0.05 compared with control (before application of Triton X-100). (C) Effect of acute hypoxic exposure for 5 min on ROS production, determined by assessing the fluorescence of the ROS detection dye H2DCF, in isolated mitochondria. (D) Effect of acute hypoxia on ATP production in isolated mitochondria. (E) Effect of hypoxia on respiration activity in isolated mitochondria. (F) Effect of hypoxia on mitochondrial inter-membrane space ROS production, examined by measuring the fluorescence of the specific ROS biosensor pHyPer, in isolated PASMCs. (G) Effect of H2O2 on HyPer signals in isolated PASMCs.

Amit S. Korde, et al. Free Radic Biol Med. ;50(8):945-952.

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