Calluses from two ecotypes of reed (Phragmites communis Trin.) plant (dune reed [DR] and swamp reed [SR]), which show different sensitivity to salinity, were used to study plant adaptations to salt stress. Under 200 mm NaCl treatment, the sodium (Na) percentage decreased, but the calcium percentage and the potassium (K) to Na ratio increased in the DR callus, whereas an opposite changing pattern was observed in the SR callus. Application of sodium nitroprusside (SNP), as a nitric oxide (NO) donor, revealed that NO affected element ratios in both DR and SR calluses in a concentration-dependent manner. N -nitro-l-arginine (an NO synthase inhibitor) and 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxyde (a specific NO scavenger) counteracted NO effect by increasing the Na percentage, decreasing the calcium percentage and the K to Na ratio. The increased activity of plasma membrane (PM) H ϩ -ATPase caused by NaCl treatment in the DR callus was reversed by treatment with N -nitro-l-arginine and 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxyde. Western-blot analysis demonstrated that NO stimulated the expression of PM H ϩ -ATPase in both DR and SR calluses. These results indicate that NO serves as a signal in inducing salt resistance by increasing the K to Na ratio, which is dependent on the increased PM H ϩ -ATPase activity.When plants are exposed to NaCl, cellular ion homeostasis may be impaired. Under salinity conditions, tolerant plants typically maintain high potassium (K ϩ ) and low sodium (Na ϩ ) in the cytosol of cells (Greenway and Munns, 1980; Jeschke, 1984). Such mechanisms involve Na ϩ compartmentalization into vacuoles and/or extrusion to the external medium and K ϩ accumulation in the cytoplasm. These processes appear to be mediated by several transport systems, such as H ϩ -ATPase, carriers (symporters and antiporters), and channels associated with plasma membranes (PMs) and tonoplasts (Niu et al., 1995; Rausch et al., 1996).Control of Na ϩ movement across the PM and tonoplast to maintain a low Na ϩ concentration in the cytoplasm is a key factor of cellular adaptation to salt stress (Niu et al., 1995; Rausch et al., 1996). Na ϩ transport across the PM is dependent on the electrochemical gradient created by the PM H ϩ -ATPase (Serrano, 1996). PM H ϩ -ATPase belongs to a family of P-type ATPase, which has a catalytic subunit of approximately 100 kD. This enzyme is a proton pump, whose major role couples ATP hydrolysis to proton transport and creates electrochemical gradient across the PM used by secondary transporters (Serrano, 1989). In addition, this membrane protein is involved in many physiological processes, including salt tolerance, intracellular pH regulation, stomatal opening, and cell elongation (Rayle and Cleland, 1992;Niu et al., 1993; Michelet and Boutry, 1995; Cosgrove, 1997; Kerkeb et al., 2001; Yang et al., 2003). The PM H ϩ -ATPase is encoded by a multigene family, and at least 10 isoforms of the H ϩ -ATPase exist in plants. Krysan et al. (1996) analyzed T-DNA knockout Arab...

Limb remote ischemic preconditioning (RIPC) is an effective means of protection against ischemia/reperfusion (IR)–induced injury to multiple organs. Many studies are focused on identifying endocrine mechanisms that underlie the cross-talk between muscle and RIPC-mediated organ protection. We report that RIPC releases irisin, a myokine derived from the extracellular portion of fibronectin domain–containing 5 protein (FNDC5) in skeletal muscle, to protect against injury to the lung. Human patients with neonatal respiratory distress syndrome show reduced concentrations of irisin in the serum and increased irisin concentrations in the bronchoalveolar lavage fluid, suggesting transfer of irisin from circulation to the lung under physiologic stress. In mice, application of brief periods of ischemia preconditioning stimulates release of irisin into circulation and transfer of irisin to the lung subjected to IR injury. Irisin, via lipid raft–mediated endocytosis, enters alveolar cells and targets mitochondria. Interaction between irisin and mitochondrial uncoupling protein 2 (UCP2) allows for prevention of IR-induced oxidative stress and preservation of mitochondrial function. Animal model studies show that intravenous administration of exogenous irisin protects against IR-induced injury to the lung via improvement of mitochondrial function, whereas in UCP2-deficient mice or in the presence of a UCP2 inhibitor, the protective effect of irisin is compromised. These results demonstrate that irisin is a myokine that facilitates RIPC-mediated lung protection. Targeting the action of irisin in mitochondria presents a potential therapeutic intervention for pulmonary IR injury.

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