Nitric oxide down‐regulates caveolin‐1 expression in rat brains during focal cerebral ischemia and reperfusion injury

Shen, Jiangang; Ma, Stephanie; Chan, P.; Lee, Waisin; Fung, Peter C. W.; Cheung, Raymond Tak Fai; Tong, Yao; Liu, Ke Jian

doi:10.1111/j.1471-4159.2005.03589.x

Cited by 75 publications

(72 citation statements)

References 58 publications

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“…The knockdown of Cav-1 reduces matrix metalloproteinase (MMPs) activity in endothelial cells and their angiogenic response to vascular endothelial growth factor (VEGF) [12]. On the contrary, the loss of Cav-1 is crucial in the activation of MMPs and BBB breakdown in stroke animal models [13]. Cav-1 regulates expression of junction-associated proteins in brain microvascular endothelial cells, and attenuated Cav-1 levels are correlated with heightened permeability of endothelia [14].…”

Section: Electronic Supplementary Materialsmentioning

confidence: 99%

Regulation of Caveolin-1 and Junction Proteins by bFGF Contributes to the Integrity of Blood–Spinal Cord Barrier and Functional Recovery

Xia

et al. 2016

Neurotherapeutics

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The blood-spinal cord barrier (BSCB) plays important roles in the recovery of spinal cord injury (SCI), and caveolin-1 is essential for the integrity and permeability of barriers. Basic fibroblast growth factor (bFGF) is an important neuroprotective protein and contributes to the survival of neuronal cells. This study was designed to investigate whether bFGF is beneficial for the maintenance of junction proteins and the integrity of the BSCB to identify the relations with caveolin-1 regulation. We examined the integrity of the BSCB with Evans blue dye and fluorescein isothiocyanate-dextran extravasation, measured the junction proteins and matrix metalloproteinases, and evaluated the locomotor function recovery. Our data indicated that bFGF treatment improved the recovery of BSCB and functional locomotion in contusive SCI model rats, reduced the expression and activation of matrix metalloproteinase-9, and increased the expressions of caveolin-1 and junction proteins, including occludin, claudin-5, p120-catenin, and β-catenin. In the brain, in microvascular endothelial cells, bFGF treatment increased the levels of junction proteins, caveolin-1 small interfering RNA abolished the protective effect of bFGF under oxygen-glucose deprivation conditions, and the expression of fibroblast growth factor receptor 1 and co-localization with caveolin-1 decreased significantly, which could not be reversed by bFGF treatment. These findings provide a novel mechanism underlying the beneficial effects of bFGF on the BSCB and recovery of SCI, especially the regulation of caveolin-1.

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Section: Electronic Supplementary Materialsmentioning

confidence: 99%

Regulation of Caveolin-1 and Junction Proteins by bFGF Contributes to the Integrity of Blood–Spinal Cord Barrier and Functional Recovery

Xia

et al. 2016

Neurotherapeutics

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“…Transient middle cerebral artery occlusion (MCAO) was induced using the intraluminal filament technique (22,23). After 1 h of ischemia, the rats in the treatment groups were administered ISF-1 orally twice daily at the dose of 2.5 g dry powder per kg body weight until their sacrifice.…”

Section: Rat Ischemic Stroke Model and Drug Treatmentmentioning

confidence: 99%

Induction of heme oxygenase-1 by traditional Chinese medicine formulation ISF-1 and its ingredients as a cytoprotective mechanism against oxidative stress

Cheung¹,

Lau²,

Shen³

et al. 2008

Int J Mol Med

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Abstract. Traditional medicines are clinically used to treat post-stroke disorders in China. In search of alternative medicines for post-stroke rehabilitation, we recently identified the heme oxygenase-1 (HO-1) pathway as a key mechanism underlying the biological activities of the ischemic stroke formulation ISF-1. This study was designed to further investigate ISF-1 for HO-1 induction in cultured human cells and corresponding cytoprotective effects against oxidative injury. A rat stroke model induced by middle cerebral artery occlusion was employed to verify the activity of ISF-1 in vivo. It was found that HO-1 expression was induced by ISF-1 in a dose-and time-dependent manner. Four ingredients from ISF-1 were identified to be responsible for HO-1 induction. The appropriate combinations of these active ingredients or purified compounds resulted in synergistic induction of HO-1 expression. A minimal HO-1-inducing formulation was prepared and showed significant cytoprotection against H 2 O 2 -induced oxidative stress. Collectively, the herbal formulation ISF-1 was capable of inducing HO-1 expression, in vitro and in vivo, offering a potential mechanism for post-stroke rehabilitation. This study may shed light on the development of mechanism-defined therapies based on traditional herbal remedies.

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“…A substantial increase in the expression of iNOS (Shen et al, 2006), HSP70 (Liu et al, 2005a), and S-100 ␤ activity (Buttner et al, 1997) after cerebral ischemia has been reported. Our results revealed that the overexpression of iNOS, HSP70, and S-100 ␤ were induced by ischemia and decreased significantly by PF preconditioning (Fig.…”

Section: Resultsmentioning

confidence: 99%

Involvement of Multitargets in Paeoniflorin-Induced Preconditioning

Chen¹,

Liang²,

Cai³

et al. 2006

J Pharmacol Exp Ther

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Paeoniflorin (PF) is the principal component of Paeoniae radix prescribed in traditional Chinese medicine. The delayed neuroprotection induced by PF preconditioning and its underlying mechanisms were investigated in rat middle cerebral artery occlusion (MCAO) and reperfusion model. At a dosage of 20 or 40 mg/kg, PF preconditioning 48 h before MCAO followed by 24-h reperfusion significantly reduced the mortality and infarct volume and reversed the neurological deficits caused by ischemia. Likewise, the ameliorative effects on mortality, infarct size, and neurological impairment induced by MCAO emerged as well when PF was administered 24 h, 48 h, or 5 days before MCAO at the dose of 20 mg/kg. Furthermore, comparative proteomics analysis was adopted to identify the differentially expressed proteins induced by PF preconditioning itself. The relative levels of 42 proteins were altered after PF preconditioning, among which 20 were elevated and 22 reduced. In summary, A 1 receptor-regulator of G protein signaling-K ATP signaling, arachidonic acid cascade, nitric oxide system, markers of neuronal damage, mitochondrial damage-related molecules, and the mitogen-activated protein kinase and nuclear factor-B pathway are associated with the mechanisms of PF preconditioning.Ischemic stroke is the second leading cause of death in China, leaving survivors burdened with severe disabilities. Deleterious infarctions of the middle cerebral artery (MCA) are at risk of developing massive edema because of the necrosis of cells located in the primary zone (Borlongan et al., 2005). The most effective drug, tissue plasminogen activator, the only Food and Drug Administration-approved thrombolytic drug used in ischemia, is widely employed in clinic. However, it has a very narrow therapeutic time window of 3 h, and only 1 to 3% of ischemic stroke patients have been benefited (Pulsinelli et al., 1997). Therefore, the current focus of stroke research requires investigation of novel neuroprotective agents and strategies, which could prolong the therapeutic window.Paeoniflorn (PF), the principal component of Paeoniae radix ("Shaoyao" in Chinese), has been widely investigated as antioxidant, cognitive enhancer, and endothelium-dependent vasodilator Ryu et al., 2001;Tabata et al., 2001). Recently, our laboratory found that PF could produce a dose-dependent decrease in both neurological impairment and infarct volume in acute transient cerebral ischemia through activating adenosine A 1 receptor in a manner different from its classic agonists (Liang et al., 2005;Liu et al., 2005b).Ischemic preconditioning (IPC) is an endogenous mechanism by which brief episodes of a sublethal insult induce a robust protection against the deleterious effects of subsequent, prolonged lethal ischemia. There are two kinds of protection: "classic IPC" and "delayed IPC." Various drugs ABBREVIATIONS: MCA, middle cerebral artery; PF, paeoniflorn; IPC, ischemic preconditioning; PPC, pharmacological preconditioning; DPCPX, 8-cyclopentyl-1,3-dipropylxanthine; TTC, 2,3,...

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Nitric oxide down‐regulates caveolin‐1 expression in rat brains during focal cerebral ischemia and reperfusion injury

Cited by 75 publications

References 58 publications

Regulation of Caveolin-1 and Junction Proteins by bFGF Contributes to the Integrity of Blood–Spinal Cord Barrier and Functional Recovery

Regulation of Caveolin-1 and Junction Proteins by bFGF Contributes to the Integrity of Blood–Spinal Cord Barrier and Functional Recovery

Induction of heme oxygenase-1 by traditional Chinese medicine formulation ISF-1 and its ingredients as a cytoprotective mechanism against oxidative stress

Involvement of Multitargets in Paeoniflorin-Induced Preconditioning

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