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Articles by X. L Wang
Total Records ( 3 ) for X. L Wang
  X. L Wang , W. B Lau , Y. X Yuan , Y. J Wang , W Yi , T. A Christopher , B. L Lopez , H. R Liu and X. L. Ma
 

Diabetes mellitus (DM) is closely related to cardiovascular morbidity and mortality, but the specific molecular basis linking DM with increased vulnerability to cardiovascular injury remains incompletely understood. Methylglyoxal (MG), a precursor to advanced glycation end products (AGEs), is increased in diabetic patient plasma, but its role in diabetic cardiovascular complications is unclear. Thioredoxin (Trx), a cytoprotective molecule with antiapoptotic function, has been demonstrated to be vulnerable to glycative inhibition, but whether Trx is glycatively inhibited by MG, thus contributing to increased cardiac injury, has never been investigated. Cultured H9c2 cardiomyocytes were treated with MG (200 µM) for 6 days. The following were determined pre- and post-simulated ischemia-reperfusion (SI-R; 8 h of hypoxia followed by 3 h of reoxygenation): cardiomyocyte death/apoptosis, Trx expression and activity, AGE formation, Trx-apoptosis-regulating kinase-1 (Trx-ASK1) complex formation, and p38 mitogen-activated protein kinase (MAPK) phosphorylation and activity. Compared with vehicle, MG significantly increased SI-R-induced cardiomyocyte LDH release and apoptosis (P < 0.01). Prior to SI-R, Trx activity was reduced in MG-treated cells, but Trx expression was increased moderately. Moreover, Trx-ASK1 complex formation was reduced, and both p38 MAPK activity and phosphorylation were increased. To investigate the effects of MG on Trx directly, recombinant human Trx (hTrx) was incubated with MG in vitro. Compared with vehicle, MG incubation markedly increased CML formation (a glycation footprint) and inhibited Trx activity. Finally, glycation inhibitor aminoguanidine administration during MG treatment of cultured cells reduced AGE formation, increased Trx activity, restored Trx-ASK1 interaction, and reduced p38 MAPK phosphorylation and activity, caspase-3 activation, and LDH release (P < 0.01). We demonstrated for the first time that methylglyoxal sensitized cultured cardiomyocytes to SI-R injury by posttranslational modification of Trx via glycation. Therapeutic interventions scavenging AGE precursors may attenuate ischemic-reperfusion injury in hyperglycemic state diseases such as diabetes.

  T Lu , D. M Zhang , X. L Wang , T He , R. X Wang , Q Chai , Z. S Katusic and H. C. Lee
 

Rationale: The large conductance Ca2+-activated K+ (BK) channel, a key determinant of vascular tone, is regulated by angiotensin II (Ang II) type 1 receptor signaling. Upregulation of Ang II functions and downregulation of BK channel activities have been reported in diabetic vessels. However, the molecular mechanisms underlying Ang II-mediated BK channel modulation, especially in diabetes mellitus, have not been thoroughly examined.

Objectives: The aim in this study was to determine whether caveolae-targeting facilitates BK channel dysfunction in diabetic vessels.

Methods and Results: Using patch clamp techniques and molecular biological approaches, we found that BK channels, Ang II type 1 receptor, Gq/11 (G protein q/11 subunit), nonphagocytic NAD(P)H oxidases (NOX-1), and c-Src kinases (c-Src) were colocalized in the caveolae of rat arterial smooth muscle cells and the integrity of caveolae in smooth muscle cells was critical for Ang II-mediated BK channel regulation. Most importantly, membrane microdomain targeting of these proteins was upregulated in the caveolae of streptozotocin-induced rat diabetic vessels, leading to enhanced Ang II-induced redox-mediated BK channel modification and causing BK channel and coronary dysfunction. The absence of caveolae abolished the effects of Ang II on vascular BK channel activity and preserved BK channel function in diabetes.

Conclusions: These results identified a molecular scheme of receptor/enzyme/channel/caveolae microdomain complex that facilitates the development of vascular BK channel dysfunction in diabetes.

  Y. N Yang , X. L Wang , Y. T Ma , X Xie , Z. Y Fu , X. M Li , B. D Chen and F. Liu
 

Objectives: Cytochrome P450 (CYP) 2C19 is expressed in vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which are potent endogenous vasodilators and inhibitors of vascular inflammation. The purpose of this study is to explore the relationship between the interaction of CYP2C19*3 polymorphism and smoking and coronary artery disease (CAD) in a Uighur population. Methods: In a Chinese Uighur case-control study of patients with CAD (n = 336) and healthy controls (n = 370), we investigated the roles of polymorphism in the CYP2C19 gene by the use of polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis. Results: The CYP2C19*3 AG + AA genotype was significantly more prevalent in patients with CAD (6.25.0% vs 2.96%; P = .03). Multiple logistic regression analysis showed 4 independent risk factors: the interaction of CYP2C19*3 and smoking (OR 7.22, 95% confidence interval [CI] 2.32-10.23; P = .009), smoking (OR 3.23, 95% CI 1.72-5.44; P = .003), blood sugar (OR 2.12, 95% CI 1.03-4.21; P < .01), and hypertension (OR 1.74, 95% CI 0.98-2.34; P = .013). Conclusions: The CYP2C19*3 polymorphism and CAD were synergistically and significantly associated in Chinese Uighur patients.

 
 
 
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