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Charleston, SC, United States

Charleston Southern University, founded in 1964 as Baptist College, is an independent comprehensive university located in North Charleston, South Carolina. Charleston Southern enrolls 3,300 students. Affiliated with the South Carolina Baptist Convention, the university's vision is to be nationally recognized for integrating faith in learning, leading and serving. Wikipedia.

Shen B.,Medical University of South Carolina | Gao L.,Medical University of South Carolina | Hsu Y.-T.,Medical University of South Carolina | Bledsoe G.,Charleston Southern University | And 3 more authors.
American Journal of Physiology - Heart and Circulatory Physiology | Year: 2010

Kallistatin is a regulator of vascular homeostasis capable of controlling a wide spectrum of biological actions in the cardiovascular and renal systems. We previously reported that kallistatin inhibited intracellular reactive oxygen species formation in cultured cardiac and renal cells. The present study was aimed to investigate the role and mechanisms of kallistatin in protection against oxidative stress-induced vascular injury and endothelial cell apoptosis. We found that kallistatin gene delivery significantly attenuated aortic superoxide formation and glomerular capillary loss in hypertensive DOCA-salt rats. In cultured endothelial cells, kallistatin suppressed TNF-α-induced cellular apoptosis, and the effect was blocked by the pharmacological inhibition of phosphatidylinositol 3-kinase and nitric oxide synthase (NOS) and by the knockdown of endothelial NOS (eNOS) expression. The transduction of endothelial cells with adenovirus expressing dominant-negative Akt abolished the protective effect of kallistatin on endothelial apoptosis and caspase activity. In addition, kallistatin inhibited TNF-α-induced reactive oxygen species formation and NADPH oxidase activity, and these effects were attenuated by phosphatidylinositol 3-kinase and NOS inhibition. Kallistatin also prevented the induction of Bim protein and mRNA expression by oxidative stress. Moreover, the downregulation of forkhead box O 1 (FOXO1) and Bim expression suppressed TNF-α-mediated endothelial cell death. Furthermore, the antiapoptotic actions of kallistatin were accompanied by Akt-mediated FOXO1 and eNOS phosphorylation, as well as increased NOS activity. These findings indicate a novel role of kallistatin in the protection against vascular injury and oxidative stress-induced endothelial apoptosis via the activation of Akt-dependent eNOS signaling. Copyright © 2010 the American Physiological Society.

Lo C.C.,University of Alabama | Howell R.J.,Charleston Southern University | Cheng T.C.,University of Alabama
Journal of Interpersonal Violence | Year: 2015

This study sought the factors associated with race/ethnicity disparities in the age at which homicide deaths tend to occur. We used the multiple disadvantage model to take race into account as we evaluated associations between age at time of homicide victimization and several social structural, mental health−related, and lifestyle factors. Data were derived from the 1993 National Mortality Followback Survey, a cross-sectional interview study of spouses, next of kin, other relatives, and close friends of individuals 15 years and older who died in the United States in 1993. Our results showed age at time of homicide mortality to be related to the three types of factors; race moderated some of these relationships. In general, being employed, married, and a homeowner appeared associated with reduced victimization while young. The relationship of victimization age and employment was not uniform across racial groups, nor was the relationship of victimization age and marital status uniform across groups. Among Blacks, using mental health services was associated with longer life. Homicide by firearm proved important for our Black and Hispanic subsamples, while among Whites, alcohol’s involvement in homicide exerted significant effects. Our results suggest that programs and policies serving the various racial/ethnic groups can alleviate multiple disadvantages relevant in homicide victimization at an early age. © The Author(s) 2014.

Chao J.,Medical University of South Carolina | Liu Y.,Medical University of South Carolina | Bledsoe G.,Charleston Southern University | Hagiwara M.,Medical University of South Carolina | And 2 more authors.
American Journal of Physiology - Renal Physiology | Year: 2012

Kallistatin (KS) levels are reduced in the kidney and blood vessels under oxidative stress conditions. To determine the function of endogenous KS in the renal and cardiovascular systems, KS levels were depleted by daily injection of anti-rat KS antibody into DOCA-salt hypertensive rats for 10 days. Administration of anti-KS antibody resulted in reduced KS levels in the circulation but increased levels of serum thiobarbituric acid reactive substances (an indicator of lipid peroxidation) as well as superoxide formation in the aorta. Moreover, anti-KS antibody injection resulted in increased NADH oxidase activity and superoxide production but decreased nitric oxide levels in the kidney and heart. Endogenous KS blockade aggravated renal dysfunction, damage, hypertrophy, inflammation, and fibrosis as evidenced by decreased creatinine clearance and increased serum creatinine, blood urea nitrogen and urinary protein levels, tubular dilation, protein cast formation, glomerulosclerosis, glomerular enlargement, inflammatory cell accumulation, and collagen deposition. In addition, rats receiving anti-KS antibody had enhanced cardiac injury as indicated by cardiomyocyte hypertrophy, inflammation, myofibroblast accumulation, and fibrosis. Renal and cardiac injury caused by endogenous KS depletion was accompanied by increases in the expression of the proinflammatory genes tumor necrosis factor-α and intercellular adhesion molecule-1 and the profibrotic genes collagen I and III, transforming growth factor-β;, and tissue inhibitor of metalloproteinase-1. Taken together, these results implicate an important role for endogenous KS in protection against salt-induced renal and cardiovascular injury in rats by suppressing oxidative stress, inflammation, hypertrophy, and fibrosis. © 2012 the American Physiological Society.

Zhang J.,Medical University of South Carolina | Yang Z.,Medical University of South Carolina | Li P.,Medical University of South Carolina | Bledsoe G.,Charleston Southern University | And 2 more authors.
Molecular and Cellular Biochemistry | Year: 2013

Kallistatin, a plasma protein, exerts pleiotropic effects in inhibiting angiogenesis, inflammation and tumor growth. Canonical Wnt signaling is the primary pathway for oncogenesis in the mammary gland. In this study, we demonstrate that kallistatin bound to the Wnt coreceptor low-density lipoprotein receptor-related protein 6 (LRP6), thus, blocking Wnt/β-catenin signaling and Wnt-mediated growth and migration in MDA-MB-231 breast cancer cells. Kallistatin inhibited Wnt3a-induced proliferation, migration, and invasion of cultured breast cancer cells. Moreover, kallistatin was bound to LRP6 in breast cancer cells, as identified by immunoprecipitation followed by western blot. Kallistatin suppressed Wnt3a-mediated phosphorylation of LRP6 and glycogen synthase kinase-3β, and the elevation of cytosolic β-catenin levels. Furthermore, kallistatin antagonized Wnt3a-induced expression of c-Myc, cyclin D1, and vascular endothelial growth factor. These findings indicate a novel role of kallistatin in preventing breast tumor growth and mobility by direct interaction with LRP6, leading to blockade of the canonical Wnt signaling pathway. © 2013 Springer Science+Business Media New York.

Baker L.,Charleston Southern University
Fire Rescue Magazine | Year: 2014

This incident proves that consistent, realistic and diverse training does pay off. Responders at this incident coordinated their efforts with other agencies and utilized a combination of uncommon and common tactics to successfully mitigate the incident.

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