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23 results on '"Chellan, Bijoy"'

9. Arsenic Exposure Decreases Adiposity During High‐Fat Feeding

Author

Carmean, Christopher M., primary, Kirkley, Andrew G., additional, Landeche, Michael, additional, Ye, Honggang, additional, Chellan, Bijoy, additional, Aldirawi, Hani, additional, Roberts, Austin A., additional, Parsons, Patrick J., additional, and Sargis, Robert M., additional

Published
2020
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11. S100/calgranulin-mediated inflammation accelerates left ventricular hypertrophy and aortic valve sclerosis in chronic kidney disease in a RAGE dependent manner

Author

Yan, Ling, Mathew, Liby, Chellan, Bijoy, Gardner, Brandon, Earley, Judy, Puri, Tipu S., and Hofmann Bowman, Marion A.

Subjects
Time Factors, Genotype, Receptor for Advanced Glycation End Products, Heart Valve Diseases, Mice, Transgenic, Article, Ventricular Function, Left, Mice, Ventricular Dysfunction, Left, Diastole, Animals, Calgranulin B, Humans, Calgranulin A, Receptors, Immunologic, Renal Insufficiency, Chronic, Cells, Cultured, Inflammation, Mice, Knockout, Sclerosis, Ventricular Remodeling, Myocardium, S100 Proteins, S100A12 Protein, Calcinosis, Fibroblasts, Fibroblast Growth Factors, Mice, Inbred C57BL, Disease Models, Animal, Fibroblast Growth Factor-23, Phenotype, Aortic Valve, Hypertrophy, Left Ventricular, Inflammation Mediators, Leukocyte L1 Antigen Complex, Signal Transduction
Abstract

S100A12 and fibroblast growth factor 23 are biomarkers of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). We tested the hypothesis that human S100/calgranulin would accelerate cardiovascular disease in mice subjected to CKD.A bacterial artificial chromosome of the human S100/calgranulin gene cluster containing the genes and regulatory elements for S100A8, S100A9, and S100A12 was expressed in C57BL/6J mouse (hBAC-S100) to generate a novel humanized mouse model. CKD was induced by ureteral ligation, and hBAC-S100 mice and wild-type mice were studied after 10 weeks of chronic uremia. hBAC-S100 mice with CKD showed increased fibroblast growth factor 23 in the hearts, left ventricular hypertrophy, diastolic dysfunction, focal cartilaginous metaplasia, and calcification of the mitral and aortic valve annulus together with aortic valve sclerosis. This phenotype was not observed in wild-type mice with CKD or in hBAC-S100 mice lacking the receptor for advanced glycation end products with CKD, suggesting that the inflammatory milieu mediated by S100/receptor for advanced glycation end products promotes pathological cardiac hypertrophy in CKD. In vitro, inflammatory stimuli including interleukin-6, tumor necrosis factor-α, lipopolysaccarides, or serum from hBAC-S100 mice upregulated fibroblast growth factor 23 mRNA and protein in primary murine neonatal and adult cardiac fibroblasts.Myeloid-derived human S100/calgranulin is associated with the development of cardiac hypertrophy and ectopic cardiac calcification in a receptor for advanced glycation end products-dependent manner in a mouse model of CKD. We speculate that fibroblast growth factor 23 produced by cardiac fibroblasts in response to cytokines may act in a paracrine manner to accelerate left ventricular hypertrophy and diastolic dysfunction in hBAC-S100 mice with CKD.

Published
2014

22. Abstract 14884: Activation of AMPK-Activated Protein Kinases Prevents Atrial Fibrillation

Author

Ozcan, Cevher, Li, Zhenping, and Chellan, Bijoy

Abstract

Introduction:There is no effective therapy for the primary prevention of atrial fibrillation (AF). Inhibition of AMP-activated protein kinase (AMPK) causes spontaneous AF in cardiac specific LKB1 knockout (KO) mice. Yet, it is not known whether pharmacological activation of AMPK activity prevents AF. We aimed to test the efficacy of AMPK activators, metformin and aspirin, in primary prevention of AF.Hypothesis:Activation of AMPK can prevent AF in susceptible heart by preserving atrial electroanatomical property.Methods:LKB1 KO mice were treated with AMPK activators, metformin (5-20 mg/kg/day, n=108) or aspirin (20-40 mg/kg/day, n=62). The treated mice were compared with untreated littermates (n=86) and wild type (WT, n=49). Incidence of AF, atrial electroanatomical property and sex-based differences were analyzed at 8 weeks of age in all groups.Results:Incidence of spontaneous AF was significantly reduced in LKB1 KO mice with metformin 10 mg/kg/day (8.3% in male and 10.3% in female) and aspirin 20 mg/kg/day (29.4% in male and 21.4% in female) treatment compared to the age- and gender-matched untreated littermates (81% in male and 67% in female) (p<0.05). Prevention of AF was associated with activation of AMPK as pAMPK? 0.48?0.03 with metformin, 0.37?0.06 with aspirin, 0.17?0.04 in untreated and 1.01?0.05 AU in WT mice (p<0.05). In treated mice, activation of AMPK was associated with reduced atrial fibrosis and enlargement while preserving gap junction proteins (connexin 40/43), SERCA2, vasculature, intra- and inter-cellular ultrastructure in atrial myocardium.Conclusions:Activation of AMPK with metformin or aspirin prevents AF in a susceptible heart. It is an effective upstream pharmacotherapy for primary prevention of AF by preserving atrial electroanatomical substrate.

Published
2019
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23. Abstract 10900: Enzyme-Modified Non-Oxidized LDL (ELDL) Transforms Human Coronary Artery Smooth Muscle Cells to Migratory Osteoblast-Like Cells.

Author

Hofmann Bowman, Marion A, Chellan, Bijoy, and Rojas, Elizabeth

Subjects
*MUSCLE cells, *SMOOTH muscle, *CORONARY arteries, *LOW density lipoproteins, *VASCULAR smooth muscle
Abstract

Introduction: Enzyme modified non-oxidative LDL (ELDL) is effectively taken up by vascular smooth muscle cells and mediates transition into foam cells. ELDL co-localizes with calcification spots in human atherosclerotic tissue and in aortic valve calcification. Hypothesis: We hypothesize that uptake of ELDL promotes expression of osteoblastic genes in SMC and transition to osteoblast-like cells. Methods: Human coronary artery smooth muscle cells (HCASMC) were incubated with ELDL (10 μg/ml), oxidized LDL (200 μg/ml) or native LDL (200 μg/ml; p<0.01) and microarray gene analysis and bioinformatic network analysis and functional assays were performed. Results: ELDL was more potent than oxLDL or native LDL in inducing foam cell formation in HCASMC. There were distinct difference in the transcriptome of HCASMCs stimulated either with ELDL, oxLDL, native LDL or control (BSA) and activation of p38 MAPK, NFkB, and pERK were identified as top canonical pathways in ELDL-treated HCASMC. Functional studies confirmed increased activation of p38MAPK, NFkB and pERK upon stimulation with ELDL. Moreover, HCASMC had increased migration upon stimulation with ELDL (10 μg/ml) or ANGPTL4 (5 μg/ml), and a gain in osteoblastic gene expression with significant increase in mRNA levels for DMP-1, ALPL, RUNX2, OPN/SPP1, osterix/SP7, BMP and reduction in mRNA for MGP and ENPP. Enhanced calcification of HCASMC by ELDL was demonstrated by Alizarin Red staining. Conclusions: ELDL is highly potent in inducing foam cells in HCASMC and mediates a phenotypic switch with enhanced migration and osteoblastic gene profile. These results point to the potential of ELDL to induce migratory and osteoblastic effects in human smooth muscle cells with potential implications for migration and calcification of SMCs in human atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2018

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