المؤلفون: Anandan, Vinitha, Thankayyan Retnabai, Santhosh Kumar, Jaleel, Abdul, Thulaseedharan, Thushara, Mullasari, Ajit, Pillai, M. Radhakrishna, Kartha, Cheranellore Chandrasekharan, Ramachandran, Surya

المصدر: FASEB BioAdvances ; volume 3, issue 5, page 305-322 ; ISSN 2573-9832 2573-9832

الإتاحة: https://doi.org/10.1096/fba.2020-00135Test

المؤلفون: Ramachandran, Surya, Vinitha, Anandan, Kartha, Cheranellore Chandrasekharan

المساهمون: Indian Council of Medical Research

المصدر: Cardiovascular Diabetology ; volume 15, issue 1 ; ISSN 1475-2840

مصطلحات موضوعية: Cardiology and Cardiovascular Medicine, Endocrinology, Diabetes and Metabolism

الإتاحة: https://doi.org/10.1186/s12933-016-0467-5Test

المؤلفون: Ramachandran, Surya, Anandan, Vinitha, Kutty, V. R., Mullasari, Ajit, Pillai, M. Radhakrishna, Kartha, Cheranellore Chandrasekharan

المصدر: Clinical Science ; volume 132, issue 6, page 719-738 ; ISSN 0143-5221 1470-8736

مصطلحات موضوعية: General Medicine

الوصف: Growing evidence implicates cyclophilin A secreted by vascular wall cells and monocytes as a key mediator in atherosclerosis. Cyclophilin A in addition to its proliferative effects, during hyperglycemic conditions, increases lipid uptake in macrophages by increasing scavenger receptors on the cell’s surface. It also promotes macrophage migration across endothelial cells and conversion of macrophages into foam cells. Given the known effects of metformin in reducing vascular complications of diabetes, we investigated the effect of metformin on cyclophilin A action in macrophages. Using an ex vivo model of cultured macrophages isolated from patients with type 2 diabetes with and without coronary artery disease (CAD), we measured the effect of metformin on cyclophilin A expression, lipid accumulation, expression of scavenger receptors, plasma cytokine levels and AMP-activated protein kinase (AMPK) activity in macrophages. In addition, the effects of metformin on migration of monocytes, reactive oxygen species (ROS) formation, lipid uptake in the presence of cyclophilin A inhibitors and comparison with pioglitazone were studied using THP-1 monocytes. Metformin reduced cyclophilin A expression in human monocyte-derived macrophages. Metformin also decreased the effects of cyclophilin A on macrophages such as oxidized low-density lipoprotein (oxLDL) uptake, scavenger receptor expression, ROS formation and secretion of inflammatory cytokines in high-glucose conditions. Metformin reversed cyclophilin A-induced decrease in AMPK-1α activity in macrophages. These effects of metformin were similar to those of cyclophilin A inhibitors. Metformin can thus function as a suppressor of pro-inflammatory effects of cyclophilin A in high-glucose conditions by attenuating its expression and repressing cyclophilin A-induced decrease in AMPK-1α activity in macrophages.

الإتاحة: https://doi.org/10.1042/cs20171523Test
https://portlandpress.com/clinsci/article-pdf/132/6/719/446472/cs-2017-1523.pdfTest

المؤلفون: Nampi, Padmaja Parameswaran, Kartha, Cheranellore Chandrasekharan, Jose, Gin, P.R., Anil Kumar, Anilkumar, Thapasimuthu, Varma, Harikrishna

المصدر: Sensors and Actuators B: Chemical ; volume 185, page 252-257 ; ISSN 0925-4005

مصطلحات موضوعية: Materials Chemistry, Electrical and Electronic Engineering, Metals and Alloys, Surfaces, Coatings and Films, Condensed Matter Physics, Instrumentation, Electronic, Optical and Magnetic Materials

الإتاحة: https://doi.org/10.1016/j.snb.2013.04.067Test
https://api.elsevier.com/content/article/PII:S0925400513005005?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0925400513005005?httpAccept=text/plainTest

المؤلفون: Ajithkumar, Santhambika Gopinathan nair, Ramachandran, Surya, Kartha, Cheranellore Chandrasekharan

مصطلحات موضوعية: R Medicine (General)

الوصف: Reactive oxygen species (ROS) are increasingly recognised as a major cause for altering normal endothelial cell functions. Several studies have revealed that pharmacological agents in the treatment of various diseases can increase ROS load in the body and result in endothelial dysfunction. Anti cancer drugs, immunosuppressive drugs, anti-retroviral drugs, aldosterone and aldosterone antagonists, diethyldithiocarbamate, nanoparticle drugs and drug carriers have been found to cause endothelial dysfunction through oxidative stress. ROS mediated endothelial dysfunction can adversely affect bioavailability of nitric oxide, endothelium-dependent vasodilatation, cell permeability, endothelial cell growth and survival. Whether anti oxidant therapies would really be beneficial to prevent the endothelial oxidative stress associated drugs is unclear. Redox biology of drug induced endothelial dysfunction involves highly complex pathways. Understanding mechanisms of regulated generation of ROS in endothelial cells and downstream effects are necessary to design appropriate therapeutic measures. The functional role of ROS in drug induced endothelial dysfunction and currently known mechanisms are reviewed in this article.

العلاقة: Ajithkumar, Santhambika Gopinathan nair; Ramachandran, Surya; Kartha, Cheranellore Chandrasekharan (2011) Drug induced endothelial dysfunction: functional role of oxidative stress The IIOAB Journal, 2 (5). pp. 62-70. ISSN 0976-3104

الإتاحة: http://repository.ias.ac.in/96628Test/
http://www.iioab.org/Vol2%286%29July2011/2%286%2962-70.pdfTest

المؤلفون: Kuruvilla, Leena¹ leenamary24@yahoo.com, Kartha, Cheranellore Chandrasekharan^1,2 cckartha@rgcb.res.in

المصدر: Journal of Biomedical Science. 2009, Vol. 16, p1-7. 7p. 5 Graphs.

مصطلحات موضوعية: *FIBROBLASTS, *CELL-mediated cytotoxicity, *VASOMOTOR system, *TUMOR necrosis factors, *ENDOCARDIUM

مستخلص: Background: The endocardial endothelium that lines the inner cavity of the heart is distinct from the microvascular endothelial cells and modulates cardiac muscle performance in a manner similar to the vascular endothelial modulation of vascular structure and vasomotor tone. Although the modulatory effects of endocardial endothelium (EE) on cardiomyocytes are firmly established, the regulatory effects of endocardial endothelium on the cardiac interstitium and its cellular components remain ill defined. Methods and Results: We investigated whether the stimulatory effect of EE on cardiac fibroblasts would be altered when EECs are activated by the cytokine tumor necrosis factor-a (TNF-α) or the endotoxin bacterial lipopolysaccharide (LPS). Both TNF-α and LPS were found to independently attenuate the stimulatory effect of EE on cardiac fibroblasts. These agents lowered the synthesis or release of ET-1 and increased the secretion of TGF-β and NO. Conclusion: The findings of this study using endocardial endothelial cells (EECs) and neonatal cardiac fibroblasts demonstrate that pro-inflammatory cytokines cause altered secretion of paracrine factors by EECs and inhibit proliferation and lower collagen synthesis in fibroblasts. These changes may influence fibroblast response and extra cellular matrix remodeling in pathological conditions of the heart. [ABSTRACT FROM AUTHOR]