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Your search keyword '"Bandyopadhyay, Chirosree"' showing total 14 results
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14 results on '"Bandyopadhyay, Chirosree"'

1. Caveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation

Author

Ramírez, Cristina M., Zhang, Xinbo, Bandyopadhyay, Chirosree, Rotllan, Noemi, Sugiyama, Michael G., Aryal, Binod, Liu, Xinran, He, Shun, Kraehling, Jan R., Ulrich, Victoria, Lin, Chin Sheng, Velazquez, Heino, Lasunción, Miguel A., Li, Guangxin, Suárez, Yajaira, Tellides, George, Swirski, Filip K., Lee, Warren L., Schwartz, Martin A., Sessa, William C., and Fernández-Hernando, Carlos

Published
2019
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3. Endothelial fluid shear stress sensing in vascular health and disease

Author

Baeyens, Nicolas, Bandyopadhyay, Chirosree, Coon, Brian G., Yun, Sanguk, and Schwartz, Martin A.

Subjects
Research, Health aspects, Forecasts and trends, Market trend/market analysis, Precision medicine -- Forecasts and trends, Disease susceptibility -- Research, Medical research, Cellular signal transduction -- Health aspects, Medicine, Experimental
Abstract

Introduction Mechanical forces guide the development and physiology of every organ system, but they are particularly crucial in the cardiovascular system, whose main function of transporting pressurized blood to every [...], Endothelial cells transduce the frictional force from blood flow (fluid shear stress) into biochemical signals that regulate gene expression and cell behavior via specialized mechanisms and pathways. These pathways shape the vascular system during development and during postnatal and adult life to optimize flow to tissues. The same pathways also contribute to atherosclerosis and vascular malformations. This Review covers recent advances in basic mechanisms of flow signaling and the involvement of these mechanisms in vascular physiology, remodeling, and these diseases. We propose that flow sensing pathways that govern normal morphogenesis can contribute to disease under pathological conditions or can be altered to induce disease. Viewing atherosclerosis and vascular malformations as instances of pathological morphogenesis provides a unifying perspective that may aid in developing new therapies.

Published
2016
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6. Caveolin-1 regulates atherogenesis by attenuating LDL transcytosis and vascular inflammation independent of endothelial nitric oxide synthase activation

Author

Ramírez, Cristina M., Zhang, Xinbo, Bandyopadhyay, Chirosree, Rotllan, Noemi, Sugiyama, Michael G., Aryal, Binod, Liu, Xinran, He, Shun, Kraehling, Jan R., Ulrich, Victoria, Lin, Chin Sheng, Velazquez, Heino, Lasunción, Miguel A., Li, Guangxin, Suárez, Yajaira, Tellides, George, Swirski, Filip K., Lee, Warren L., Schwartz, Martin A., Sessa, William C., and Fernández-Hernando, Carlos

Subjects
Male, Mice, Knockout, Nitric Oxide Synthase Type III, Caveolin 1, Mice, Transgenic, Atherosclerosis, Article, Enzyme Activation, Lipoproteins, LDL, Mice, Inbred C57BL, Mice, Dogs, Animals, Humans, Female, Endothelium, Vascular, Transcytosis, Cells, Cultured
Abstract

BACKGROUND—: Atherosclerosis is driven by synergistic interactions between pathological biomechanical, inflammatory and lipid metabolic factors. Our previous studies demonstrated that absence of caveolin-1 (Cav1)/caveolae in hyperlipidemic mice strongly inhibits atherosclerosis, which was attributed to activation of endothelial nitric oxide synthase (eNOS) and increased production of nitric oxide (NO), reduced inflammation and low-density lipoprotein (LDL) trafficking. However, the contribution of eNOS activation and NO production in the athero-protection of Cav1 and the exact mechanisms by which Cav1/caveolae controls the pathogenesis of diet-induced atherosclerosis are still not clear. METHODS—: Triple knockout mouse lacking expression of eNOS, Cav1 and Ldlr were generated to explore the role of NO production in Cav1-dependent atheo-protective function. The effects of Cav1 on lipid trafficking, extracellular matrix (ECM) remodeling and vascular inflammation were studied both in vitro and in vivo using a mouse model of diet-induced atherosclerosis. The expression of Cav1 and distribution of caveolae regulated by flow were analyzed by immunofluorescence staining and transmission electron microscopy. RESULTS—: We found that absence of Cav1 significantly suppressed atherogenesis in Ldlr(−/−)eNOS(−/−) mice, demonstrating that athero-suppression is independent of increased NO production. Instead, we find that absence of Cav1/caveolae inhibited LDL transport across the endothelium, pro-atherogenic fibronectin deposition, and disturbed flow-mediated endothelial cell (EC) inflammation. Consistent with the idea that Cav1/caveolae may play a role in early flow-dependent inflammatory priming, distinct patterns of Cav1 expression and caveolae distribution were observed in athero-prone and athero-resistant areas of the aortic arch even in wild-type mice. CONCLUSIONS—: The above findings support a role for Cav1/caveolae as a central regulator of atherosclerosis that links biomechanical, metabolic and inflammatory pathways independent of endothelial eNOS activation and NO production.

Published
2019

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