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Daniela Stan

Researcher at Romanian Academy

Publications -  25
Citations -  671

Daniela Stan is an academic researcher from Romanian Academy. The author has contributed to research in topics: Resistin & Chemokine. The author has an hindex of 16, co-authored 25 publications receiving 597 citations.

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Similar effects of resistin and high glucose on P-selectin and fractalkine expression and monocyte adhesion in human endothelial cells

TL;DR: In HEC, resistin and HG induce the up-regulation of P-selectin and fractalkine and the ensuing increased monocyte adhesion by a mechanism involving oxidative stress and NF-kB and AP-1 activation.
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Cross talk between smooth muscle cells and monocytes/activated monocytes via CX3CL1/CX3CR1 axis augments expression of pro-atherogenic molecules.

TL;DR: The cross-talk between SMC and monocytes augments the inflammatory response in both cell types as revealed by the increased expression of TNFα,IL-1β, IL-6, CX3CR1 and MMPs.
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Cross-talk between macrophages and smooth muscle cells impairs collagen and metalloprotease synthesis and promotes angiogenesis

TL;DR: MAC-SMC communication affects factors and molecules that could alter ECM composition and neo-angiogenesis, features that could directly dictate the progression of atheroma towards the vulnerable plaque.
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High glucose conditions induce upregulation of fractalkine and monocyte chemotactic protein-1 in human smooth muscle cells

TL;DR: HG upregulates the expression of fractalkine and MCP-1 in SMC leading to increased monocyte-SMC adhesive interactions by a mechanism involving activation of MAPK, activator protein-1 (AP-1) and NF-kappaB.
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VCAM-1 directed target-sensitive liposomes carrying CCR2 antagonists bind to activated endothelium and reduce adhesion and transmigration of monocytes.

TL;DR: It is reported that Vp-TSL-Tj binds specifically to activated EC in vitro and in situ, release the entrapped Teijin and prevent the transmigration of monocytes through activated EC, the first evidence that nanocarriers which transport and release chemokine inhibitors at specific pathological sites can reduceChemokine-dependent inflammatory processes.