Articles by Laura Z. Vanags in JoVE
Murine Model of Wound Healing Louise Dunn1,2, Hamish C. G Prosser1,2, Joanne T. M. Tan1,2, Laura Z. Vanags1,2, Martin K. C. Ng1,2,3, Christina A. Bursill1,2 1The Heart Research Institute, 2Sydney Medical School, University of Sydney, 3Cardiology Department, Royal Prince Alfred Hospital A murine model of cutaneous wound healing that can be used to assess therapeutic compounds in physiological and pathophysiological settings.
Other articles by Laura Z. Vanags on PubMed
The Apolipoprotein A-I Mimetic Peptide, ETC-642, Reduces Chronic Vascular Inflammation in the Rabbit Lipids in Health and Disease. 2011 | Pubmed ID: 22128776 High-density lipoproteins (HDL) and their main apolipoprotein, apoA-I, exhibit anti-inflammatory properties. The development of peptides that mimic HDL apolipoproteins offers a promising strategy to reduce inflammatory disease. This study aimed to compare the anti-inflammatory effects of ETC-642, an apoA-I mimetic peptide, with that of discoidal reconstituted HDL (rHDL), consisting of full-length apoA-I complexed with phosphatidylcholine, in rabbits with chronic vascular inflammation.
High-density Lipoproteins Suppress Chemokine Expression and Proliferation in Human Vascular Smooth Muscle Cells FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology. Apr, 2013 | Pubmed ID: 23271056 The inflammatory chemokines CCL2, CCL5, and CXâ‚ƒCL1 stimulate vascular smooth muscle cell (SMC) proliferation. High-density lipoproteins (HDLs) exhibit potent cardioprotective and anti-inflammatory properties. We therefore sought to determine the effect of reconstituted HDLs (rHDLs) on SMC chemokine expression and proliferation and elucidate the mechanisms. Preincubation of primary human SMCs with rHDLs containing apolipoprotein (apo)A-I and phosphatidylcholine (20 Î¼M, final apoA-I concentration), before stimulation with TNF-Î±, inhibited CCL2 (54%), CCL5 (38%), and CX3CL1 (33%) protein levels. The chemokine receptors CCR2 (29%) and CX3CR1 (22%) were also reduced by rHDLs. Incubation with rHDLs reduced the NF-ÎºB subunit p65 in the nucleus (39%) and phosphorylated IÎºBÎ± (28%), both regulators of chemokine expression. Furthermore, rHDLs inhibited the upstream signaling proteins phosphoinositide 3-kinase (37%) and phosphorylated Akt (pAkt, 49%). Incubation with rHDLs strikingly suppressed SMC proliferation (84%) and ERK phosphorylation (pERK, 29%). Finally, siRNA knockdown of the scavenger receptor SR-B1 attenuated rHDL-induced inhibition of SMC chemokine expression, p65, and proliferation, indicating that SR-B1 plays a key role in mediating these effects. Thus, rHDLs reduce SMC chemokine expression (via NF-ÎºB/pAkt inhibition) and proliferation (via pERK inhibition). This has important implications for preventing the pathogenesis of neointimal hyperplasia, the main cause of early vein graft/stent failure.