Facial amphipathic deoxycholic acid-modified polyethyleneimine for efficient MMP-2 siRNA delivery in vascular smooth muscle cells

Kim, Dongkyu; Lee, Do Kyung; Jang, Yeon Lim; Chae, Su Young; Choi, Donghoon; Jeong, Ji Hoon; Kim, Sun Hwa

doi:10.1016/j.ejpb.2012.01.013

Cited by 37 publications

(21 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is widely believed that during the later stages of vein grafting, the promotion of apoptosis may inhibit restenosis of the grafted tissue (Fan et al, 2006;Kim et al, 2012;Liu et al, 2012;Yang et al, 2013). However, in the present study, we found that in a rabbit model of vein graft restenosis, apoptosis was maintained at a low level from the 7th day following transplantation, although the underlying reasons for this are unknown.…”

Section: Discussioncontrasting

confidence: 50%

“…They found that the existence of the late apoptosis associated with macrophage, and the inflammatory mediators secreted by macrophage can induce apoptosis. Kim et al (2012) reported that elevated expression of the gene BMP-2 inhibits VSMC proliferation and stimulates their apoptosis, preventing excessive intimal hyperplasia following autologous vein grafting (Fan et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Apoptosis, proliferation, and morphology during vein graft remodeling in rabbits

et al. 2016

View full text Add to dashboard Cite

ABSTRACT. Neo-intima development and atherosclerosis limit the long-term use of vein grafts for revascularization of ischemic tissues. Recently, studies have confirmed that proliferating cell nuclear antigen (PCNA) plays an important role in cell proliferation. Our research confirmed that 28 days after vein transplantation, PCNA expression increases significantly. Using rabbits, rather than rodents, for a more representative model of human vein grafts, we aimed to establish a time course of changes in cell proliferation and apoptosis using morphometric and immunohistochemical analyses, western blot, terminal deoxynucleotidyl transferase dUTP nick end labeling, and transmission electron microscopy (TEM). The external jugular veins of 42 healthy purebred male New Zealand white rabbits were grafted onto their common carotid arteries. The rabbits were divided into seven groups, with vein grafts being harvested before surgery, and at 1, 3, 7, 14, 28, and 90 days afterwards. The extent of stenosis and apoptosis, PCNA protein levels, and TEM morphology were subsequently examined. Intimal thickness was slightly decreased 1 day following surgery, but then increased continuously until the 90th day. Western blot and immunohistochemistry both indicated lowered PCNA expression on day 1, although levels subsequently increased, peaking at 7 days post-surgery. After surgery, apoptosis was lowest on day 7, and remained low thereafter. TEM revealed signs of apoptosis as vein graft restenosis progressed. Proliferation and apoptosis cooccurred following grafting, indicating that both processes were involved in vein graft remodeling. Apoptosis levels were highest between days 1 and 3 after surgery, whereas proliferation culminated on the 7th day.

show abstract

Section: Discussioncontrasting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Apoptosis, proliferation, and morphology during vein graft remodeling in rabbits

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The delivery system used was amphipathic deoxycholic acid-modified polyethyleneimine. This was synthesized to be used as a carrier system for siRNA in order to prevent neointima formation secondary to migration of vascular SMCs (VSMCs) 9. This work has profound implications for patient care.…”

Section: Mmps and Differential Function Of Mmp-2 And Mmp-9mentioning

confidence: 99%

Matrix metalloproteinases in atherosclerosis: role of nitric oxide, hydrogen sulfide, homocysteine, and polymorphisms

Vacek

Rehman

Neamtu

et al. 2015

VHRM

119

View full text Add to dashboard Cite

Atherosclerosis is an inflammatory process that involves activation of matrix metalloproteinases (MMPs); MMPs degrade collagen and allow for smooth-muscle cell migration within a vessel. Moreover, this begets an accumulation of other cellular material, resulting in occlusion of the vessel and ischemic events to tissues in need of nutrients. Homocysteine has been shown to activate MMPs via an increase in oxidative stress and acting as a signaling molecule on receptors like the peroxisome proliferator activated receptor-γ and N-methyl-D-aspartate receptor. Nitric oxide has been shown to be beneficial in some cases of deactivating MMPs. However, in other cases, it has been shown to be harmful. Further studies are warranted on the scenarios that are beneficial versus destructive. Hydrogen sulfide (H2S) has been shown to decrease MMP activities in all cases in the literature by acting as an antioxidant and vasodilator. Various MMP-knockout and gene-silencing models have been used to determine the function of the many different MMPs. This has allowed us to discern the role that each MMP has in promoting or alleviating pathological conditions. Furthermore, there has been some study into the MMP polymorphisms that exist in the population. The purpose of this review is to examine the role of MMPs and their polymorphisms on the development of atherosclerosis, with emphasis placed on pathways that involve nitric oxide, hydrogen sulfide, and homocysteine.

show abstract

“…[130]. To combat plaque destabilization, matrix metalloproteinase-2 siRNA was encapsulated in polymeric nanostructures and was found to inhibit SMC migration in vitro , suggesting the potential to reduce atherosclerosis and restenosis [131]. …”

Section: Nanomaterials For Gene Therapymentioning

confidence: 99%

Engineering Nanomaterials to Address Cell-Mediated Inflammation in Atherosclerosis

Allen

Liu²,

Scott

2016

Regen. Eng. Transl. Med.

View full text Add to dashboard Cite

Atherosclerosis is an inflammatory disorder with a pathophysiology driven by both innate and adaptive immunity and a primary cause of cardiovascular disease (CVD) worldwide. Vascular inflammation and accumulation of foam cells and their products induce maturation of atheromas, or plaques, which can rupture by metalloprotease action, leading to ischemic stroke or myocardial infarction. Diverse immune cell populations participate in all stages of plaque maturation, many of which directly influence plaque stability and rupture via inflammatory mechanisms. Current clinical treatments for atherosclerosis focus on lowering serum levels of low-density lipoprotein (LDL) using therapeutics such as statins, administration of antithrombotic drugs, and surgical intervention. Strategies that address cell-mediated inflammation are lacking, and consequently have recently become an area of considerable research focus. Nanomaterials have emerged as highly advantageous tools for these studies, as they can be engineered to target specific inflammatory cell populations, deliver therapeutics of wide-ranging solubilities and enhance analytical methods that include imaging and proteomics. Furthermore, the highly phagocytic nature of antigen presenting cells (APCs), a diverse cell population central to the initiation of immune responses and inflammation, make them particularly amenable to targeting and modulation by nanoscale particulates. Nanomaterials have therefore become essential components of vaccine formulations and treatments for inflammation-driven pathologies like autoimmunity, and present novel opportunities for immunotherapeutic treatments of CVD. Here, we review recent progress in the design and use of nanomaterials for therapeutic assessment and treatment of atherosclerosis. We will focus on promising new approaches that utilize nanomaterials for cell-specific imaging, gene therapy and immunomodulation.

show abstract

Facial amphipathic deoxycholic acid-modified polyethyleneimine for efficient MMP-2 siRNA delivery in vascular smooth muscle cells

Cited by 37 publications

References 44 publications

Apoptosis, proliferation, and morphology during vein graft remodeling in rabbits

Apoptosis, proliferation, and morphology during vein graft remodeling in rabbits

Matrix metalloproteinases in atherosclerosis: role of nitric oxide, hydrogen sulfide, homocysteine, and polymorphisms

Engineering Nanomaterials to Address Cell-Mediated Inflammation in Atherosclerosis

Contact Info

Product

Resources

About