Regulatory crosstalk between KLF5, miR-29a and Fbw7/CDC4 cooperatively promotes atherosclerotic development.

Atherogenesis is a chronic inflammatory process that involves complex interactions between endothelial dysfunction, lipid deposition and vascular smooth-muscle cell (VSMC) proliferation. However, the molecular mechanism is still unclear. We found that a pro-atherosclerotic factor (oxLDL) induced the expression of Krüppel-like factor 5 (KLF5), which in turn increased miR-29a expression levels.

Exosome-Mediated miR-155 Transfer from Smooth Muscle Cells to Endothelial Cells Induces Endothelial Injury and Promotes Atherosclerosis.

The vascular response to pro-atherosclerotic factors is a multifactorial process involving endothelial cells (ECs), macrophages (MACs), and smooth muscle cells (SMCs), although the mechanism by which these cell types communicate with each other in response to environmental cues is yet to be understood. Here, we show that miR-155, which is significantly expressed and secreted in Krüppel-like factor 5 (KLF5)-overexpressing vascular smooth muscle cells (VSMCs), is a potent regulator of endothelium barrier function through regulating endothelial targeting tight junction protein expression. VSMCs-derived exosomes mediate the transfer of KLF5-induced miR-155 from SMCs to ECs, which, in turn, destroys tight junctions and the integrity of endothelial barriers, leading to an increased endothelial permeability and enhanced atherosclerotic progression.

miR-29a regulates vascular neointimal hyperplasia by targeting YY1.

Objectives: The formation of vascular neointima is mainly related to impairment of the vascular endothelial barrier and abnormal proliferation and migration of smooth muscle cells. The objective of this study was to investigate whether miR-29a exerts any promoting effect on the vascular neointimal hyperplasia and if so, its mechanism.

Materials And Methods: RT-qPCR was performed to determine expression of miR-29a in vascular smooth muscle cells (VSMC) and vascular neointimal hyperplasia.

1, 25(OH)D-induced interaction of vitamin D receptor with p50 subunit of NF-κB suppresses the interaction between KLF5 and p50, contributing to inhibition of LPS-induced macrophage proliferation.

KLF5 and nuclear factor κB (NF-κB) regulate cell proliferation and inflammation. Vitamin D signaling through vitamin D receptor (VDR) exerts anti-proliferative and anti-inflammatory actions. However, an actual relationship between KLF5, NF-κB and VDR in the inflammation and proliferation of macrophages is still unclear.

Interictal epileptiform discharges were associated with poorer cognitive performance in adult epileptic patients.

Objective: Cognitive impairment is one of the major consequences of epilepsy and has been shown to reduce quality of life. Interictal epileptiform discharges (IEDs) were associated with poorer cognitive performance in children, and the aim of this study was to determine whether there was a similar association in adults.

Methods: A prospective cohort of 167 seizure-free adult patients underwent EEG recording and extensive cognitive evaluations.

SUMOylation of KLF4 acts as a switch in transcriptional programs that control VSMC proliferation.

The regulation of vascular smooth muscle cell (VSMC) proliferation is an important issue due to its major implications for the prevention of pathological vascular conditions. The objective of this work was to assess the function of small ubiquitin-like modifier (SUMO)ylated Krϋppel-like transcription factor 4 (KLF4) in the regulation of VSMC proliferation in cultured cells and in animal models with balloon injury. We found that under basal conditions, binding of non-SUMOylated KLF4 to p300 activated p21 (p21(WAF1/CIP1))transcription, leading to VSMC growth arrest.

Photo-Activatable Substrates for Site-Specific Differentiation of Stem Cells.

In this report, a UV sensitive, PEGylated PFSSTKTC (Pro-Phe-Ser-Ser-Thr-Lys-Thr-Cys) peptide was modified on quartz substrate to investigate the spatial controlled differentiation of stem cells. This substrate could restrict the cell adhesion due to the steric hindrance of PEG shell. With UV irradiation, PFSSTKTC became exposed owing to the breakage of o-nitrobenzyl group with the detachment of PEG shell.

A novel function of BMHP1 and cBMHP1 peptides to induce the osteogenic differentiation of mesenchymal stem cells.

Bone marrow homing peptide 1 (BMHP1), which was derived from a phage display peptide library (PDPL), is known to be home to bone marrow and bind to stem cells. For the first time, the effect of BMHP1 on the differentiation behavior of mesenchymal stem cells (MSCs) was evaluated. BMHP1 was tethered to modified quartz substrates, and MSCs were seeded on the substrates.

Virus-Surface-Mimicking Surface Clustering of AuNPs onto DNA-Entrapped Polymeric Nanoparticle for Enhanced Cellular Internalization and Nanocluster-Induced NIR Photothermal Therapy.

is demonstrated to lead to enhanced cellular uptake, improved gene transfection, and particularly efficient near-infrared photothermal therapy that cannot be achieved by both of them separately. This hybrid nanosystem represents a novel paradigm of multipurpose organic-inorganic nanoplatform, especially for cancer treatments.

Evaluating the effects of charged oligopeptide motifs coupled with RGD on osteogenic differentiation of mesenchymal stem cells.

Mesenchymal stem cells, due to their multilineage differentiation potential, have emerged as a promising cell candidate for cell-based therapy. In recent years, biomaterials were artificially synthesized to control the differentiation of mesenchymal stem cells. In this study, a series of charged or neutral oligopeptide motifs coupled with RGD were synthesized and used for surface modification using quartz substrates as model.

The synergistic effect of a BMP-7 derived peptide and cyclic RGD in regulating differentiation behaviours of mesenchymal stem cells.

Precisely controlling the behaviours of stem cells has far-reaching application potential in clinical trials. In this study, we have developed a self-assembled monolayer (SAM) of a cyclic RGD peptide (cycRGD) and bone forming peptide-1 (BFP-1) on a quartz substrate to regulate the behaviours of mesenchymal stem cells (MSCs). The results demonstrated that cycRGD can accelerate the cell adhesion on the substrate, thereby enhancing the ability of BFP-1 in mediating the osteogenic activity.