Bioprinted optoelectronically active cardiac tissues.

Electrical stimulation of existing three-dimensional bioprinted tissues to alter tissue activities is typically associated with wired delivery, invasive electrode placement, and potential cell damage, minimizing its efficacy in cardiac modulation. Here, we report an optoelectronically active scaffold based on printed gelatin methacryloyl embedded with micro-solar cells, seeded with cardiomyocytes to form light-stimulable tissues. This enables untethered, noninvasive, and damage-free optoelectronic stimulation-induced modulation of cardiac beating behaviors without needing wires or genetic modifications to the tissue solely with light.

Brain-targeted exosome-mimetic cell membrane nanovesicles with therapeutic oligonucleotides elicit anti-tumor effects in glioblastoma animal models.

The brain-targeted delivery of therapeutic oligonucleotides has been investigated as a new treatment modality for various brain diseases, such as brain tumors. However, delivery efficiency into the brain has been limited due to the blood-brain barrier. In this research, brain-targeted exosome-mimetic cell membrane nanovesicles (CMNVs) were designed to enhance the delivery of therapeutic oligonucleotides into the brain.

Antisense-oligonucleotide co-micelles with tumor targeting peptides elicit therapeutic effects by inhibiting microRNA-21 in the glioblastoma animal models.

Introduction: miRNA-21 (miR-21) is highly expressed in glioblastoma, facilitating tumor growth by blocking the expression of apoptosis-related genes. Therefore, an antisense microRNA oligonucleotide (AMO) against miR-21 was suggested as a therapeutic nucleic acid for glioblastoma.

Objectives: AMO21 co-micelles were developed with tumor-targeting T7 peptides as an AMO21 delivery system by intranasal administration.

Intranasal delivery of self-assembled nanoparticles of therapeutic peptides and antagomirs elicits anti-tumor effects in an intracranial glioblastoma model.

MicroRNA-21 (miR-21) is involved in the progression of glioblastoma through inhibition of pro-apoptotic genes. Antisense RNA against miR-21 (antagomir-21) has been developed as a potential therapeutic reagent for the treatment of glioblastoma. The receptor for advanced glycation end-products (RAGE) is also involved in the progression of glioblastoma through induction of angiogenic factors.

Delivery of MiRNA-92a Inhibitor Using RP1-Linked Peptide Elicits Anti-Inflammatory Effects in an Acute Lung Injury Model.

Acute lung injury (ALI) is an inflammatory lung disease. miRNA-92a (miR92a) is induced in the lungs of ALI patients and mediates inflammatory reactions. In this study, a RP1-linked R3V6 (RP1R3V6) peptide was synthesized and evaluated as a carrier of anti-microRNA-92a oligonucleotide (AMO92a) into the lungs of an ALI animal model.

Engineering exosomes for pulmonary delivery of peptides and drugs to inflammatory lung cells by inhalation.

Exosomes have been investigated as delivery vesicles for various drugs. However, exosome-mediated peptide delivery into the lungs has not been studied. In this study, exosomes were engineered for the pulmonary delivery of RAGE-binding peptide (RBP), an anti-inflammatory peptide.

A RAGE-antagonist peptide potentiates polymeric micelle-mediated intracellular delivery of plasmid DNA for acute lung injury gene therapy.

Acute lung injury (ALI) is a severe inflammatory lung disease. A high mobility group box-1 (HMGB-1) derived RAGE-antagonist peptide (RAP) was previously developed for anti-inflammatory therapy for ALI. Due to its specific binding to RAGE on the surface of inflammatory cells, the RAP may facilitate polymer-mediated intracellular delivery of plasmid DNA (pDNA) into the inflammatory cells.

Inhalable Gene Delivery System Using a Cationic RAGE-Antagonist Peptide for Gene Delivery to Inflammatory Lung Cells.

Acute lung injury (ALI) is a severe lung inflammatory disease. In ALI, the receptor for advanced glycation end-products (RAGE) is overexpressed in lung epithelial cells and involved in inflammatory reactions. A previous report showed that a RAGE-antagonist peptide (RAP), from high-mobility group box-1, bound to RAGE and reduced inflammatory reactions.