Cholesterol-Anchored Ac-SDKP Modified Platelet sEVs Effectively Deliver Anti-Inflammatory Peptides

Small extracellular vesicles (sEVs) released from thrombin-activated platelets carry adhesion proteins inherited from the parent cell membrane. Whether these vesicles can function as carriers for short anti-inflammatory peptides depends on a methodical evaluation of loading performance, biological compatibility, and intrinsic inflammatory potential. This protocol describes the isolation of platelet sEVs by thrombin-triggered vesiculation and differential ultracentrifugation, followed by surface decoration with the anti-inflammatory tetrapeptide Ac-SDKP via a cholesterol-polyhistidine anchor. The isolated vesicles were 90-300 nm in diameter, spherical by transmission electron microscopy, and positive for the platelet markers CD41 and CD62P. Cholesterol-directed membrane insertion gave loading efficiencies of 93.7% to 97.0% across four peptide-to-vesicle feeding ratios. The drug payload rose from 9.75% to 37.5% (w/w) as peptide input increased, without measurable change in vesicle diameter or zeta potential. Incubation with human coronary artery endothelial cells or human umbilical vein endothelial cells for 24 h produced no loss of metabolic activity at the concentrations tested. A single intravenous dose of unmodified sEVs at 20 mg/kg in mice did not prolong tail bleeding time or alter serum ALT, AST, BUN, or creatinine over a 7-day observation window. Histological examination of the lung, liver, spleen, and kidney showed no evidence of injury. Thrombin stimulation triggered substantial release of TNF-alpha, IL-6, and IL-1beta from intact platelets; the sEV fraction released negligible amounts of these cytokines, irrespective of thrombin exposure. In lipopolysaccharide-treated endothelial monolayers, Ac-SDKP-decorated sEVs suppressed cytokine secretion more effectively than an equal concentration of free Ac-SDKP. These results describe a practical method for generating peptide-functionalized platelet sEVs and provide an initial dataset on their pharmaceutical properties, supporting further investigation of this platform for anti-inflammatory delivery in vascular disorders.

Authors

Institutions

Publication Details

Journal
Journal of Visualized Experiments
Published
2026-08-25
DOI
https://doi.org/10.3791/73065
Primary Topic
Platelet Disorders and Treatments
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Cholesterol-Anchored Ac-SDKP Modified Platelet sEVs Effectively Deliver Anti-Inflammatory Peptides

Chunlei Wei, C J Tan, Z. Y. Xu, Lijun Jiang et al.
Journal of Visualized Experiments
Platelet Disorders and Treatments
article

Cholesterol-Anchored Ac-SDKP Modified Platelet sEVs Effectively Deliver Anti-Inflammatory Peptides

Chunlei Wei, C J Tan, Z. Y. Xu, Lijun Jiang, Yue Cao, Jie Huang, Shiyu Su, He Zhao
article en

Abstract

Small extracellular vesicles (sEVs) released from thrombin-activated platelets carry adhesion proteins inherited from the parent cell membrane. Whether these vesicles can function as carriers for short anti-inflammatory peptides depends on a methodical evaluation of loading performance, biological compatibility, and intrinsic inflammatory potential. This protocol describes the isolation of platelet sEVs by thrombin-triggered vesiculation and differential ultracentrifugation, followed by surface decoration with the anti-inflammatory tetrapeptide Ac-SDKP via a cholesterol-polyhistidine anchor. The isolated vesicles were 90-300 nm in diameter, spherical by transmission electron microscopy, and positive for the platelet markers CD41 and CD62P. Cholesterol-directed membrane insertion gave loading efficiencies of 93.7% to 97.0% across four peptide-to-vesicle feeding ratios. The drug payload rose from 9.75% to 37.5% (w/w) as peptide input increased, without measurable change in vesicle diameter or zeta potential. Incubation with human coronary artery endothelial cells or human umbilical vein endothelial cells for 24 h produced no loss of metabolic activity at the concentrations tested. A single intravenous dose of unmodified sEVs at 20 mg/kg in mice did not prolong tail bleeding time or alter serum ALT, AST, BUN, or creatinine over a 7-day observation window. Histological examination of the lung, liver, spleen, and kidney showed no evidence of injury. Thrombin stimulation triggered substantial release of TNF-alpha, IL-6, and IL-1beta from intact platelets; the sEV fraction released negligible amounts of these cytokines, irrespective of thrombin exposure. In lipopolysaccharide-treated endothelial monolayers, Ac-SDKP-decorated sEVs suppressed cytokine secretion more effectively than an equal concentration of free Ac-SDKP. These results describe a practical method for generating peptide-functionalized platelet sEVs and provide an initial dataset on their pharmaceutical properties, supporting further investigation of this platform for anti-inflammatory delivery in vascular disorders.

Journal of Visualized Experiments(234)
Soochow University (TW), Soochow University (CN), Second Affiliated Hospital of Soochow University (CN), First Affiliated Hospital of Soochow University (CN)
Openalex Percentile: Top 10%
Platelet Disorders and Treatments
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.