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Isolation of Low Endotoxin Content Extracellular Vesicles Derived from Cancer Cell Lines

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Streptococcus mutans-derived extracellular vesicles disrupt endothelial function via eNOS and endothelin-1

Yang Liu¹, Xinxin Li¹, Zhengshuo Cui¹

¹The Key Laboratory of Remodeling Cardiovascular Diseases, Ministry of Education, Collaborative Innovation Center for Cardiovascular Disorders, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing an Zhen Hospital, Capital Medical University, Beijing, 100029, China.

Biochemical and Biophysical Research Communications

|December 26, 2025

Summary

Dental caries pathogen Streptococcus mutans (S.m) releases extracellular vesicles (EVs) that impair blood vessel function. These S.m EVs disrupt endothelial-dependent relaxation, linking oral health to cardiovascular disease risk.

Keywords:

Endothelial function Extracellular vesicle Streptococcus mutans

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Area of Science:

Cardiovascular Biology
Microbiology
Oral Health Research

Background:

Epidemiological studies suggest a link between dental caries and cardiovascular diseases.
Endothelial dysfunction is a key factor in cardiovascular diseases.
Bacterial extracellular vesicles (EVs) play a crucial role in host-microbe interactions.

Purpose of the Study:

To investigate the impact of Streptococcus mutans (S.m)-derived extracellular vesicles (S.m EVs) on endothelial function.
To elucidate the underlying mechanisms linking dental caries to cardiovascular diseases via S.m EVs.

Main Methods:

Oral administration of S.m in vivo to assess effects on endothelial-dependent relaxation (EDR).
In vitro treatment with isolated S.m EVs to evaluate dose- and time-dependent effects on EDR.
Analysis of molecular pathways including Akt, eNOS, p38 MAPK, and endothelin-1 expression.

Main Results:

S.m administration impaired EDR in vivo.
S.m EVs significantly diminished EDR in a dose- and time-dependent manner.
S.m EVs altered key signaling pathways: inhibiting Akt/eNOS phosphorylation and promoting p38 MAPK phosphorylation and endothelin-1 expression.

Conclusions:

S.m EVs adversely affect endothelial function through specific molecular pathways.
The Akt/eNOS and p38 MAPK/endothelin-1 pathways are implicated in S.m EVs-induced endothelial dysfunction.
This study establishes a mechanistic link between Streptococcus mutans, dental caries, and cardiovascular diseases via bacterial EVs.