Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism

Shiwakoti, Saugat; Ko, Ju-Young; Gong, Dal-Seong; Dhakal, Bikalpa; Lee, Jeong-Hye; Adhikari, Radhika; Gwak, Yeonhyang; Park, Sin‐Hee; Choi, Ik Jun; Schini‐Kerth, Valérie B.; Kang, Ki‐Woon; Oak, Min–Ho

doi:10.1016/j.envint.2022.107248

Cited by 28 publications

(18 citation statements)

References 63 publications

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“…The effect of NP exposure on the expression of SGLT1 and SGLT2 was assessed using western blot analysis by incubating PCAECs with different concentrations of NPs (1, 10 μg/mL) for 24 h. The treatment dose and duration of NPs was selected referred to our previous study, where NPs at 1 and 10 µg/mL for 24 h could significantly induce endothelial senescence and dysfunction 4 . The expression of SGLT2, not SGLT1, was significantly increased by NPs with increasing concentrations (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…NPs-induced endothelial senescence is associated with decreased cell proliferation 4 . Therefore, the effect of SGLT2 inhibition on cell proliferation in NPs-induced endothelial senescence was studied.…”

Section: Resultsmentioning

confidence: 99%

“…Since NPs-induced oxidative stress involves NADPH oxidase, known to be a major source of ROS in the ECs 4 , 15 , further studies explored the role of SGLT2 inhibition on NADPH oxidase. Western blotting analysis indicated that Nox2 and p22 phox , membrane catalytic subunits of NADPH oxidase, were significantly upregulated by NPs and that SGLT2 inhibition suppressed the response significantly in 0.1 and 1 µM concentrations (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Some studies have shown that NPs exposure is mainly via ingestion, inhalation, or dermal contact and is linked with numerous cardiovascular, pulmonary, metabolic & neuronal complications 3 . NPs induce premature endothelial senescence and dysfunction which is accompanied by an increase in intracellular oxidative stress 4 . Endothelial cells (ECs) senescence is characterized by irreversible cell cycle arrest, inflammation, oxidative stress, and downregulation of endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) formation.…”

Section: Introductionmentioning

confidence: 99%

“…Endothelial cells (ECs) senescence is characterized by irreversible cell cycle arrest, inflammation, oxidative stress, and downregulation of endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) formation. ECs senescence can be induced by various factors like DNA damage, pollutants, high glucose, angiotensin II, and radiation, which promotes endothelial dysfunction and is a significant risk factor for the development of cardiovascular disorders (CVDs) 4 – 6 .…”

Section: Introductionmentioning

confidence: 99%

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SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction

Dhakal

Shiwakoti

Park

et al. 2023

Sci Rep

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Nano plastics (NPs) have been a significant threat to human health and are known to cause premature endothelial senescence. Endothelial senescence is considered one of the primary risk factors contributing to numerous cardiovascular disorders. Recent studies have suggested that inhibition of sodium glucose co-transporter (SGLT2) ameliorates endothelial senescence and dysfunction. Therefore, our study intends to explore the role of SGLT2 in NPs-induced endothelial senescence and dysfunction. Porcine coronary artery and its endothelial cells were treated with NPs in the presence or absence of Enavogliflozin (ENA), a SGLT2 inhibitor and then SGLTs expression, senescence markers and vascular function were evaluated. NPs significantly up-regulated SGLT2 and ENA significantly decreased NPs-induced senescence-associated-β‐gal activity, cell‐cycle arrest, and senescence markers p53 and p21 suggesting that inhibition of SGLT2 prevents NPs-induced endothelial senescence. In addition, ENA decreased the formation of reactive oxygen species with the downregulation of Nox2, and p22phox. Furthermore, SGLT2 inhibition also up regulated the endothelial nitric oxide synthase expression along with improving vascular function. In conclusion, premature endothelial senescence by NPs is, at least in part, associated with SGLT2 and it could be a potential therapeutic target for preventing and/or treating environmental pollutants-induced cardiovascular disorders mediated by endothelial senescence and dysfunction.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction

Dhakal

Shiwakoti

Park

et al. 2023

Sci Rep

Self Cite

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Human Toxicity of Nano‐ and Microplastics

Cruz Salas,

Perez,

Bobadilla

et al. 2024

Toxic Effects of Micro‐ and Nanoplastics

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Polystyrene nanoplastics induce haematotoxicity with cell oxeiptosis and senescence involved in C57BL/6J mice

Guo

Cheng

Wang

et al. 2023

Environmental Toxicology

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Nanoplastics (NPs) has become a worrying serious environmental problem. However, the toxicological effects and mechanisms of NPs on hematopoiesis are still unknown. To this end, male C57BL/6J mice were directly exposed to the serial concentration gradient of polystyrene NPs (PSNPs, 0, 30, 60, and 120 μg d), respectively, for 42 days by intragastric administration. Results show that PSNPs were clearly visible in bone tissues, meanwhile, induced the count of major blood indicators (WBC, RBC, and LYM) decreased. H&E staining displayed that exposed to PSNPs can cause hematopoietic damage of BM and extramedullary hematopoiesis in spleen. Flow cytometry result show that the proportion of LSK represented a dose‐dependent significantly decreased after PSNPs exposure. Further research found that PSNPs can cause the systemic oxidative stress occurs manifested as MDA accumulated. In addition, as the dose of PSNPs increased, the fluorescence intensity of Keap1 and p53 in femur sections gradually increased, meanwhile, the expression of cell oxeiptosis signal pathway Keap1/PGAM5/AIFM1 and the cell senescence signal pathway p53/p21 was all increased, markedly. Overall, our study demonstrated that PSNPs exposure caused oxidative stress, potentially resulting in cell oxeiptosis and senescence to develop haematotoxicity in C57BL/6J mice.

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Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism

Cited by 28 publications

References 63 publications

SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction

SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction

Human Toxicity of Nano‐ and Microplastics

Polystyrene nanoplastics induce haematotoxicity with cell oxeiptosis and senescence involved in C57BL/6J mice

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