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Effects of the Particulate Matter₂.₅ (PM₂.₅) on Lipoprotein Metabolism, Uptake and Degradation, and Embryo Toxicity.

Kim JY, Lee EY, Choi I, Kim J, Cho KH - Mol. Cells (2015)

Bottom Line: In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism.PM2.5 extract resulted in degradation and aggregation of high-density lipoprotein (HDL) as well as low-density lipoprotein (LDL); apoA-I in HDL aggregated and apo-B in LDL disappeared.In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

View Article: PubMed Central - PubMed

Affiliation: School of Biotechnology, Korea.

ABSTRACT
Particulate matter2.5 (PM2.5) is notorious for its strong toxic effects on the cardiovascular, skin, nervous, and reproduction systems. However, the molecular mechanism by which PM2.5 aggravates disease progression is poorly understood, especially in a water-soluble state. In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism. Collected PM2.5 from Seoul, Korea was dissolved in water, and the water extract (final 3 and 30 ppm) was treated to human serum lipoproteins, macrophages, and dermal cells. PM2.5 extract resulted in degradation and aggregation of high-density lipoprotein (HDL) as well as low-density lipoprotein (LDL); apoA-I in HDL aggregated and apo-B in LDL disappeared. PM2.5 treatment (final 30 ppm) also induced cellular uptake of oxidized LDL (oxLDL) into macrophages, especially in the presence of fructose (final 50 mM). Uptake of oxLDL along with production of reactive oxygen species was accelerated by PM2.5 solution in a dose-dependent manner. Further, PM2.5 solution caused cellular senescence in human dermal fibroblast cells. Microinjection of PM2.5 solution into zebrafish embryos induced severe mortality accompanied by impairment of skeletal development. In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

No MeSH data available.


Related in: MedlinePlus

Uptake of LDL into human macrophages in the presence of PM2.5 extract and fructose (Frc). (A) Oil red O-stained area for visualization of LDL phagocytosis. Quantification of stained area by computer-assisted image analysis.
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f4-molce-38-12-1096: Uptake of LDL into human macrophages in the presence of PM2.5 extract and fructose (Frc). (A) Oil red O-stained area for visualization of LDL phagocytosis. Quantification of stained area by computer-assisted image analysis.

Mentions: As shown in Fig. 4, uptake of native LDL into macrophages resulted in 42% oil-red O staining. However, PM2.5 solution caused 2.2-fold increased LDL uptake into cells, indicating that PM2.5 accelerated atherogenesis. In the presence of fructose (final 50 mM in cell media), LDL uptake was also accelerated to a similar extent as PM2.5 treatment. Interestingly, co-presence of PM2.5 and fructose cause 2.4-fold higher LDL uptake with increased cell death.


Effects of the Particulate Matter₂.₅ (PM₂.₅) on Lipoprotein Metabolism, Uptake and Degradation, and Embryo Toxicity.

Kim JY, Lee EY, Choi I, Kim J, Cho KH - Mol. Cells (2015)

Uptake of LDL into human macrophages in the presence of PM2.5 extract and fructose (Frc). (A) Oil red O-stained area for visualization of LDL phagocytosis. Quantification of stained area by computer-assisted image analysis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4697001&req=5

f4-molce-38-12-1096: Uptake of LDL into human macrophages in the presence of PM2.5 extract and fructose (Frc). (A) Oil red O-stained area for visualization of LDL phagocytosis. Quantification of stained area by computer-assisted image analysis.
Mentions: As shown in Fig. 4, uptake of native LDL into macrophages resulted in 42% oil-red O staining. However, PM2.5 solution caused 2.2-fold increased LDL uptake into cells, indicating that PM2.5 accelerated atherogenesis. In the presence of fructose (final 50 mM in cell media), LDL uptake was also accelerated to a similar extent as PM2.5 treatment. Interestingly, co-presence of PM2.5 and fructose cause 2.4-fold higher LDL uptake with increased cell death.

Bottom Line: In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism.PM2.5 extract resulted in degradation and aggregation of high-density lipoprotein (HDL) as well as low-density lipoprotein (LDL); apoA-I in HDL aggregated and apo-B in LDL disappeared.In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

View Article: PubMed Central - PubMed

Affiliation: School of Biotechnology, Korea.

ABSTRACT
Particulate matter2.5 (PM2.5) is notorious for its strong toxic effects on the cardiovascular, skin, nervous, and reproduction systems. However, the molecular mechanism by which PM2.5 aggravates disease progression is poorly understood, especially in a water-soluble state. In the current study, we investigated the putative physiological effects of aqueous PM2.5 solution on lipoprotein metabolism. Collected PM2.5 from Seoul, Korea was dissolved in water, and the water extract (final 3 and 30 ppm) was treated to human serum lipoproteins, macrophages, and dermal cells. PM2.5 extract resulted in degradation and aggregation of high-density lipoprotein (HDL) as well as low-density lipoprotein (LDL); apoA-I in HDL aggregated and apo-B in LDL disappeared. PM2.5 treatment (final 30 ppm) also induced cellular uptake of oxidized LDL (oxLDL) into macrophages, especially in the presence of fructose (final 50 mM). Uptake of oxLDL along with production of reactive oxygen species was accelerated by PM2.5 solution in a dose-dependent manner. Further, PM2.5 solution caused cellular senescence in human dermal fibroblast cells. Microinjection of PM2.5 solution into zebrafish embryos induced severe mortality accompanied by impairment of skeletal development. In conclusion, water extract of PM2.5 induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

No MeSH data available.


Related in: MedlinePlus