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Functionally defective high-density lipoprotein and paraoxonase: a couple for endothelial dysfunction in atherosclerosis.

Eren E, Yilmaz N, Aydin O - Cholesterol (2013)

Bottom Line: HDL-C is capable of opposing LDL's inductive effects and avoiding the ox-LDL's inhibition of eNOS.Paraoxonase 1 (PON1) is an HDL-associated enzyme esterase which appears to contribute to the antioxidant and antiatherosclerotic capabilities of HDL-C. "Healthy HDL," namely the particle that contains the active Paraoxonase 1, has the power to suppress the formation of oxidized lipids. "Dysfunctional HDL," on the contrary, has reduced Paraoxonase 1 enzyme activity and not only fails in its mission but also potentially leads to greater formation of oxidized lipids/lipoproteins to cause endothelial dysfunction.The association of HDL-C PON1 and endothelial dysfunction depends largely on the molecules with exact damaging effect on NO synthase coupling.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Atatürk Hospital, 07040 Antalya, Turkey.

ABSTRACT
The endothelium is the primary target for biochemical or mechanical injuries caused by the putative risk factors of atherosclerosis. Endothelial dysfunction represents the ultimate link between atherosclerotic risk factors that promote atherosclerosis. HDL-C is thought to exert at least some parts of its antiatherogenic facilities via stimulating endothelial NO production, nearby inhibiting oxidative stress and inflammation. HDL-C is capable of opposing LDL's inductive effects and avoiding the ox-LDL's inhibition of eNOS. Paraoxonase 1 (PON1) is an HDL-associated enzyme esterase which appears to contribute to the antioxidant and antiatherosclerotic capabilities of HDL-C. "Healthy HDL," namely the particle that contains the active Paraoxonase 1, has the power to suppress the formation of oxidized lipids. "Dysfunctional HDL," on the contrary, has reduced Paraoxonase 1 enzyme activity and not only fails in its mission but also potentially leads to greater formation of oxidized lipids/lipoproteins to cause endothelial dysfunction. The association of HDL-C PON1 and endothelial dysfunction depends largely on the molecules with exact damaging effect on NO synthase coupling. Loss of nitric oxide bioavailability has a pivotal role in endothelial dysfunction preceding the appearance of atherosclerosis. Analyses of HDL-C and Paraoxonase1 would be more important in the diagnosis and treatment of atherosclerosis in the very near future.

No MeSH data available.


Related in: MedlinePlus

H-HDLs perform functions including several immunological activities.
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fig2: H-HDLs perform functions including several immunological activities.

Mentions: H-HDL also has well-documented antioxidative properties. The antioxidant property of H-HDL is thought to be involved in potential antiatherogenic effects, but the exact mechanism is not known. H-HDL has been shown to prevent oxidative modification of LDL-C, thus reducing macrophage foam cell generation in the vessel wall [13]. Oxidized low-density lipoprotein (oxLDL) is the approved culprit in endothelial dysfunction. oxLDL induces endothelial damage, monocyte adhesion, and platelet aggregation and inhibits apoptosis and endothelial nitric oxide synthase (eNOS) expression/activity, all of which contribute to atherosclerotic process [14]. The other atheroprotective functions of H-HDL that have more recently attracted attention among other actions include its antiapopitotic, antithrombotic, and anti-infectious functions [1] (Figure 2).


Functionally defective high-density lipoprotein and paraoxonase: a couple for endothelial dysfunction in atherosclerosis.

Eren E, Yilmaz N, Aydin O - Cholesterol (2013)

H-HDLs perform functions including several immunological activities.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3814057&req=5

fig2: H-HDLs perform functions including several immunological activities.
Mentions: H-HDL also has well-documented antioxidative properties. The antioxidant property of H-HDL is thought to be involved in potential antiatherogenic effects, but the exact mechanism is not known. H-HDL has been shown to prevent oxidative modification of LDL-C, thus reducing macrophage foam cell generation in the vessel wall [13]. Oxidized low-density lipoprotein (oxLDL) is the approved culprit in endothelial dysfunction. oxLDL induces endothelial damage, monocyte adhesion, and platelet aggregation and inhibits apoptosis and endothelial nitric oxide synthase (eNOS) expression/activity, all of which contribute to atherosclerotic process [14]. The other atheroprotective functions of H-HDL that have more recently attracted attention among other actions include its antiapopitotic, antithrombotic, and anti-infectious functions [1] (Figure 2).

Bottom Line: HDL-C is capable of opposing LDL's inductive effects and avoiding the ox-LDL's inhibition of eNOS.Paraoxonase 1 (PON1) is an HDL-associated enzyme esterase which appears to contribute to the antioxidant and antiatherosclerotic capabilities of HDL-C. "Healthy HDL," namely the particle that contains the active Paraoxonase 1, has the power to suppress the formation of oxidized lipids. "Dysfunctional HDL," on the contrary, has reduced Paraoxonase 1 enzyme activity and not only fails in its mission but also potentially leads to greater formation of oxidized lipids/lipoproteins to cause endothelial dysfunction.The association of HDL-C PON1 and endothelial dysfunction depends largely on the molecules with exact damaging effect on NO synthase coupling.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Atatürk Hospital, 07040 Antalya, Turkey.

ABSTRACT
The endothelium is the primary target for biochemical or mechanical injuries caused by the putative risk factors of atherosclerosis. Endothelial dysfunction represents the ultimate link between atherosclerotic risk factors that promote atherosclerosis. HDL-C is thought to exert at least some parts of its antiatherogenic facilities via stimulating endothelial NO production, nearby inhibiting oxidative stress and inflammation. HDL-C is capable of opposing LDL's inductive effects and avoiding the ox-LDL's inhibition of eNOS. Paraoxonase 1 (PON1) is an HDL-associated enzyme esterase which appears to contribute to the antioxidant and antiatherosclerotic capabilities of HDL-C. "Healthy HDL," namely the particle that contains the active Paraoxonase 1, has the power to suppress the formation of oxidized lipids. "Dysfunctional HDL," on the contrary, has reduced Paraoxonase 1 enzyme activity and not only fails in its mission but also potentially leads to greater formation of oxidized lipids/lipoproteins to cause endothelial dysfunction. The association of HDL-C PON1 and endothelial dysfunction depends largely on the molecules with exact damaging effect on NO synthase coupling. Loss of nitric oxide bioavailability has a pivotal role in endothelial dysfunction preceding the appearance of atherosclerosis. Analyses of HDL-C and Paraoxonase1 would be more important in the diagnosis and treatment of atherosclerosis in the very near future.

No MeSH data available.


Related in: MedlinePlus