Limits...
Oxidized low density lipoprotein, stem cells, and atherosclerosis.

Yang H, Mohamed AS, Zhou SH - Lipids Health Dis (2012)

Bottom Line: Researchers have proposed that stem cells participate in the formation of atherosclerotic plaque.Also, because ox-LDL is capable of inducing toxic effects on stem cells, it is reasonable to postulate that ox-LDL promotes the progress of atherosclerosis via acting on stem cells.In the present article, we review the relationship between ox-LDL, stem cells, and atherosclerosis and a portion of the associated mechanisms.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cardiology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.

ABSTRACT
Oxidized low density lipoprotein (ox-LDL), a risk factor of atherosclerosis, facilitates the formation and vulnerability of atherosclerotic plaque, thus contributing to several clinical complications. Stem cells participate in vascular repair after damage and atherosclerosis is a process of inflammation accompanied with vascular injury. Researchers have proposed that stem cells participate in the formation of atherosclerotic plaque. Also, because ox-LDL is capable of inducing toxic effects on stem cells, it is reasonable to postulate that ox-LDL promotes the progress of atherosclerosis via acting on stem cells. In the present article, we review the relationship between ox-LDL, stem cells, and atherosclerosis and a portion of the associated mechanisms.

Show MeSH

Related in: MedlinePlus

The molecular events included in the direct toxic effects of ox-LDL on stem cells. ?: whether receptors mediate phagocytosis of ox-LDL in MSCs is not clear; →: positive effects; ⊥: negative effects.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3475066&req=5

Figure 1: The molecular events included in the direct toxic effects of ox-LDL on stem cells. ?: whether receptors mediate phagocytosis of ox-LDL in MSCs is not clear; →: positive effects; ⊥: negative effects.

Mentions: LDLs in the blood could enter the intima, where they are retained through binding to the extracellular matrix. LDLs are then modified by oxygen radicals, myeloperoxidase, secretory phospholipase A2 and sphingomyelinase [32]. The rate of oxidants liberated by cultured cells and their ability to oxidize LDL is largely variable and is dependent on species, cell type, proliferation rate, and culture medium [36]. Monocyte-derived macrophages and neutrophils are able to initiate and propagate lipid peroxidation [43]. To the best of our knowledge, whether stem cells could modificate LDLs and/or the involved mechanisms are not clear. Even if stem cells have no effect on LDL oxidation, the LDL oxidized by other cells, such as monocytes, may contribute to the participation of stem cells in the process of atherosclerosis. However, it is important to know the direct effects of stem cells on LDL and its role in atherogenesis, which would let us to know whether stem cells can initiate atherosclerosis without the help of other cell types. Systemic lipids from diet can be delivered to the bone marrow by chylomicron and chylomicron remnants [44,45]. Hyperlipidemia may negatively influence the stem cells in both bone marrow and systemic circulation pool. There are large number of evidences that ox-LDL could act on stem cells, especially EPCs, SMPCs, and MSCs to influence the cellular physical activities in almost every aspects, such as proliferation, differentiation, apoptosis, mobilization, migration, senescence, and so on. The associated mechanisms might include membrane receptors mediated phagocytosis and signal transduction, oxidative stress, mitogen activated protein kinase (MAPK) pathway and others, which may be further divided into direct (Figure 1) and indirect effects.


Oxidized low density lipoprotein, stem cells, and atherosclerosis.

Yang H, Mohamed AS, Zhou SH - Lipids Health Dis (2012)

The molecular events included in the direct toxic effects of ox-LDL on stem cells. ?: whether receptors mediate phagocytosis of ox-LDL in MSCs is not clear; →: positive effects; ⊥: negative effects.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475066&req=5

Figure 1: The molecular events included in the direct toxic effects of ox-LDL on stem cells. ?: whether receptors mediate phagocytosis of ox-LDL in MSCs is not clear; →: positive effects; ⊥: negative effects.
Mentions: LDLs in the blood could enter the intima, where they are retained through binding to the extracellular matrix. LDLs are then modified by oxygen radicals, myeloperoxidase, secretory phospholipase A2 and sphingomyelinase [32]. The rate of oxidants liberated by cultured cells and their ability to oxidize LDL is largely variable and is dependent on species, cell type, proliferation rate, and culture medium [36]. Monocyte-derived macrophages and neutrophils are able to initiate and propagate lipid peroxidation [43]. To the best of our knowledge, whether stem cells could modificate LDLs and/or the involved mechanisms are not clear. Even if stem cells have no effect on LDL oxidation, the LDL oxidized by other cells, such as monocytes, may contribute to the participation of stem cells in the process of atherosclerosis. However, it is important to know the direct effects of stem cells on LDL and its role in atherogenesis, which would let us to know whether stem cells can initiate atherosclerosis without the help of other cell types. Systemic lipids from diet can be delivered to the bone marrow by chylomicron and chylomicron remnants [44,45]. Hyperlipidemia may negatively influence the stem cells in both bone marrow and systemic circulation pool. There are large number of evidences that ox-LDL could act on stem cells, especially EPCs, SMPCs, and MSCs to influence the cellular physical activities in almost every aspects, such as proliferation, differentiation, apoptosis, mobilization, migration, senescence, and so on. The associated mechanisms might include membrane receptors mediated phagocytosis and signal transduction, oxidative stress, mitogen activated protein kinase (MAPK) pathway and others, which may be further divided into direct (Figure 1) and indirect effects.

Bottom Line: Researchers have proposed that stem cells participate in the formation of atherosclerotic plaque.Also, because ox-LDL is capable of inducing toxic effects on stem cells, it is reasonable to postulate that ox-LDL promotes the progress of atherosclerosis via acting on stem cells.In the present article, we review the relationship between ox-LDL, stem cells, and atherosclerosis and a portion of the associated mechanisms.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cardiology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.

ABSTRACT
Oxidized low density lipoprotein (ox-LDL), a risk factor of atherosclerosis, facilitates the formation and vulnerability of atherosclerotic plaque, thus contributing to several clinical complications. Stem cells participate in vascular repair after damage and atherosclerosis is a process of inflammation accompanied with vascular injury. Researchers have proposed that stem cells participate in the formation of atherosclerotic plaque. Also, because ox-LDL is capable of inducing toxic effects on stem cells, it is reasonable to postulate that ox-LDL promotes the progress of atherosclerosis via acting on stem cells. In the present article, we review the relationship between ox-LDL, stem cells, and atherosclerosis and a portion of the associated mechanisms.

Show MeSH
Related in: MedlinePlus