Atorvastatin enhances cellular uptake of oxidized LDL in adipocytes from hypercholesterolemic rabbits

Zhao, Shui‐Ping; Zhang, Daqing

doi:10.1016/j.cccn.2003.10.007

Cited by 20 publications

(11 citation statements)

References 25 publications

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“…The expression of CD36 undoubtedly reflects its very significant role in the function of the adipose cell. Looking beyond its implication in the transport of fatty acids, this new data enables us to postulate that the adipose tissue could play a major role in the elimination of LDL oxidized within the human body (Kuniyasu et al 2002;Stanton et al 1997;Zhao et al 2004). Thus, CD36 can be regarded as a very good marker of differentiated adipocyte (Teboul et al 2001).…”

Section: Discussionmentioning

confidence: 90%

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

Festy¹,

Hoareau²,

Bès-Houtmann³

et al. 2005

Histochem Cell Biol

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Adipose tissue contains a stroma that can be easily isolated. Thus, human adipose tissue presents an source of multipotent stromal cells. In order to determine the implication of hematopoietic markers in adipocyte biology, we have defined part of the phenotype of the human adipose tissue-derived stromal cells, and compared this to fully differentiated adipocytes. Flow cytometry demonstrates that the protein expression phenotype of both cell types are similar and includes the expression of CD10, CD13, CD34, CD36, CD55, CD59 and CD65. No significant difference between subcutaneous and omental adipose tissue could be demonstrated concerning the expression of these markers. However, the expression of CD34, CD36 and CD65 is cell-dependent. While the expression of CD36 and CD65 doubled between stromal cells and mature adipocytes, the expression of CD34 decreased, despite this protein being present on the mature adipocyte. As CD34 is described as a stem cell marker and it being unlikely to be expressed on differentiated cells, this result was confirmed by immunostaining and western blot. The clear function of this protein on the adipocyte membrane remains to be determined. The characterization of new proteins on mature adipocytes could have broad implications for the comprehension of the biology of this tissue.

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Section: Discussionmentioning

confidence: 90%

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

Festy¹,

Hoareau²,

Bès-Houtmann³

et al. 2005

Histochem Cell Biol

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“…PPARγ is a central regulator of adipocyte differentiation and lipid accumulation through transcriptional regulation of genes encoding proteins involved in lipid metabolism and the inflammatory reaction. Several PPARγ-responsive genes have been identified such as CD36 are highly expressed in adipocytes 29 . CD36 is a major regulator of long-chain FA transport across the cell membrane and acts as a scavenger receptor for oxLDL in macrophages.…”

Section: Discussionmentioning

confidence: 99%

High-density Lipoprotein Increases the Uptake of Oxidized Low Density Lipoprotein via PPARγ/CD36 Pathway in Inflammatory Adipocytes

Zhong¹,

Zhao²,

Yu³

et al. 2015

Int. J. Biol. Sci.

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Aim: Previous studies have demonstrated that the dysregulated-secretion of adipokines by adipocytes may contribute to obesity-associated atherosclerosis (As) and high density lipoprotein (HDL) may protect against atherogenesis through multiple pathways. This study was to explore the effect of HDL on the oxLDL uptake in inflammatory adipocytes stimulated by endotoxin lipopolysaccharide (LPS) and the possible mechanism.Methods and Results: 3T3-L1 adipocytes were cultured and induced to differentiation and maturation. Acute inflammation in adipocytes was induced by LPS (100 ng/ml) for 6 hours. The adipocytes were pretreated with HDL in various concentrations (10, 50, 100 μg/ml) for 16 hours or with specific PPARγ antagonist (GW9662, 10 μM) or agonist (Rosiglitazone, 10 μM) for 30 min before administration of LPS. The results showed that LPS significantly increased the release of inflammation-related adipokines, such as monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor 1 (PAI-1), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-8 and IL-6, while decreasing the release of leptin and adiponectin. Meanwhile, LPS reduced the uptake and degradation of 125I-oxLDL, and down-regulated the expression of PPARγ and CD36. Pretreatment with HDL dose-dependently affected the release of IL-8 and IL-6 and the reduced uptake and degradation of oxLDL of adipocytes stimulated by LPS, accompanied with marked upregulation of PPARγ and CD36 expression. Pretreatment with GW9662 markedly inhibited the upregulation of CD36 expression mediated by HDL (100 μg/ml), while the effects of Rosiglitazone were opposite to GW9662.Conclusions: HDL may increase oxLDL uptake of inflammatory adipocytes stimulated by LPS via upregulation of PPARγ/CD36 pathway, which may be a new mechanism of anti-atherosclerosis mediated by HDL.

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“…Statins also reduce oxygen species generation [54]. Atorvastatin promotes adipocyte uptake of oxLDL in rabbits by increasing the expression of CD36 and peroxisome proliferators-activated receptor γ (PPARγ) in adipocytes [58]. The increased expression of such receptors by adipocytes results to internalization of oxLDL and clearance from plasma, converting adipocytes to an oxLDLbuffering pool [58].…”

Section: Discussionmentioning

confidence: 99%

“…Atorvastatin promotes adipocyte uptake of oxLDL in rabbits by increasing the expression of CD36 and peroxisome proliferators-activated receptor γ (PPARγ) in adipocytes [58]. The increased expression of such receptors by adipocytes results to internalization of oxLDL and clearance from plasma, converting adipocytes to an oxLDLbuffering pool [58]. Reduction of oxLDL in patients with CHD with atorvastatin 10mg parallel with an increase of adiponectin, which has anti-atherogenic [55], anti-inflammatory and antidiabetic [55] properties through reduction of insulin resistance [55].…”

Section: Discussionmentioning

confidence: 99%

Oxidised Low Density Lipoprotein (LDL) Modification with Statin Therapy is Associated with Reduction in Carotid Stenosis

Skopelitis¹,

Levisianou²,

Lydataki³

et al. 2014

Carotid Artery Disease - From Bench to Bedside and Beyond

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Atorvastatin enhances cellular uptake of oxidized LDL in adipocytes from hypercholesterolemic rabbits

Cited by 20 publications

References 25 publications

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

High-density Lipoprotein Increases the Uptake of Oxidized Low Density Lipoprotein via PPARγ/CD36 Pathway in Inflammatory Adipocytes

Oxidised Low Density Lipoprotein (LDL) Modification with Statin Therapy is Associated with Reduction in Carotid Stenosis

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