Low density lipoprotein receptor expression and function in human polymorphonuclear leucocytes

Leclerc, Lara; Rivera, Humberto Fernando Cantú; Perez-P, C.; Blanca, Isaac; Bianco, N. E.; Sanctis, Juan B. De

doi:10.1046/j.1365-2249.1997.d01-888.x

Cited by 22 publications

(17 citation statements)

References 26 publications

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“…Ca +2 dependent PKC is the main enzyme involved in both these phenomena, while MAPK pathway mediated both the inflammatory and the antioxidant gene expression regulation. PKC is also involved in the oxidative burst of human polymorphonuclear leucocytes, activated with PMA, observed after interaction of LDL with its receptor (LDLR) [86] (Fig. 2).…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Peluso

Morabito²,

Urban³

et al. 2012

EMIDDT

197

133

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The involvement of both oxidative stress and hyperlipaemia in atherosclerosis development is well established. Oxidative burst is an innate immune response to infection, the latter being associated also with marked changes in lipid and lipoprotein metabolism, aimed to neutralize endotoxin toxic effects. On the other hand, lipid overload may increase lipopolysaccharide circulating levels and oxidative stress. Whilst these changes may be beneficial from the perspective of host defense, if they become chronic, they likely increase the risk of atherosclerosis. In particular, oxidation of lipoproteins, resulting from an imbalance of the pro- and antioxidant equilibrium, is involved in the pathologic process of atherosclerosis, changing cellular functions. Lipid oxidation, induced by leukocytes derived reactive oxygen species, can amplify foam cell formation through oxidized low density lipoproteins LDL (oxLDL) formation and uptake. The main enzymes, operating during oxidative burst, involved in LDL oxidation are NADPH oxidase and myeloperoxidase. In vitro studies have shown that oxLDL are able to induce many proatherogenic processes, including modulation of oxidative burst. OxLDL may also induce maturation of dendritic cells and regulate the shift from classical (M1) to alternative (M2) macrophage activation and from T helper 1 to T helper 2 response, suggesting that these could act as a bridge between innate and adaptative immunity, both involved in plaque development. Understanding the relationship between oxLDL and leukocyte oxidative burst helps to explain the involvement of innate immune responses in the early phases of atherosclerosis. The present review focuses on this interplay.

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Peluso

Morabito²,

Urban³

et al. 2012

EMIDDT

197

133

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show abstract

“…Although the liver is the central organ for receptor-mediated clearance of LDL, circulating leukocytes also abundantly express LDLR which internalizes and degrades LDL molecules, contributing a large mass to the body. [21][22][23][24] Thus, peripheral leukocytes could also serve as the target for adjunct gene therapy for familial hypercholesterolemia. Our results have also implications for applying this technology to other human diseases, especially those in which deficiency of a single gene can be replaced by transfer of an exogenous gene into circulating cells.…”

mentioning

confidence: 99%

Intravenous gene therapy for familial hypercholesterolemia using ligand-facilitated transfer of a liposome:LDL receptor gene complex

2003

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“…Briefly, we assessed proliferation of purified BC, and nitrite and peroxide production of RAW 264.7 cells and Nph, respectively [10]. The specificity of the biological activity was confirmed by addition of Ab or Ig-CD40 (Ancell, Bayport, MN, USA), both specifically neutralizing the activity of sCD154.…”

Section: Methodsmentioning

confidence: 99%

Total and biologically active CD154 in patients with SLE

et al. 2009

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CD154, a member of the tumor necrosis factor receptor family, is involved in several biological responses. In the sera of systemic lupus erythematosus (SLE) patients, the levels of sCD154 have been shown to be increased, however, few reports have dealt with the biologically active tetramer. Here, we assessed the biological activity of the serum CD154 tetramer using bioassays for BC activation and production nitrite or peroxide. The patients showed a markedly increased total sCD154 serum concentration (12.5 +/- 8.2 vs. 3.9 +/- 1.2 ng/ml; p < 0.001). ba-sCD154 was significantly increased in non-treated patients (7.4 +/- 3.4 ng/ml, n = 22; p < 0.001) and patients with the highest SLE disease activity index (SLEDAI) scores (5.3 +/- 2.9 ng/ml, n = 8), but not in stable patients (1.3 +/- 1.2 ng/ml, n = 30) whose values were similar to normal healthy donors (NHD; 0.8 +/- 0.2 ng/ml). Patients with SLEDAI above 8 that recovered after successful treatment displayed significantly decreased levels of ba-sCD154. We conclude that the bioassay is a useful tool discriminating active and stable SLE, as well as non-treated patients.

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Low density lipoprotein receptor expression and function in human polymorphonuclear leucocytes

Cited by 22 publications

References 26 publications

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Intravenous gene therapy for familial hypercholesterolemia using ligand-facilitated transfer of a liposome:LDL receptor gene complex

Total and biologically active CD154 in patients with SLE

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