Role of acid lipase in cholesteryl ester accumulation during atherogenesis

Davis, Harry R.; Glagov, Seymour; Zarins, C K

doi:10.1016/0021-9150(85)90099-1

Cited by 14 publications

(3 citation statements)

References 23 publications

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“…Previous studies in atherosclerotic tissue have indicated that LAL activity is increased relative to non-atherosclerotic arteries (Brecher et al, 1977 ; Takano, 1978 ; Subbiah, 1979 ; Haley et al, 1980 ; Davis et al, 1985 ). The analytical procedures for those studies, however, involved ex vivo acidic pH adjustment and therefore reflects the total amount of potentially active LAL present, but not what may be actually active in vivo within intact cells under the influence of excess lipids and altered lysosomal pH.…”

Section: Lysosomal Cholesterol Accumulation In Atherosclerosismentioning

confidence: 96%

“…Haley et al ( 1980 ) indicated a 2-fold increase in LAL activity in lipid-laden lysosomes isolated by density centrifugation from atherosclerotic tissue homogenates. Davis et al ( 1985 ) reported that increased LAL activity in human aortic lesions at various stages of disease correlated with increased macrophage infiltration. These studies do not support the LAL deficiency hypothesis of atherosclerosis.…”

Section: Lysosomal Acid Lipasementioning

confidence: 99%

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Lysosomal acid lipase: at the crossroads of normal and atherogenic cholesterol metabolism

Dubland

Francis

2015

Front. Cell Dev. Biol.

109

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Unregulated cellular uptake of apolipoprotein B-containing lipoproteins in the arterial intima leads to the formation of foam cells in atherosclerosis. Lysosomal acid lipase (LAL) plays a crucial role in both lipoprotein lipid catabolism and excess lipid accumulation as it is the primary enzyme that hydrolyzes cholesteryl esters derived from both low density lipoprotein (LDL) and modified forms of LDL. Evidence suggests that as atherosclerosis progresses, accumulation of excess free cholesterol in lysosomes leads to impairment of LAL activity, resulting in accumulation of cholesteryl esters in the lysosome as well as the cytosol in foam cells. Impaired metabolism and release of cholesterol from lysosomes can lead to downstream defects in ATP-binding cassette transporter A1 regulation, needed to offload excess cholesterol from plaque foam cells. This review focuses on the role LAL plays in normal cholesterol metabolism and how the associated changes in its enzymatic activity may ultimately contribute to atherosclerosis progression.

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Section: Lysosomal Cholesterol Accumulation In Atherosclerosismentioning

confidence: 96%

Section: Lysosomal Acid Lipasementioning

confidence: 99%

Lysosomal acid lipase: at the crossroads of normal and atherogenic cholesterol metabolism

Dubland

Francis

2015

Front. Cell Dev. Biol.

109

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“…Macrophages in atherosclerotic plaques have lysosomal accumulation of cholesteryl ester and free cholesterol [22], implicating impaired lysosomal lipolysis. However, several studies have reported higher LAL activity in atherosclerotic tissue and lipid-laden lysosomes isolated from atherosclerotic tissue homogenates [23,24], although it is not yet clear whether this increased LAL activity is a result of a higher number of LAL-expressing cells in the lesion and/or an up-regulation of LAL within cells. Furthermore, the mRNA expression levels or the activity measured in vitro may not be correlated to the lipolytic capacity of LAL in an atherosclerotic environment when lysosomal acidification is compromised.…”

Section: Lysosomal Acid Lipase and Macrophage Lysosome Biogenesis In mentioning

confidence: 99%

Lysosomal acid lipase and lipid metabolism: new mechanisms, new questions, and new therapies

Zhang

2018

Current Opinion in Lipidology

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Tissue interactions and measurement of ablation rates with ultraviolet and visible lasers in canine and human arteries

et al. 1987

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Ablation rates measured as the depth of tissue excavation per unit time were determined in human and canine aortas subjected to radiation with ultraviolet (UV) excimer (ArF 193 nm, KrF 248 nm, XeF 351 nm) and visible lasers [continuous wave (cw) and 50-ms chopped argon ion, 478 nm-514 nm; pulsed double-frequency Nd:YAG, 532 nm]. For UV and pulsed double-frequency Nd:YAG lasers ablation rates were constant in time and depended linearly on average laser power, but for cw and chopped argon lasers ablation rates varied with irradiation time and were nonlinearly dependent on laser power. In human aortas, atherosclerosis without gross calcification had no influence on ablation rates. Charring and tissue disruption were observed with cw and chopped argon ion, whereas excimer and pulsed Nd:YAG lasers produced only minimal injury to surrounding tissue. We conclude that the determination of ablation rates is useful for the selection of laser wavelengths and power densities applicable to angioplasty and that UV and pulsed visible laser permit a better control of ablation compared to continuous wave lasers.

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Role of acid lipase in cholesteryl ester accumulation during atherogenesis

Cited by 14 publications

References 23 publications

Lysosomal acid lipase: at the crossroads of normal and atherogenic cholesterol metabolism

Lysosomal acid lipase: at the crossroads of normal and atherogenic cholesterol metabolism

Lysosomal acid lipase and lipid metabolism: new mechanisms, new questions, and new therapies

Tissue interactions and measurement of ablation rates with ultraviolet and visible lasers in canine and human arteries

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