September 1, 1991Journal of Biological ChemistryOpen Access

Mechanisms of inhibition by apolipoprotein C of apolipoprotein E-dependent cellular metabolism of human triglyceride-rich lipoproteins through the low density lipoprotein receptor pathway.

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Population

Cultured human skin fibroblasts

Comparison

Apolipoprotein C added to very low density… vs VLDL and IDL without added apoC, or with…

Design

Preclinical

Authors

ESEphraim SehayekCleveland Clinic SES. EisenbergHadassah Academic College

Discussion

Member takes

Implication

Apolipoprotein C inhibition of apoE-VLDL uptake should not change practice; leaves open isoform-specific roles in human dyslipidemia.

Structured PICO

Population

Cultured human skin fibroblasts

Intervention

Apolipoprotein C (total and individual C-I, C-II, C-III-1, and C-III-2) added to very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) with or without exogenous recombinant apolipoprotein E-3

Comparator

VLDL and IDL without added apoC, or with apoA-I/apoA-II

Outcome

Uptake and degradation of triglyceride-rich lipoproteins via the low density lipoprotein (LDL) receptor pathwaysurrogate

Apolipoprotein C inhibits the apoE-3-dependent interaction of triglyceride-rich lipoproteins with the LDL receptor in cultured fibroblasts, driven by the ratio of apoE-3 to apoC at the lipoprotein surface.

Cite This Study

Sehayek et al. (1991) studied this question.

synapsesocial.com/papers/6a702e4e5d37378ac1dd400f https://doi.org/10.1016/s0021-9258(18)55263-7

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