Evidence map›Paper›PMID 27381048›Full record

ArticleJournal of lipid research2016

Intracellular cholesterol transport proteins enhance hydrolysis of HDL-CEs and facilitate elimination of cholesterol into bile.

Jing Wang, Jinghua Bie, Shobha Ghosh

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Triglyceride Metabolism in the Liver.Comprehensive Physiology · 2017
    Review
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jing WangDepartment of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, VA 23298.
Jinghua BieDepartment of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, VA 23298.
Shobha GhoshDepartment of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, VA 23298 shobha@vcu.edu.
Virginia Commonwealth University Medical Center · US

Funding

Hepatic Cholesteryl Ester Metabolism and Cholesterol EliminationR01HL097346 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GHOSH, SHOBHA · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL097346
6 · The paper itself

Abstract

While HDL-associated unesterified or free cholesterol (FC) is thought to be rapidly secreted into the bile, the fate of HDL-associated cholesteryl esters (HDL-CEs) that represent >80% of HDL-cholesterol, is only beginning to be understood. In the present study, we examined the hypothesis that intracellular cholesterol transport proteins [sterol carrier protein 2 (SCP2) and fatty acid binding protein-1 (FABP1)] not only facilitate CE hydrolase-mediated hydrolysis of HDL-CEs, but also enhance elimination of cholesterol into bile. Adenovirus-mediated overexpression of FABP1 or SCP2 in primary hepatocytes significantly increased hydrolysis of HDL-[(3)H]CE, reduced resecretion of HDL-CE-derived FC as nascent HDL, and increased its secretion as bile acids. Consistently, the flux of [(3)H]cholesterol from HDL-[(3)H]CE to biliary bile acids was increased by overexpression of SCP2 or FABP1 in vivo and reduced in SCP2(-/-) mice. Increased flux of HDL-[(3)H]CE to biliary FC was noted with FABP1 overexpression and in SCP2(-/-) mice that have increased FABP1 expression. Lack of a significant decrease in the flux of HDL-[(3)H]CE to biliary FC or bile acids in FABP1(-/-) mice indicates the likely compensation of its function by an as yet unidentified mechanism. Taken together, these studies demonstrate that FABP1 and SCP2 facilitate the preferential movement of HDL-CEs to bile for final elimination.

Indexed as

AdenoviridaeAnimalsBileBile Acids and SaltsCarrier ProteinsCholesterolCholesterol EstersCholesterol, HDLFatty Acid-Binding ProteinsGene Expression RegulationHydrolysisLipoproteins, HDLLiverMiceBile Acids and SaltsCarrier ProteinsCholesterolCholesterol EstersCholesterol, HDLFabp1 protein, mouseFatty Acid-Binding ProteinsHDL cholesteryl esterLipoproteins, HDLsterol carrier proteinsbile acid secretioncholesterol eliminationcholesteryl estersfatty acid binding protein-1hepatocytehigh density lipoproteinreverse cholesterol transportsterol carrier protein 2

Identifiers

PMID27381048
PMCPMC5003163
OpenAlexW2514672305

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.