Evidence map›Paper›PMID 27253994›Full record

ArticleEndocrinology2016

Synthetic High-Density Lipoprotein (sHDL) Inhibits Steroid Production in HAC15 Adrenal Cells.

Matthew J Taylor, Aalok R Sanjanwala, Emily E Morin, Elizabeth Rowland-Fisher, Kyle Anderson, Anna Schwendeman, William E Rainey

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Lipid metabolism in the adrenal gland.Frontiers in endocrinology · 2025
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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

7 authors at 1 institution in 1 country.

Matthew J TaylorDepartments of Molecular and Integrative Physiology and Internal Medicine (M.J.T., A.R.S., K.A.,W.E.R.)., University of Michigan, Ann Arbor, Michigan 48109; Medical College of Georgia (A.R.S.), Georgia Regents University, Augusta, Georgia 30912; Department of Pharmaceutical Science (E.E.M., A.S.), Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109; and Department of Medicinal Chemistry (E.R.-F.), College of Pharmacy, University of Michigan, Ann Arbor, Michigan 48109.
Aalok R SanjanwalaDepartments of Molecular and Integrative Physiology and Internal Medicine (M.J.T., A.R.S., K.A.,W.E.R.)., University of Michigan, Ann Arbor, Michigan 48109; Medical College of Georgia (A.R.S.), Georgia Regents University, Augusta, Georgia 30912; Department of Pharmaceutical Science (E.E.M., A.S.), Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109; and Department of Medicinal Chemistry (E.R.-F.), College of Pharmacy, University of Michigan, Ann Arbor, Michigan 48109.
Emily E MorinDepartments of Molecular and Integrative Physiology and Internal Medicine (M.J.T., A.R.S., K.A.,W.E.R.)., University of Michigan, Ann Arbor, Michigan 48109; Medical College of Georgia (A.R.S.), Georgia Regents University, Augusta, Georgia 30912; Department of Pharmaceutical Science (E.E.M., A.S.), Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109; and Department of Medicinal Chemistry (E.R.-F.), College of Pharmacy, University of Michigan, Ann Arbor, Michigan 48109.
Elizabeth Rowland-FisherDepartments of Molecular and Integrative Physiology and Internal Medicine (M.J.T., A.R.S., K.A.,W.E.R.)., University of Michigan, Ann Arbor, Michigan 48109; Medical College of Georgia (A.R.S.), Georgia Regents University, Augusta, Georgia 30912; Department of Pharmaceutical Science (E.E.M., A.S.), Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109; and Department of Medicinal Chemistry (E.R.-F.), College of Pharmacy, University of Michigan, Ann Arbor, Michigan 48109.
Kyle AndersonDepartments of Molecular and Integrative Physiology and Internal Medicine (M.J.T., A.R.S., K.A.,W.E.R.)., University of Michigan, Ann Arbor, Michigan 48109; Medical College of Georgia (A.R.S.), Georgia Regents University, Augusta, Georgia 30912; Department of Pharmaceutical Science (E.E.M., A.S.), Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109; and Department of Medicinal Chemistry (E.R.-F.), College of Pharmacy, University of Michigan, Ann Arbor, Michigan 48109.
Anna SchwendemanDepartments of Molecular and Integrative Physiology and Internal Medicine (M.J.T., A.R.S., K.A.,W.E.R.)., University of Michigan, Ann Arbor, Michigan 48109; Medical College of Georgia (A.R.S.), Georgia Regents University, Augusta, Georgia 30912; Department of Pharmaceutical Science (E.E.M., A.S.), Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109; and Department of Medicinal Chemistry (E.R.-F.), College of Pharmacy, University of Michigan, Ann Arbor, Michigan 48109.
William E RaineyDepartments of Molecular and Integrative Physiology and Internal Medicine (M.J.T., A.R.S., K.A.,W.E.R.)., University of Michigan, Ann Arbor, Michigan 48109; Medical College of Georgia (A.R.S.), Georgia Regents University, Augusta, Georgia 30912; Department of Pharmaceutical Science (E.E.M., A.S.), Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan 48109; and Department of Medicinal Chemistry (E.R.-F.), College of Pharmacy, University of Michigan, Ann Arbor, Michigan 48109.
University of Michigan–Ann Arbor · US

Funding

Cellular Biotechnology Training Program (CBTP)T32GM008353 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCHWENDEMAN, ANNA · 1991 to 2021
$9.3M
SYTEMS AND INTEGRATIVE BIOLOGYT32GM008322 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOW, MALCOLM JAMES · 1990 to 2020
$5.7M
Molecular Mechanisms of AdrenarcheR01DK069950 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RAINEY, WILLIAM E · 2005 to 2019
$4.4M
Synthetic HDL_a potential sepsis therapyR01GM113832 · NIGMS · UNIVERSITY OF KENTUCKY · PI LI, XIANG-AN, SCHWENDEMAN, ANNA · 2015 to 2019
$3.0M
Cellular Biotechnology Training Program (CBTP) - Years 31-35T32GM145304 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Guizhi Zhu · 2022 to 2026
$2.6M
Training Program in Translational Cardiovascular Research and EntrepreneurshipT32HL125242 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MICHELE, DANIEL E · 2015 to 2024
$1.9M
NHLBI NIH HHS T32 HL125242NIDDK NIH HHS R01 DK069950NIGMS NIH HHS R01 GM113832NIGMS NIH HHS T32 GM008322NIGMS NIH HHS T32 GM008353NIGMS NIH HHS T32 GM145304
6 · The paper itself

Abstract

High density lipoprotein (HDL) transported cholesterol represents one of the sources of substrate for adrenal steroid production. Synthetic HDL (sHDL) particles represent a new therapeutic option to reduce atherosclerotic plaque burden by increasing cholesterol efflux from macrophage cells. The effects of the sHDL particles on steroidogenic cells have not been explored. sHDL, specifically ETC-642, was studied in HAC15 adrenocortical cells. Cells were treated with sHDL, forskolin, 22R-hydroxycholesterol, or pregnenolone. Experiments included time and concentration response curves, followed by steroid assay. Quantitative real-time RT-PCR was used to study mRNA of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase, lanosterol 14-α-methylase, cholesterol side-chain cleavage enzyme, and steroid acute regulatory protein. Cholesterol assay was performed using cell culture media and cell lipid extracts from a dose response experiment. sHDL significantly inhibited production of cortisol. Inhibition occurred in a concentration- and time-dependent manner and in a concentration range of 3μM-50μM. Forskolin (10μM) stimulated cortisol production was also inhibited. Incubation with 22R-hydroxycholesterol (10μM) and pregnenolone (10μM) increased cortisol production, which was unaffected by sHDL treatment. sHDL increased transcript levels for the rate-limiting cholesterol biosynthetic enzyme, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase. Extracellular cholesterol assayed in culture media showed a positive correlation with increasing concentration of sHDL, whereas intracellular cholesterol decreased after treatment with sHDL. The current study suggests that sHDL inhibits HAC15 adrenal cell steroid production by efflux of cholesterol, leading to an overall decrease in steroid production and an adaptive rise in adrenal cholesterol biosynthesis.

Indexed as

Adrenal Cortex HormonesAdrenal GlandsAdrenocorticotropic HormoneCell Line, TumorCholesterolGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansHydrocortisoneLipoproteins, HDLMetabolic Networks and PathwaysAdrenal Cortex HormonesAdrenocorticotropic HormoneCholesterolHydrocortisoneLipoproteins, HDL

Identifiers

PMID27253994
PMCPMC4967112
OpenAlexW2416230234

What OpenQuestion 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 OpenQuestion graph.