Remnant lipoproteins inhibit malaria sporozoite invasion of hepatocytes

Research output: Contribution to journalArticle

Abstract

Remnants of lipoproteins (chylomicron remnants and very low density lipoprotein remnants) are rapidly cleared from plasma and enter hepatocytes. The catabolism of the lipoproteins is apolipoprotein E (apoE) dependent. It has been suggested that the lipoproteins are initially captured in the space of Disse by heparan sulfate proteoglycans and then internalized by members of the LDL-receptor gene family. Within minutes after injection by Anopheles mosquitoes, malaria sporozoties are also removed from the blood circulation by the liver. The sporozoite's surface is covered by the circumsporozoite protein (CS), and its region ll-plus has been implicated in the initial binding of the parasites to the hepatocytes. Here we provide evidence that CS and remnant lipoproteins compete in vitro and in vivo for the same liver receptors. As predicted by these observations, apoE-enriched remnant lipoproteins inhibit sporozoite invasion of HepG2 cells, and malaria parasites are less infective in LDL-receptor knockout mice maintained on a high fat diet.

Original languageEnglish (US)
JournalJournal of Investigative Medicine
Volume44
Issue number3
StatePublished - 1996
Externally publishedYes

Fingerprint

Sporozoites
Lipoproteins
Malaria
Hepatocytes
LDL Receptors
Apolipoproteins E
Liver
Parasites
Chylomicron Remnants
Heparan Sulfate Proteoglycans
Anopheles
VLDL Lipoproteins
Blood Circulation
Hep G2 Cells
Hemodynamics
High Fat Diet
Nutrition
Culicidae
Knockout Mice
Proteins

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Remnant lipoproteins inhibit malaria sporozoite invasion of hepatocytes. / Sinnis, Photini.

In: Journal of Investigative Medicine, Vol. 44, No. 3, 1996.

Research output: Contribution to journalArticle

@article{ef06cfc8e8fb4a028daacc8bfb6429d6,
title = "Remnant lipoproteins inhibit malaria sporozoite invasion of hepatocytes",
abstract = "Remnants of lipoproteins (chylomicron remnants and very low density lipoprotein remnants) are rapidly cleared from plasma and enter hepatocytes. The catabolism of the lipoproteins is apolipoprotein E (apoE) dependent. It has been suggested that the lipoproteins are initially captured in the space of Disse by heparan sulfate proteoglycans and then internalized by members of the LDL-receptor gene family. Within minutes after injection by Anopheles mosquitoes, malaria sporozoties are also removed from the blood circulation by the liver. The sporozoite's surface is covered by the circumsporozoite protein (CS), and its region ll-plus has been implicated in the initial binding of the parasites to the hepatocytes. Here we provide evidence that CS and remnant lipoproteins compete in vitro and in vivo for the same liver receptors. As predicted by these observations, apoE-enriched remnant lipoproteins inhibit sporozoite invasion of HepG2 cells, and malaria parasites are less infective in LDL-receptor knockout mice maintained on a high fat diet.",
author = "Photini Sinnis",
year = "1996",
language = "English (US)",
volume = "44",
journal = "Journal of Investigative Medicine",
issn = "1081-5589",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Remnant lipoproteins inhibit malaria sporozoite invasion of hepatocytes

AU - Sinnis, Photini

PY - 1996

Y1 - 1996

N2 - Remnants of lipoproteins (chylomicron remnants and very low density lipoprotein remnants) are rapidly cleared from plasma and enter hepatocytes. The catabolism of the lipoproteins is apolipoprotein E (apoE) dependent. It has been suggested that the lipoproteins are initially captured in the space of Disse by heparan sulfate proteoglycans and then internalized by members of the LDL-receptor gene family. Within minutes after injection by Anopheles mosquitoes, malaria sporozoties are also removed from the blood circulation by the liver. The sporozoite's surface is covered by the circumsporozoite protein (CS), and its region ll-plus has been implicated in the initial binding of the parasites to the hepatocytes. Here we provide evidence that CS and remnant lipoproteins compete in vitro and in vivo for the same liver receptors. As predicted by these observations, apoE-enriched remnant lipoproteins inhibit sporozoite invasion of HepG2 cells, and malaria parasites are less infective in LDL-receptor knockout mice maintained on a high fat diet.

AB - Remnants of lipoproteins (chylomicron remnants and very low density lipoprotein remnants) are rapidly cleared from plasma and enter hepatocytes. The catabolism of the lipoproteins is apolipoprotein E (apoE) dependent. It has been suggested that the lipoproteins are initially captured in the space of Disse by heparan sulfate proteoglycans and then internalized by members of the LDL-receptor gene family. Within minutes after injection by Anopheles mosquitoes, malaria sporozoties are also removed from the blood circulation by the liver. The sporozoite's surface is covered by the circumsporozoite protein (CS), and its region ll-plus has been implicated in the initial binding of the parasites to the hepatocytes. Here we provide evidence that CS and remnant lipoproteins compete in vitro and in vivo for the same liver receptors. As predicted by these observations, apoE-enriched remnant lipoproteins inhibit sporozoite invasion of HepG2 cells, and malaria parasites are less infective in LDL-receptor knockout mice maintained on a high fat diet.

UR - http://www.scopus.com/inward/record.url?scp=33749437462&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33749437462&partnerID=8YFLogxK

M3 - Article

VL - 44

JO - Journal of Investigative Medicine

JF - Journal of Investigative Medicine

SN - 1081-5589

IS - 3

ER -