Distinct APOL1 functions in trypanosomes and kidney podocytes.

Trends Parasitol

Laboratory of Molecular Parasitology, Institute of Molecular Biology and Medicine, Université Libre de Bruxelles, Gosselies, Belgium. Electronic address:

Published: February 2022

The human serum protein apolipoprotein L1 (APOL1) kills Trypanosoma brucei but not the sleeping sickness agent Trypanosoma rhodesiense. APOL1 C-terminal variants can kill T. rhodesiense but they also induce kidney disease. Given topological and functional differences between intracellular and extracellular APOL1 isoforms, I propose that trypanolysis and kidney disease result from distinct APOL1 activities.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.pt.2021.11.005DOI Listing

Publication Analysis

Top Keywords

distinct apol1
8
kidney disease
8
apol1 functions
4
functions trypanosomes
4
trypanosomes kidney
4
kidney podocytes
4
podocytes human
4
human serum
4
serum protein
4
protein apolipoprotein
4

Similar Publications

Apolipoprotein-L Functions in Membrane Remodeling.

Cells

December 2024

Laboratory of Molecular Parasitology, Institut de Biologie et de Médecine Moléculaires (IBMM), Université Libre de Bruxelles, 6041 Gosselies, Belgium.

The mammalian Apolipoprotein-L families (APOLs) contain several isoforms of membrane-interacting proteins, some of which are involved in the control of membrane dynamics (traffic, fission and fusion). Specifically, human APOL1 and APOL3 appear to control membrane remodeling linked to pathogen infection. Through its association with Non-Muscular Myosin-2A (NM2A), APOL1 controls Golgi-derived trafficking of vesicles carrying the lipid scramblase Autophagy-9A (ATG9A).

View Article and Find Full Text PDF
Article Synopsis
  • Studies show kidney disease is linked to viral infections, causing kidney injury through systemic inflammation and direct infection of kidney cells.
  • Research using an immortalized human podocyte cell line (HPC) infected with lentivirus revealed strong immune responses and pathways related to cell death, indicating compromised cell viability.
  • The findings suggest that these lentivirus-infected HPC cells serve as a valuable model for studying how viral infections specifically damage podocytes, separate from other stressors like Adriamycin.
View Article and Find Full Text PDF

Focal segmental glomerulosclerosis (FSGS) defines a distinct histologic pattern observed in kidney tissue that is linked to several distinct underlying causes, all converging on the common factor of podocyte injury. It presents a considerable challenge in terms of classification because of its varied underlying causes and the limited correlation between histopathology and clinical outcomes. Critically, precise nomenclature is key to describe and delineate the pathogenesis, subsequently guiding the selection of suitable and precision therapies.

View Article and Find Full Text PDF

Key Points: Apolipoprotein L1 (APOL1)-G1 induced kidney disease in the two APOL1 transgenic mouse models, HIV-associated nephropathy and IFN- administration. Glomerular single-nuclear RNA-sequencing identified genes differentially expressed among mice with APOL1-G1 and G0 variants at single-cell resolution.

Background: Apolipoprotein L1 () high-risk variants contribute to kidney disease among individuals with African ancestry.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!