GPIHBP1 and ANGPTL4 Utilize Protein Disorder to Orchestrate Order in Plasma Triglyceride Metabolism and Regulate Compartmentalization of LPL Activity

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Intravascular processing of triglyceride-rich lipoproteins (TRLs) is crucial for delivery of dietary lipids fueling energy metabolism in heart and skeletal muscle and for storage in white adipose tissue. During the last decade, mechanisms underlying focal lipolytic processing of TRLs along the luminal surface of capillaries have been clarified by fresh insights into the functions of lipoprotein lipase (LPL); LPL’s dedicated transporter protein, glycosylphosphatidylinositol-anchored high density lipoprotein–binding protein 1 (GPIHBP1); and its endogenous inhibitors, angiopoietin-like (ANGPTL) proteins 3, 4, and 8. Key discoveries in LPL biology include solving the crystal structure of LPL, showing LPL is catalytically active as a monomer rather than as a homodimer, and that the borderline stability of LPL’s hydrolase domain is crucial for the regulation of LPL activity. Another key discovery was understanding how ANGPTL4 regulates LPL activity. The binding of ANGPTL4 to LPL sequences adjacent to the catalytic cavity triggers cooperative and sequential unfolding of LPL’s hydrolase domain resulting in irreversible collapse of the catalytic cavity and loss of LPL activity. Recent studies have highlighted the importance of the ANGPTL3–ANGPTL8 complex for endocrine regulation of LPL activity in oxidative organs (e.g., heart, skeletal muscle, brown adipose tissue), but the molecular mechanisms have not been fully defined. New insights have also been gained into LPL–GPIHBP1 interactions and how GPIHBP1 moves LPL to its site of action in the capillary lumen. GPIHBP1 is an atypical member of the LU (Ly6/uPAR) domain protein superfamily, containing an intrinsically disordered and highly acidic N-terminal extension and a disulfide bond–rich three-fingered LU domain. Both the disordered acidic domain and the folded LU domain are crucial for the stability and transport of LPL, and for modulating its susceptibility to ANGPTL4-mediated unfolding. This review focuses on recent advances in the biology and biochemistry of crucial proteins for intravascular lipolysis.

OriginalsprogEngelsk
Artikelnummer702508
TidsskriftFrontiers in Cell and Developmental Biology
Vol/bind9
Antal sider20
ISSN2296-634X
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
Research in the authors’ laboratories that was instrumental for writing this review was supported by grants from the Lundbeck Foundation (R230–2016–2930), NOVO Nordisk Foundation Grants (NNF17OC0026868, NNF18OC0033864, NNF20OC0063444), The John and Birthe Meyer Foundation, a Transatlantic Network grant (12CVD04) from the Leducq Foundation, the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No 801481, The Capital Region (RegionH) grant No A6867, and the National Heart, Lung, and Blood Institute (HL146358, HL087228, HL139725).

Publisher Copyright:
© Copyright © 2021 Kristensen, Leth-Espensen, Kumari, Grønnemose, Lund-Winther, Young and Ploug.

Antal downloads er baseret på statistik fra Google Scholar og www.ku.dk


Ingen data tilgængelig

ID: 283775545