Immature surfactant protein-B impairs the antioxidant capacity of HDL.

Authors:
Cristina Banfi
Cristina Banfi
University of Milan
Italy
Maura Brioschi
Maura Brioschi
University of Milan
Italy
Minna K Karjalainen
Minna K Karjalainen
University of Oulu
Finland
Johanna M Huusko
Johanna M Huusko
Institute of Clinical Medicine
Finland
Erica Gianazza
Erica Gianazza
University of Milano-Bicocca
Italy
Piergiuseppe Agostoni
Piergiuseppe Agostoni
Centro Cardiologico Monzino
Italy

Int J Cardiol 2019 Jun 27;285:53-58. Epub 2019 Feb 27.

Centro Cardiologico Monzino, IRCCS, Milano, Italy; Dipartimento di Scienze Cliniche e di Comunità, Sezione Cardiovascolare, Università di Milano, Italy.

Circulating immature surfactant protein B (proSP-B) forms emerged as the most reliable lung-specific circulating marker for alveolar-capillary membrane (ACM) dysfunction and for the overall clinical status of heart failure (HF). Notably, in terms of HF hospitalization, immature SP-B overwhelms the prognostic role of other most frequently used clinical parameters such as those related to lung dysfunction. The strong prognostic value of circulating proSP-B in HF suggests more widespread and possible systemic effects. Thus, we assessed the plasma distribution of proSP-B evaluating whether it exists in a lipoprotein-bound form and its impact on lipoprotein structure and function. ProSP-B forms were detectable in high-density lipoprotein (HDL) only. To assess the impact of proSP-B on HDL, HDL from healthy subjects were enriched with proSP-B produced by a stably transfected CHO cell line that specifically expresses and releases the human proSP-B. After enrichment, HDL size and lipoprotein electrophoretic mobility, and protein composition did not show apparent differences. HDL antioxidant capacity (HOI), assessed as their ability to inhibit air-induced LDL oxidation, was impaired after proSP-B enrichment. HOI was also higher in HF patients with respect to age-matched control healthy subjects (p = 0.013). Circulating proSP-B, besides its potential role as a specific marker for ACM dysfunction in HF patients with diagnostic and prognostic value, binds to human HDL impairing their antioxidant capacity. These findings shed light on proSP-B as a molecule that contributes to the reduction of the defense against oxidative stress, a key mediator in the pathogenesis of HF.

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Source
https://linkinghub.elsevier.com/retrieve/pii/S01675273183592
Publisher Site
http://dx.doi.org/10.1016/j.ijcard.2019.02.057DOI Listing
June 2019
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