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Aging Suppresses Sphingosine-1-Phosphate Chaperone ApoM in Circulation Resulting in Maladaptive Organ Repair.

Abstract：

:Here, we show that the liver-derived apolipoprotein M (ApoM) protects the lung and kidney from pro-fibrotic insults and that this circulating factor is attenuated in aged mice. Aged mouse hepatocytes exhibit transcriptional suppression of ApoM. This leads to reduced sphingosine-1-phosphate (S1P) signaling via the S1P receptor 1 (S1PR1) in the vascular endothelial cells of lung and kidney. Suboptimal S1PR1 angiocrine signaling causes reduced resistance to injury-induced vascular leak and leads to organ fibrosis. Plasma transfusion from Apom transgenic mice but not Apom knockout mice blocked fibrosis in the lung. Similarly, infusion of recombinant therapeutics, ApoM-Fc fusion protein enhanced kidney and lung regeneration and attenuated fibrosis in aged mouse after injury. Furthermore, we identified that aging alters Sirtuin-1-hepatic nuclear factor 4α circuit in hepatocytes to downregulate ApoM. These data reveal an integrative organ adaptation that involves circulating S1P chaperone ApoM+ high density lipoprotein (HDL), which signals via endothelial niche S1PR1 to spur regeneration over fibrosis.

journal_name

Dev Cell

journal_title

Developmental cell

authors

Ding BS,Yang D,Swendeman SL,Christoffersen C,Nielsen LB,Friedman SL,Powell CA,Hla T,Cao Z

doi

10.1016/j.devcel.2020.05.024

subject

Has Abstract

pub_date

2020-06-22 00:00:00

pages

677-690.e4

issue

6

eissn

1534-5807

issn

1878-1551

pii

S1534-5807(20)30413-5

journal_volume

53

pub_type

杂志文章

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