Human Platelets Are Internalized By Liver Sinusoidal Endothelial Cells and Enhance Secretion of EGF.

Lejmi, Esma; Meyer, Jérémy; Sadoul, Karin; Fontana, Pierre; Perroud, Elodie; Bollinger, A.; Morel, Philippe; Gonelle‐Gispert, Carmen; Bühler, Léo H.

doi:10.1097/00007890-201407151-01379

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“…After partial hepatectomy, platelets accumulate in sinusoids or are translocated into the space of Disse, which separates the liver sinusoidal endothelial cells (LSEC) lining from hepatocytes [2]. Platelets may act through the release of granule-derived proliferative factors or by mechanisms such as platelet internalization by hepatocytes [4] or LSEC [5,6].…”

Section: Introductionmentioning

confidence: 99%

Platelet Transforming Growth Factor-β1 Induces Liver Sinusoidal Endothelial Cells to Secrete Interleukin-6

Balaphas

Meyer

Perozzo

et al. 2020

Cells

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The roles and interactions of platelets and liver sinusoidal endothelial cells in liver regeneration are unclear, and the trigger that initiates hepatocyte proliferation is unknown. We aimed to identify the key factors released by activated platelets that induce liver sinusoidal endothelial cells to produce interleukin-6 (IL-6), a cytokine implicated in the early phase of liver regeneration. We characterized the releasate of activated platelets inducing the in vitro production of IL-6 by mouse liver sinusoidal endothelial cells and observed that the stimulating factor was a thermolabile protein. Following gel filtration, a single fraction of activated platelet releasate induced a maximal IL-6 secretion by liver sinusoidal endothelial cells (90.2 ± 13.9 versus control with buffer, 9.0 ± 0.8 pg/mL, p < 0.05). Mass spectroscopy analysis of this fraction, followed by in silico processing, resulted in a reduced list of 18 candidates. Several proteins from the list were tested, and only recombinant transforming growth factor β1 (TGF-β1) resulted in an increased IL-6 production up to 242.7 ± 30.5 pg/mL, which was comparable to non-fractionated platelet releasate effect. Using neutralizing anti-TGF-β1 antibody or a TGF-β1 receptor inhibitor, IL-6 production by liver sinusoidal endothelial cells was dramatically reduced. These results support a role of platelet TGF-β1 β1 in the priming phase of liver regeneration.

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