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. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: Hepatology. 2019 Feb 7;69(3):1259–1272. doi: 10.1002/hep.30227

Fig. 1. Capillarization is due to engraftment of BM-derived LSECs that fail to completely differentiate.

Fig. 1.

(A) In control rats (BMT-CTR), fewer than 5% of LSECs were BM-derived (GFP+, •), whereas 65% of LSECs were BM-derived in cirrhosis (****P<0.0001). (B) The number of sprocs (CD133+) increased during cirrhosis (***P<0.001). (C) Representative images of LSECs isolated from wild-type control rats (CTR, upper left), and from resident LSECs (GFP-, lower left) and BM-derived LSECs (GFP+, lower right) from cirrhotic liver. Inserts are magnified portions of the cytoplasm. Resident LSECs from cirrhotic liver had fenestrae organized in sieve plates (arrowheads) comparable to control rat (CTR) whereas BM-derived LSECs lacked fenestration. (D) Calculation of porosity confirms that capillarization is only observed in BM-derived LSECs isolated from cirrhotic liver (***P<0.001). Scale bars, 5μm. Data are mean ± s.e.m. See Supporting Table S3 for numbers of replicates and details of statistical analysis.