Rat liver sinusoidal endothelial cells survive without exogenous VEGF in 3D perfused co-cultures with hepatocytes

被引:90
作者
Hwa, Albert J.
Fry, Rebecca C.
Sivaraman, Anand
So, Peter T.
Samson, Leona D.
Stolz, Donna B.
Griffith, Linda G.
机构
[1] MIT, Biol Engn Div, Dept Biol Engn, Cambridge, MA 02139 USA
[2] MIT, Ctr Environm Hlth Sci, Cambridge, MA 02139 USA
[3] MIT, Dept Mech Engn, Cambridge, MA 02139 USA
[4] Univ Pittsburgh, Ctr Biol Imaging, Pittsburgh, PA USA
关键词
tissue engineering; liver; microvascular;
D O I
10.1096/fj.06-7473com
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Liver sinusoidal endothelial cells (SECs) are generally refractory to extended in vitro culture. In an attempt to recreate some features of the complex set of cues arising from the liver parenchyma, we cocultured adult rat liver SECs, identified by the expression of the marker SE-1, with primary adult rat hepatocytes in a 3D culture system that provides controlled microscale perfusion through the tissue mass. The culture was established in a medium containing serum and VEGF, and these factors were then removed to assess whether cells with the SE-1 phenotype could be supported by the local microenvironment in vitro. Rats expressing enhanced green fluorescent protein (EGFP) in all liver cells were used for isolation of the SE-1-positive cells added to cocultures. By the 13th day of culture, EGFP-expressing cells had largely disappeared from 2D control cultures but exhibited moderate proliferation in 3D perfused cultures. SE-1-positive cells were present in 3D cocultures after 13 days, and these cultures also contained Kupffer cells, stellate cells, and CD31-expressing endothelial cells. Global transcriptional profiling did not reveal profound changes between 2D and 3D cultures in expression of most canonical angiogenic factors but suggested changes in several pathways related to endothelial cell function.
引用
收藏
页码:2564 / 2579
页数:16
相关论文
共 79 条
[1]
[Anonymous], LIVER DIS HEPATIC SI
[2]
Growth factor-binding sequence in human α2-macroglobulin targets the receptor-binding site in transforming growth factor-β [J].
Arandjelovic, S ;
Freed, TA ;
Gonias, SL .
BIOCHEMISTRY, 2003, 42 (20) :6121-6127
[3]
ARIAS IM, 2001, LIVER BIOL PATHOBIOL
[4]
Population expansion, clonal growth, and specific differentiation patterns in primary cultures of hepatocytes induced by HGF/SF, EGF and TGF alpha in a chemically defined (HGM) medium [J].
Block, GD ;
Locker, J ;
Bowen, WC ;
Petersen, BE ;
Katyal, S ;
Strom, SC ;
Riley, T ;
Howard, TA ;
Michalopoulos, GK .
JOURNAL OF CELL BIOLOGY, 1996, 132 (06) :1133-1149
[5]
Drying cells for SEM, AFM and TEM by hexamethyldisilazane: A study on hepatic endothelial cells [J].
Braet, F ;
deZanger, R ;
Wisse, E .
JOURNAL OF MICROSCOPY-OXFORD, 1997, 186 :84-87
[6]
BRAET F, 1994, LAB INVEST, V70, P944
[7]
Braet Filip, 2004, Comp Hepatol, V3, P7, DOI 10.1186/1476-5926-3-7
[8]
Braet Filip, 2002, Comp Hepatol, V1, P1, DOI 10.1186/1476-5926-1-1
[9]
Exposure to bacterial cell wall products triggers an inflammatory phenotype in hepatic stellate cells [J].
Brun, P ;
Castagliuolo, I ;
Pinzani, M ;
Palù, G ;
Martines, D .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2005, 289 (03) :G571-G578
[10]
Transgenic pigs expressing human CD59 and decay-accelerating factor produce an intrinsic barrier to complement-mediated damage [J].
Byrne, G ;
McCurry, KR ;
Martin, MJ ;
McClellan, SM ;
Platt, JL ;
Logan, JS .
TRANSPLANTATION, 1997, 63 (01) :149-155