|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Hepatic stellate cell (vitamin A-storing cell) and its relative – past, present and future
Haruki Senoo*1, Kiwamu Yoshikawa*, Mayako Morii†, Mitsutaka Miura*, Katsuyuki Imai* and Yoshihiro Mezaki*
*Departments of Cell Biology and Morphology, Akita University Graduate School of Medicine, 111 Hondo, Akita City, Akita 0108543, Japan, and †Department of Pediatric Surgery, Akita University Graduate School of Medicine, 111 Hondo, Akita City, Akita 0108543, Japan
HSCs (hepatic stellate cells) (also called vitamin A-storing cells, lipocytes, interstitial cells, fat-storing cells or Ito cells) exist in the space between parenchymal cells and liver sinusoidal endothelial cells of the hepatic lobule and store 50–80% of vitamin A in the whole body as retinyl palmitate in lipid droplets in the cytoplasm. In physiological conditions, these cells play pivotal roles in the regulation of vitamin A homoeostasis. In pathological conditions, such as hepatic fibrosis or liver cirrhosis, HSCs lose vitamin A and synthesize a large amount of extracellular matrix components including collagen, proteoglycan, glycosaminoglycan and adhesive glycoproteins. Morphology of these cells also changes from the star-shaped SCs (stellate cells) to that of fibroblasts or myofibroblasts. The hepatic SCs are now considered to be targets of therapy of hepatic fibrosis or liver cirrhosis. HSCs are activated by adhering to the parenchymal cells and lose stored vitamin A during hepatic regeneration. Vitamin A-storing cells exist in extrahepatic organs such as the pancreas, lungs, kidneys and intestines. Vitamin A-storing cells in the liver and extrahepatic organs form a cellular system. The research of the vitamin A-storing cells has developed and expanded vigorously. The past, present and future of the research of the vitamin A-storing cells (SCs) will be summarized and discussed in this review.
Key words: hepatic stellate cell, retinoid-binding protein, vitamin A, vitamin A-storing cell
Abbreviations: αSMA, α smooth muscle actin, 9RA, 9-cis retinoic acid, ADRP, adipose differentiation-related protein, ARAT, acyl-CoA/retinol acyltransferase, Asc 2-P, l-ascorbic acid 2-phosphate, ATRA, all-trans retinoic acid, CRBP, cellular retinol-binding protein, CTGF, connective tissue growth factor, ECM, extracellular matrix, EGF, epidermal growth factor, EMT, epithelial to mesenchymal transition, ER, endoplasmic reticulum, FGFs, fibroblast growth factors, FoxO, Forkhead box gene, group O, FXR, farnesoid X receptor, GFAP, glial fibrillary acidic protein, HSCs, hepatic stellate cells, KCs, Kupffer cells, LRAT, lecithin/retinol acyltransferase, LSCs, lung stellate cells, LSECs, liver sinusoidal endothelial cells, MEF2, myocyte enhancer factor 2, MMPs, matrix metalloproteinases, MVB, multivesicular body, N-CAM, neural cell adhesion molecule, NPCs, non-parenchymal cells, PCs, parenchymal cells, PHx, partial hepatectomy, PI3K, phosphatidylinositol 3-kinase, PPARs, peroxisome proliferator-activated receptors, PSCs, pancreatic SCs, PXR, Pregnane X receptor, RARs, retinoic acid receptors, RBP, retinol-binding protein, SCs, stellate cells, STAP, stellate cell activation-associated protein, STRA6, stimulated by retinoic acid 6, TIMP, tissue inhibitor of metalloproteinases, VFSC, vocal fold SCs
1To whom correspondence should be addressed (email firstname.lastname@example.org).
Part of a series marking the 70th birthday of the Cell Biology International Editor-in-Chief Denys Wheatley
Received 14 May 2010; accepted 22 July 2010
Published online 11 November 2010, doi:10.1042/CBI20100321
© The Author(s) Journal compilation © 2010 Portland Press Limited