Hepatic stellate cells (HSCs) — also called interstitial cells, fat-storing cells, Vitamin A-storing cells, or Ito cells — are perisinusoidal cells distributed throughout the liver, located in the space of Disse between the hepatocytes and sinusoidal endothelial cells. The stellate cells arise embryologically from the septum transversum mesenchyme from precursor cells that invade the liver parenchyma from the hepatic capsule. In the normal adult liver, these important cells store retinoids as retinyl palmitate in cytoplasmic lipid droplets and are pivotal in the regulation of retinoid homeostasis. Other functions ascribed to hepatic stellate cells include vasoregulation (through interactions with endothelial cells), extracellular matrix homeostasis, immune regulation, drug detoxification, and production of mitogens and morphogens (such as hepatocyte growth factor) that serve to preserve and/or restore hepatocyte mass.

Under physiological conditions, HSCs exhibit a quiescent phenotype (qHSCs). They express neural markers, such as GFAP, synemin, synaptophysin, and nerve growth factor receptor p75 and store vitamin A in lipid droplets. In response to liver injury, such as chronic exposure to certain drugs or chemicals, steatosis, and/or persistent inflammation, qHSCs decrease vitamin A storage and peroxisome proliferator-activated receptor (PPAR) expression, and activate into collagen type I and αSMA expressing myofibroblasts (aHSCs). Persistent activation of HSCs and intrahepatic presence of myofibroblasts leads to fibrosis, portal hypertension, and cirrhosis, thus aHSCs are the primary target for anti-fibrosis therapies. Active areas of research involving stellate cells are broad, and include mechanisms of activation, fibrosis and resolution of fibrosis, inflammation, regeneration, and the development of hepatocellular cancer.

In vitro monolayer culture of hepatic stellate cells typically results in the development of a culture-activated phenotype, with progressive increases in expression of αSMA and loss of phenotypic features associated with quiescence, including lipid droplets and expression of GFAP. However, study results have suggested that culture-activated stellate cells may re-gain a quiescent phenotype when implanted into the in vivo microenvironment1, 2 or incorporated into multicellular 3D tissues comprising other liver cell types3, 4. Click here to download a general product information sheet.


Kupffer cells are the resident macrophages in the liver and are involved in normal physiology and homeostasis as well as mediating response to toxic injury and disease. When Kupffer cells are activated, they release cytokines, growth factors, and reactive oxygen species, all of which can have acute effects on hepatocytes and other cell types. Persistent activation of Kupffer cells may contribute to chronic disease processes, including chronic drug-induced liver injury, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatotic hepatitis (NASH), alcoholic steatohepatitis, and hepatic cancer. Within the liver, the mobile Kupffer cells are able to traverse the sinusoidal endothelial barrier and interact with cells and signals present in the sinusoidal blood flow and in the space of Disse between the sinusoidal endothelial cells and hepatocytes. Both phagocytosis and inducible cytokine release are considered important functional measures of Kupffer cells. Marker expression may vary in human Kupffer cells depending on activation state, but generally includes significant populations of cells that are immunopositive for CD11b and CD68. Click here to download a general product information sheet. Available Kupffer Cells (KC) lots can be found in the Liver Cell Inventory Table.


Samsara’s primary liver-derived endothelial cells (LEC) are isolated by elutriation and are comprised of cells that express general endothelial cell markers, such as CD31 and von Willebrand Factor (vWF) and more specific sinusoidal endothelial cell-associated markers, such as CD32b and LYVE-1. Liver-derived endothelial cells may be important components of co-culture or 3D tissue systems, due to their highly specialized, tissue-specific nature. Samsara’s LEC are capable of tube formation in vitro and can be propagated through limited serial passage for use in assays. Click here to download a general product information sheet. Available LEC lots can be found in the Liver Cell Inventory Table.

Inflammation Grade*Fibrosis Score*NAFLD
Inflammation Grade*Fibrosis Score*NAFLD
Inflammation Grade*Fibrosis Score*NAFLD
Inflammation Grade*Fibrosis Score*NAFLD
HL160016Near normal0.66 / M12.8Muscular Dystrophy000FFPE, LEC
HL160018Near normal35 / F24.7None000FFPE, SFT
HL150002Near normal,
24 / M22.9None0-100FFPE, SC
HL160026Near normal25 / F26Pulmonary Arterial Hypertension Lung Transplant000FFPE, SFT, SCp2
HL160033Near normal22 / M29.1Acute Drug Toxicity, Metabolic acidosis000FFPE, SFT
HL170057Near normal35 / F22.2Anoxia / drowning000FFPE, SFT, LEC, HCP
HL170063Near normal59 / F27.4ICH / Stroke000FFPE, SFT, SC, KC, LEC, HCS
HL180067Near normal12 / M17.7Head trauma000FFPE, SFT, SC, KC, LEC
HL180070Near normal52 / F35.4ICH / Stroke000FFPE, SFT, SC, KC, LEC, HCS
HL170044Near Normal, minimal periportal inflammation47 / M32.9Anoxia0-100FFPE, SFT, SC, LEC, HCS
HL150004Near normal, ductal plate malformation54 / M32None110FFPE, SC
HL150006Near Normal, Vascular outflow defect31 / F28.7Sepsis (confirmed)100FFPE
HL150008Near normal59 / M34None100-1FFPE, SFT, SC
HL150010Inflammmation (mild)69 / M21Diabetes (Type 2), Hypertension, Renal Failure100FFPE, SFT, SC
HL160020Inflammation (mild,
43 / M23.8None100FFPE, SFT, SC
HL160023Inflammation (mild, chronic), bile duct
57 / M27Diabetes (Type 2) Hypertension100FFPE, SFT, SC
HL160034Inflammation (mild,
57 / F35.2Cardiac Arrest/ Anoxia100FFPE, SFT, HCS , LEC, SC, KC
HL160036Inflammation (mild)25 / M30.8Acute Drug Toxicity0-100FFPE, SFT, SC, EC
HL160038Minimal portal inflammation23 / M30.56Head Trauma / GSW100SC, LEC
HL170047No steatohepatitis, Very mild portal inflammation.34 / M23Anoxia/ respiratory failure100FFPE, SFT, SC, LEC,HCS
HL170062Minimal portal, focal periductal fibrosis79 / F27.8ICH / Stroke100FFPE, SFT, KC, LEC, HC
HL160037Inflammation (mild, portal)47 / F34.6Hypertension100-1FFPE, SFT, HCS , LEC
HL170051Minimal portal inflammation64 / M37.2GERD, Depression, Orchidectomy for testicular cancer (2002 cured)101FFPE, SFT, HCP, SC, LEC
HL180068Minimal steatosis59 / F36.2Anoxia / Cardiac arrest101FFPE, SFT, SC, KC, LEC
HL170052Peri-portal iron with stage 0-1 fibrosis, minimal portal inflammation29 / M23.1Chronic alcoholism10-11FFPE, SFT, LEC
HL160031Inflammation (mild), oxidative/toxic injury, fibrosis42 / M24.1GERD120FFPE, SFT, SC, HCP
HL160025Inflammation (mild), glycogen accumulation70 / M25.6None1-200FFPE, SFT, SC, HCP , LEC
HL160019Inflammation (mild)53 / M25.3None1-200FFPE, SFT, LEC
42 / MHypertension200FFPE, SFT
HL150001Steatosis47 / M27.1Diabetes (Type 2)001FFPE, SFT
HL150007peri-portal small droplet fat29 / M23.1Head trauma/MVA001FFPE, SFT
HL160024Inflammation (chronic), Sepsis (possible), biliary
62 / M35.2Diabetes (Type 2), Hypertension, Gout201FFPE, SFT, SC, HCP , LEC
HL150009Steatosis, Drug-
induced injury
37 / M29.4Chronic drug exposure002FFPE
HL160027Steatosis26 / M24.8None102FFPE, SFT, SC
HL160017Steatosis, cholangitis, fibrosis31 / M24.7Chronic Alcoholism, Hypertension122FFPE, SFT, SC, LEC
HL170053Mild portal inflammation. Very mild steatohepatitis.62 / M33.4Hypertension, Hyperlipidemia, stent placement103FFPE, HCP, SC, LEC
HL150013Steatosis, inflammation, fibrosis45 / M35Diabetes (Type 2),
HL160014Cirrhosis, steatosis, inflammation (chronic)60 / M23.1Hypertension34ASHFFPE, SFT
HL160030Steatosis29 / M30.2Diabetes (type 2), Hypertension, Asthma002FFPE, SFT
HL180069No fibrosis, no steatohepatitis22 / M23.2Head Trauma / MVA002FFPE, SFT, SC, KC, LEC
HL160032Inflammation (mild), Steatosis23 / M29.4None reported102FFPE, SFT, KC, LEC
HL160015Steatosis, fibrosis59 / M28.1Hypertension, Hyperlipidemia11a3FFPE, SFT
HL17004653 / F48.06Cardiac Arrest/ Anoxia11a3FFPE, SFT, SC, KC, LEC, HCS
HL170048Minimally active steatohepatitis48 / F32Cardiac Arrest/ Anoxia113FFPE, SFT, SC, KC, LEC, HCS
HL170058Chronic steatohepatitis, but not active58 / F38.3CVA/ Stroke123FFPE, SFT, SC, LEC, HCS
HL170065Hypertension, CHF, CHD, COPD57 / F60.6Anoxia/Cardiac Arrest, Type II Diabetes1-204FFPE, SFT, SC, LEC, HCS
HL170064lobular inflammation and mild fibrosis66 / M37Cardiac Arrest/ Anoxia215FFPE, SFT, SC, LEC, HCS
HL180071No active steatohepatitis52 / F44.4ICH/ Stroke104FFPE, SFT, SC, KC, LEC, HCP
HL170059Chronic steatohepatitis with 1C fibrosis67 / F37.5ICH / Stroke0-114FFPE, SFT, KC, LEC, HCS
HL160021Steatohepatitis (chronic, active), fibrosis44 / F34.5Diabetes (Type 2), Chronic Kidney Disease11a4FFPE, SFT, SC
HL160022Steatohepatitis (chronic, active),
45 / F29.8Epilepsy125FFPE, SFT
HL170049Cirrhosis, steatohepatitis34 / F23.8Anoxia / seizure14ASHFFPE, SFT, SC, KC, LEC
HL170066Hypertension, kidney stones51 / M37.7ICH / Stroke226FFPE, SFT, SC, LEC, HC
HL160041Steatohepatitis, fibrosis, ascending cholangitis, possible drug injury33 / M35.4None reported22ASHFFPE, SFT

FFPE = formalin-fixed, paraffin-embedded tissue of origin
SFT = snap-frozen tissue of origin
SC = stellate cells
KC = Kupffer cells
LEC = liver-derived endothelial cell

All histopathology assessment conducted by board certified liver pathologist and scored according to standard clinical practice.
*Inflammation and fibrosis were assessed using standard Batts-Ludwig scoring methodology (Scale, 0-4).
**NAFLD score (NAS) was assigned according to the standards of the NASH CRN Scoring System (Hepatology 2005; 41:1313-1321).

  1. Crespo Yanguas, S., et al., Experimental models of liver fibrosis. Arch Toxicol, 2015.
  2. Dusabineza, A.C., et al., Hepatic stellate cells improve engraftment of human primary hepatocytes: A pre-clinical transplantation study in animal model. Cell Transplant, 2015.
  3. Robbins, J., et al., Bioprinted Human Liver Tissue With iPSC-Derived Hepatocyte-Like Cells 2013: Boston. View SCOM Poster
  4. Roskos, K., S. Pentoney, and S. Presnell, Bioprinting: An Industrial Perspective, in Essentials of 3D Biofabrication and Translation, J. Yoo and A. Atala, Editors. 2015, Elsevier: Academic Press.