Hepatic stellate cells (HSteC) are intralobular connective tissue cells presenting myofibroblastlike or lipocyte phenotypes. They participate in the homeostasis of liver extracellular matrix, repair, regeneration, fibrosis and control retinol metabolism, storage and release. Following liver injury, HSteC transform into myofibroblast-like cells and are the major source of type I collagen in the fibrotic liver. Beyond these feature, HSteC have been implicated as regulators of hepatic microcirculation via cell contraction, and in disease states, in the pathogenesis of intrahepatic portal hypertension. Proliferation and migration of HSteC and expression of chemokines are involved in the pathogenesis of liver inflammation and fibrogenesis. HSteC possess voltageactivated calcium current, express the low affinity nerve growth factor receptor p75, and undergo apoptosis in response to nerve growth factor stimulation. Therefore, the new insight into the molecular regulation of HSteC activation will lead to therapeutic approaches in treatment of hepatic fibrosis in the future, and could lead to reduced morbidity and mortality in patients with chronic liver injury.
RHSteC are isolated from neonate day 2 rat liver tissue. RHSteC are cryopreserved immediately after purification and delivered frozen. Each vial contains >5 x 10^5 cells in 1 ml volume. RHSteC are characterized by immunofluorescent method with antibodies to desmin and ?-actin. RHSteC are negative for mycoplasma, bacteria, yeast and fungi. RHSteC are guaranteed to further expand for 5 population doublings in the conditions provided by Creative Bioarray.
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