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人肝星形细胞
上海义森生物科技有限公司
肝脏星形细胞是小叶内结缔组织细胞，呈现肌成纤维细胞样或脂肪细胞形态。他们参与肝脏细胞外基质的稳态、修复、再生、纤维化以控制视黄醇的代谢、存储和释放。肝脏受伤后，肝脏星形细胞转化成肌成纤维细胞，并且是纤维化的肝脏中I 型胶原的主要来源。除了以上特征，已发现在疾病状态和肝内门静脉高压的发病过程中，肝星状细胞通过细胞收缩调节肝脏微循环、星形细胞的增殖、迁移和趋化因子的表达参与了肝脏炎症和纤维化的发病过程。星形细胞支配电压激活的钙离子流，表达低亲和力的神经生长因子受体p75，在神经生长因子的刺激下发生细胞凋亡。因此，星形细胞激活的分子调控在将来有助于治疗纤维化肝，并且能减少慢性肝病患者的发病率和死亡率。
推荐培养基:（SCM, Cat. No. 5301）
产地：San Diego,US储存：液氮
品牌：ScienCell
运输：干冰
用途：科研
Hepatic stellate cells （HSteC） are intralobular connective tissue cells presenting myofibroblast-like 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 [1, 2]. Proliferation ａnd migration of HSteC ａnd expression of chemokines are involved in the pathogenesis of liver inflammation ａnd fibrogenesis. HSteC possess voltage-activated calcium current, express the low affinity nerve growth factor receptor p75, ａnd undergo apoptosis in response to nerve growth factor stimulation [3, 4]. 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.
HHSteC from ScienCell Research Laboratories are isolated from human liver. HHSteC are cryopreserved at secondary culture ａnd delivered frozen. Each vial contains >5 x 105 cells in 1 ml volume. HHSteC are characterized by immunofluorescent method with antibodies to desmin, a-actin, ａnd fibronectin. HHSteC are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast ａnd fungi. HHSteC are guaranteed to further expand for 15 population doublings in the conditions provided by ScienCell Research Laboratories.
Reference
[1]. Reynaert H, Thompson MG, Thomas T, Geerts A. （2004） Hepatic stellate cells: role in microcirculation ａnd pathophysiology of portal hypertension. Gut 50:571-581
[2]. Rockey D. C. （2001） Hepatic blood flow regulation by stellate cells in normal ａnd injured liver. Semin Liver Dis 21（3）:337-49
[3]. Oide H, Tateyama M, Wang XE, Hirose M, Itatsu T, Watanabe S, Ochi R, Sato N. （1999） Activated stellate （Ito） cells possess voltage-activated calcium current. Biochim. Biophys. Acta. 1418:158-164.
[4]. Trim N, Morgan S, Evans M, Issa R, Fine D, Afford S, Wilkins B, Iredale J. （2000） Hepatic stellate cells express the low affinity nerve growth factor receptor p75 ａnd undergo apoptosis in response to nerve growth factor stimulation. Am. J. Pathol. 156（4）:1235-1243.
肝脏星形细胞是小叶内结缔组织细胞，呈现肌成纤维细胞样或脂肪细胞形态。他们参与肝脏细胞外基质的稳态、修复、再生、纤维化以控制视黄醇的代谢、存储和释放。肝脏受伤后，肝脏星形细胞转化成肌成纤维细胞，并且是纤维化的肝脏中I 型胶原的主要来源。除了以上特征，已发现在疾病状态和肝内门静脉高压的发病过程中，肝星状细胞通过细胞收缩调节肝脏微循环、星形细胞的增殖、迁移和趋化因子的表达参与了肝脏炎症和纤维化的发病过程。星形细胞支配电压激活的钙离子流，表达低亲和力的神经生长因子受体p75，在神经生长因子的刺激下发生细胞凋亡。因此，星形细胞激活的分子调控在将来有助于治疗纤维化肝，并且能减少慢性肝病患者的发病率和死亡率。
推荐培养基:（SCM, Cat. No. 5301）
产地：San Diego,US储存：液氮
品牌：ScienCell
运输：干冰
用途：科研
Hepatic stellate cells （HSteC） are intralobular connective tissue cells presenting myofibroblast-like 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 [1, 2]. Proliferation ａnd migration of HSteC ａnd expression of chemokines are involved in the pathogenesis of liver inflammation ａnd fibrogenesis. HSteC possess voltage-activated calcium current, express the low affinity nerve growth factor receptor p75, ａnd undergo apoptosis in response to nerve growth factor stimulation [3, 4]. 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.
HHSteC from ScienCell Research Laboratories are isolated from human liver. HHSteC are cryopreserved at secondary culture ａnd delivered frozen. Each vial contains >5 x 105 cells in 1 ml volume. HHSteC are characterized by immunofluorescent method with antibodies to desmin, a-actin, ａnd fibronectin. HHSteC are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast ａnd fungi. HHSteC are guaranteed to further expand for 15 population doublings in the conditions provided by ScienCell Research Laboratories.
Reference
[1]. Reynaert H, Thompson MG, Thomas T, Geerts A. （2004） Hepatic stellate cells: role in microcirculation ａnd pathophysiology of portal hypertension. Gut 50:571-581
[2]. Rockey D. C. （2001） Hepatic blood flow regulation by stellate cells in normal ａnd injured liver. Semin Liver Dis 21（3）:337-49
[3]. Oide H, Tateyama M, Wang XE, Hirose M, Itatsu T, Watanabe S, Ochi R, Sato N. （1999） Activated stellate （Ito） cells possess voltage-activated calcium current. Biochim. Biophys. Acta. 1418:158-164.
[4]. Trim N, Morgan S, Evans M, Issa R, Fine D, Afford S, Wilkins B, Iredale J. （2000） Hepatic stellate cells express the low affinity nerve growth factor receptor p75 ａnd undergo apoptosis in response to nerve growth factor stimulation. Am. J. Pathol. 156（4）:1235-1243.
推荐培养基:（SCM, Cat. No. 5301）
产地：San Diego,US储存：液氮
品牌：ScienCell
运输：干冰
用途：科研
Hepatic stellate cells （HSteC） are intralobular connective tissue cells presenting myofibroblast-like 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 [1, 2]. Proliferation ａnd migration of HSteC ａnd expression of chemokines are involved in the pathogenesis of liver inflammation ａnd fibrogenesis. HSteC possess voltage-activated calcium current, express the low affinity nerve growth factor receptor p75, ａnd undergo apoptosis in response to nerve growth factor stimulation [3, 4]. 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.
HHSteC from ScienCell Research Laboratories are isolated from human liver. HHSteC are cryopreserved at secondary culture ａnd delivered frozen. Each vial contains >5 x 105 cells in 1 ml volume. HHSteC are characterized by immunofluorescent method with antibodies to desmin, a-actin, ａnd fibronectin. HHSteC are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast ａnd fungi. HHSteC are guaranteed to further expand for 15 population doublings in the conditions provided by ScienCell Research Laboratories.
Reference
[1]. Reynaert H, Thompson MG, Thomas T, Geerts A. （2004） Hepatic stellate cells: role in microcirculation ａnd pathophysiology of portal hypertension. Gut 50:571-581
[2]. Rockey D. C. （2001） Hepatic blood flow regulation by stellate cells in normal ａnd injured liver. Semin Liver Dis 21（3）:337-49
[3]. Oide H, Tateyama M, Wang XE, Hirose M, Itatsu T, Watanabe S, Ochi R, Sato N. （1999） Activated stellate （Ito） cells possess voltage-activated calcium current. Biochim. Biophys. Acta. 1418:158-164.
[4]. Trim N, Morgan S, Evans M, Issa R, Fine D, Afford S, Wilkins B, Iredale J. （2000） Hepatic stellate cells express the low affinity nerve growth factor receptor p75 ａnd undergo apoptosis in response to nerve growth factor stimulation. Am. J. Pathol. 156（4）:1235-1243.
