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The effect of cytokines on the proliferation and migration of bovine meniscal cells

AMERICAN JOURNAL OF SPORTS MEDICINE 1999年第5期27卷 636-643页

作者： Bhargava, MM Attia, ET Murrell, GAC Dolan, MM Warren, RF Hannafin, JA Cornell Univ Med Ctr New York Hosp Hosp Special SurgLab Soft Tissue Res New York NY 10021 USA

We determined the effect of cytokines on the proliferation and migration of cells isolated from the inner-third (white-white), middle-third (red-white), and outer-third (red-red) regions of bovine meniscus. Cells from the outer, or peripheral, region of the meniscus exhibited higher DNA synthesis in the presence of 10% serum compared with cells from the inner or central regions. Recombinant human platelet-derived growth factor-AB, hepatocyte growth factor/scatter factor, and bone morphogenic protein-2 stimulated DNA synthesis of all meniscal cells in a dose-dependent manner, with a two- to threefold maximal stimulation at 10 ng/ml. Cell migration was also stimulated by addition of cytokines. Platelet-derived growth factor and hepatocyte growth factor caused an increase in the migration of cells derived from all three zones, while interleukin-1 selectively stimulated the migration of outer-zone meniscal cells. Epidermal growth factor was much less effective and stimulated the migration of cells in the inner and outer zones by 40% to 50%, while bone morphogenic protein-2 and insulin-like growth factor-1 stimulated the migration of meniscal cells from the middle zone by 40% to 50%. The identification of cytokines that stimulate both the growth and migration of meniscal cells may provide new tools for modulation of meniscal healing.

关键词：骨形态发生蛋白质类/药理学细胞分裂细胞运动细胞培养的软骨细胞/细胞学细胞因子类/药理学 DNA/生物合成剂量效应关系药物表皮生长因子/药理学成纤维细胞生长因子/药理学成纤维细胞/细胞学肝细胞生长因子/药理学胰岛素样生长因子Ⅰ/药理学胰岛素样生长因子Ⅱ/药理学白细胞介素1/药理学半月板胫骨/细胞学血小板源性生长因子/药理学放射性药物/诊断应用重组蛋白质类转化生长因子β/药理学氚/诊断应用动物牛人类

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Signaling of hepatocyte growth factor/scatter factor (HGF) to the small GTPase Rap1 via the large docking protein Gab1 and the adapter protein CRKL

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第15期275卷 10772-10778页

作者： Sakkab, D Lewitzky, M Posern, G Schaeper, U Sachs, M Birchmeier, W Feller, SM Univ Wurzburg Inst Med Strahlenkunde & Zellforsch Oncol Mol Lab MSZ D-97078 Wurzburg Germany Max Delbruck Ctr Mol Med D-13125 Berlin Germany

Hepatocyte growth factor (HGF;scatter factor) is a multipotent protein with mitogenic, motogenic, and developmental functions. Upon activation, the HGF-receptor c-Met binds and phosphorylates the multisite docking protein Gab1. Besides binding motifs for phosphatidylinositol 3-kinase and Grb2, Gab 1 contains multiple Tyr-X-X-Pro (YXXP) motifs which, when phosphorylated, are potential binding sites for the adapter proteins c-Crk and Crk-like (CRKL). Stimulation of human embryonic kidney cells (HEK293) with HGF leads to Gab1 association with CRKL. The Gab1-CRKL interaction requires both, the SH2 domain of CRKL and the region containing the YXXP motifs in Gab1, CRKL binds via its first SH3 domain to several downstream signal transducers, including C3G an activator of the small GTPase Rap1. Indeed, Rap1 was rapidly activated after HGF stimulation of HEK293 cells. Rap1 activation through HGF was suppressed through transfection of a truncated C3G protein which only contains the SH3-binding motifs of C3G. Transfection of nonmutated Gab1 led to a strong increase of *** in the absence of HGF. In contrast, transfection of the Gab Delta YXXP mutant abolished the elevation of *** by HGF. A replating assay indicated that HGF decreases the adhesion of HEK293 cells. The results presented here delineate a novel signaling pathway from HGF to the GTPase Rap1 which depends on the interaction of the adapter protein CRKL with the exchange factor C3G and could be linked to cell migration.

关键词：衔接蛋白质类信号转导细胞培养的酶激活/药物作用肝细胞生长因子/药理学核蛋白质类/生理学磷蛋白类/生理学磷酰化酪氨酸/代谢 rap1GTP结合蛋白质类/生理学人类

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c-MET expression in myofibroblasts -: Role in autocrine activation and prognostic significance in lung adenocarcinoma

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AMERICAN JOURNAL OF PATHOLOGY 2001年第4期158卷 1451-1463页

作者： Tokunou, M Niki, T Eguchi, K Iba, S Tsuda, H Yamada, T Matsuno, Y Kondo, H Saitoh, Y Imamura, H Hirohashi, S Natl Canc Ctr Res Inst Div Pathol Chuo Ku Tokyo 1040045 Japan Natl Canc Ctr Hosp Div Surg Tokyo Japan Kansai Med Univ Dept Thorac & Cardiovasc Surg Osaka Japan

Hepatocyte growth factor (HGF) plays important rots in tumor development and progression. It is currently thought that the main action of HGF is of a paracrine nature: HGF produced by mesenchymal cells acts on epithelial cells that express its receptor c-MET. In this investigation, we explored the significance of c-MET expression in myofibroblasts, both in culture and in patients with lung adenocarcinoma. We first showed that human myofibroblasts derived from primary lung cancer expressed c-MET mRNA and protein by reverse transcription-polymerase chain reaction and Western blot analysis. Proliferation of myofibroblasts was stimulated in a dose-dependent manner by exogenously added recombinant human HGF whereas it was inhibited in a dose-dependent manner by neutralizing antibody to HGF. The addition of HGF in the culture medium stimulated tyrosine phosphorylation of c-MET. The c-MET protein was immunohistochemically detected in myofibroblasts in the invasive area of lung adenocarcinoma. Finally, the prognostic significance of c-MET expression in stromal myofibroblasts was explored in patients with small-sized lung adenocarcinomas. c-MET-positive myofibroblasts were observed in 69 of 131 cases (53%). A significant relationship between myofibroblast c-MET expression and shortened patient survival was observed in a whole cohort of patients including ah pathological stages (two-sided P = 0.0089 by log-rank test) and in patients with stage IA disease (two-sided P = 0.0019 by log-rank test). These data suggest that the HGF/c-MET system constitutes an autocrine activation loop in cancer-stromal myofibroblasts. This autocrine system may play a role in invasion and metastasis of lung adenocarcinoma.

关键词：腺癌/代谢腺癌/病理学自身分泌性细胞间通讯/生理学细胞系计算机系统解剖/方法成纤维细胞/代谢肝细胞生长因子/遗传学肝细胞生长因子/药理学激光肺肿瘤/代谢肺肿瘤/病理学肌平滑/细胞学肌平滑/代谢磷酰化/药物作用预后原癌基因蛋白质c-met/遗传学原癌基因蛋白质c-met/代谢原癌基因蛋白质c-met/生理学 RNA 信使/代谢逆转录聚合酶链反应酪氨酸/代谢人类

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Papillary carcinoma of the thyroid - Hepatocyte growth factor (HGF) stimulates tumor cells to release chemokines active in recruiting dendritic cells

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AMERICAN JOURNAL OF PATHOLOGY 2000年第3期156卷 831-837页

作者： Scarpino, S Stoppacciaro, A Ballerini, F Marchesi, M Prat, M Stella, MC Sozzani, S Allavena, P Mantovani, A Ruco, LP Univ La Sapienza Dipartimento Med Sperimentale & Patol I-00161 Rome Italy Univ La Sapienza Cattedra Chirurg Gen Ist Clin Chirurg 3 Rome Italy Univ Piemonte Orientale A Avogadro Dipartimento Sci Med Novara Italy Univ Turin Ist Ric Canc IRCC Turin Italy Ist Ric Farmacol Mario Negri Milan Italy

Tissue distribution of dendritic cells was investigated in eight cases of papillary carcinoma of the thyroid using immunohistochemistry. Most dendritic cells had an immature phenotype (CD1a++, CD11c+, CD40+, CD86-, HLA-DR-) and were located at the invasion edge of the tumor. This pattern of distribution was profoundly different from that of CD68+ macrophages, which were evenly distributed throughout the tumor. The ability of tumor cells to release chemotactic factors active on dendritic cells was investigated in primary cultures of the same cases of papillary carcinoma, and was compared to that of the corresponding normal thyroid cells obtained from the tumor-free contralateral lobe. Chemotactic activity of culture supernatants was tested against dendritic cells in a chemotaxis chamber. It was found that papillary carcinoma cells were active in releasing chemotactic activity, that hepatocyte growth factor (HGF;100 ng/ml) or interleukin (IL)-1 beta (10(3) U/ml) induced a fourfold increase in the amount of chemotactic activity released, and that normal thyroid cells obtained from the same patients were as effective as tumor cells. Characterization of chemokines at RNA level revealed that unstimulated cells contain large amounts of IL-8 and monocyte chemotactic protein (MCP)-1 RNAs, and that stimulation with HGF or IL-1 beta induced RNAs for regulated upon activation normal T expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-3 alpha, interferon-gamma-inducible protein 10 (IP-10), and, to a lesser extent, MIP-1 alpha and MIP-1 beta, The possibility that HGF/Met interaction has a biological role in vivo was investigated in serial sections of six tumors immunostained for CD1a+, Met protein, and HGF. It was found that all six tumors were intensely and diffusely positive for Met protein, that HGF staining was present in tumor cells of the advancing edge, and that HGF+/Met+ tumor cell nests were infiltrated by CD1a+ dendritic cells. The foregoing observa

关键词：抗原 CD/代谢抗原分化髓单核细胞/代谢癌髓样/代谢癌髓样/病理学癌乳头状/代谢癌乳头状/病理学趋化因子CCL2/代谢趋化因子CCL5/代谢炎症趋化因子类/遗传学炎症趋化因子类/代谢趋化作用/药物作用树突细胞/病理学树突细胞/生理学肝细胞生长因子/药理学免疫酶技术白细胞介素1/药理学 RNA 信使/代谢 RNA 肿瘤/分析重组蛋白质类/药理学逆转录聚合酶链反应 S100蛋白质类/代谢甲状腺肿瘤/代谢甲状腺肿瘤/病理学肿瘤细胞培养的青少年成年人女(雌)性人类男(雄)性中年人

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Enhanced transformation by a plasma membrane-associated met oncoprotein:: Activation of a phosphoinositide 3′-kinase-dependent autocrine loop involving hyaluronic acid and CD44

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MOLECULAR AND CELLULAR BIOLOGY 2000年第10期20卷 3482-3496页

作者： Kamikura, DM Khoury, H Maroun, C Naujokas, MA Park, M McGill Univ Royal Victoria Hosp Dept Med Mol Oncol Grp Montreal PQ H3A 1A1 Canada McGill Univ Royal Victoria Hosp Dept Oncol Montreal PQ H3A 1A1 Canada McGill Univ Royal Victoria Hosp Dept Biochem Montreal PQ H3A 1A1 Canada

A Met-hepatocyte growth factor receptor oncoprotein, Tpr-Met, generated by chromosomal rearrangement, fuses a protein dimerization motif with the cytoplasmic domain of the Met receptor, producing a cytosolic, constitutively activated tyrosine kinase. Although both the Met receptor and the Tpr-Met oncoprotein associate with the same substrates, activating mutations of the Met receptor in hereditary papillary;renal carcinomas have different signaling requirements for transformation than Tpr-Met. This suggests differential activation of membrane-localized pathways by oncogenic forms of the membrane-bound Met receptor but not by the cytoplasmic Tpr-Met oncoprotein. To establish which pathways might be differentially regulated, we have localized the constitutively activated Tpr-Met oncoprotein to the membrane using the c-src myristoylation signal. Membrane localization enhances cellular transformation, focus formation, and anchorage-independent growth and induces tumors with a distinct myxoid phenotype. This correlates with the induction of hyaluronic acid (HA) and the presence of a distinct form of its receptor, CD44. A pharmacological inhibitor of phosphoinositide 3' kinase (PI3'K), inhibits the production of HA, and conversely, an activated, plasma membrane-targeted form of PI3'K is sufficient to enhance HA production. Furthermore, the multisubstrate adapter protein Gab-1, which couples the Met receptor with PI3'K enhances Met receptor-dependent IU synthesis in a PI3'K-dependent manner. These results provide a positive huh to a role for HA and CD44 in Met receptor-mediated oncogenesis and implicate PI3'K in these events.

关键词：自身分泌性细胞间通讯细胞膜/代谢细胞转化肿瘤肝细胞生长因子/药理学透明质酸/代谢膜蛋白质类/代谢小鼠裸肉豆蔻酸/代谢核孔复合蛋白质类癌基因蛋白质类融合/代谢磷酸肌醇3-激酶类/代谢磷蛋白类/代谢蛋白质加工转译后原癌基因蛋白质类/代谢原癌基因蛋白质c-met/代谢原癌基因蛋白质pp60(c-src) 肉瘤实验性/遗传学动物小鼠

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Hepatocyte growth factor enhances vascular endothelial growth factor-induced angiogenesis in vitro and in vivo

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AMERICAN JOURNAL OF PATHOLOGY 2001年第3期158卷 1111-1120页

作者： Xin, XH Yang, SY Ingle, G Zlot, C Rangell, L Kowalski, J Schwall, R Ferrara, N Gerritsen, ME Genentech Inc Dept Cardiovasc Res S San Francisco CA 94080 USA Genentech Inc Dept Mol Oncol S San Francisco CA 94080 USA Genentech Inc Dept Pharmacol Sci S San Francisco CA 94080 USA

Vascular endothelial growth factor (VEGF) is an important mediator of angiogenesis in both physiological and pathological processes. Hepatocyte growth factor (HGF) is a mesenchyme-derived mitogen that also stimulates cell migration, and branching and/or tubular morphogenesis of epithelial and endothelial cells. In the present study, we tested the hypothesis that simultaneous administration of HGF and VEGF would synergistically promote new blood vessel formation. HGF acted in concert with VEGF to promote human endothelial cell survival and tubulogenesis in 3-D type I collagen gels, a response that did not occur with either growth factor alone. The synergistic effects of VEGF and HGF on endothelial survival correlated with greatly augmented mRNA levels for the anti-apoptotic genes Bcl-2 and A1. Go-culture experiments with human neonatal dermal fibroblasts and human umbilical vein endothelial cells demonstrated that neonatal dermal fibroblasts, in combination with VEGF, stimulated human umbilical vein endothelial cells tubulogenesis through the paracrine secretion of HGF. Finally, in vivo experiments demonstrated that the combination of HGF and VEGF increased neovascularization in the rat corneal assay greater than either growth factor alone. We suggest that combination therapy using HGF and VEGF co-administration may provide a more effective strategy to achieve therapeutic angiogenesis.

关键词：细胞培养技术/方法细胞系细胞存活/药物作用胶原/生理学角膜/血液供给角膜/药物作用药物协同作用内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用成纤维细胞/生理学肝细胞生长因子/药理学淋巴因子/药理学新生血管化生理性/药物作用大鼠 Sprague-Dawley 血管内皮生长因子A 血管内皮生长因子类动物人类男(雄)性大鼠

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Expression and action of hepatocyte growth factor in human and bovine normal ovarian surface epithelium and ovarian cancer

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BIOLOGY OF REPRODUCTION 2000年第3期62卷 491-500页

作者： Parrott, JA Skinner, MK Washington State Univ Dept Genet & Cell Biol Ctr Reprod Biol Pullman WA 99164 USA

More than 95% of ovarian cancers originate from the epithelial cells on the surface of the ovary, which are termed ovarian surface epithelium (OSE). These OSE cells are modified peritoneal mesothelial cells separated from underlying ovarian surface stromal tissue by a basal lamina of dense collagenous connective tissue. Mesenchymal-epithelial cell interactions between stromal cells and OSE cells are postulated to be important for normal OSE biology and for the onset of ovarian cancer. Hepatocyte growth factor (HGF) is a mesenchymal-derived growth factor that mediates mesenchymal-epithelial cell interactions in a number of different tissues. The current study was an investigation of the expression and actions of HGF in normal OSE and ovarian cancer. Human epithelial cells from borderline and stage III ovarian cancer cases were found to express HGF protein in the epithelial cell component by immunocytochemistry analysis. The stromal cell component of human ovarian tumors contained little or no HGF immunostaining. Normal bovine ovaries have a similar physiology and endocrinology to human ovaries and are used as a model system to investigate normal OSE functions. HGF protein was detected in the OSE from both normal human and bovine ovaries. Adjacent ovarian stromal tissue contained light but positive HGF immunostaining. RNA was collected from normal bovine ovarian stromal cells to examine HGF gene expression. HGF transcripts were detected in cultured OSE and stromal cells by Northern blot analysis. Using a quantitative reverse transcription-polymerase chain reaction procedure, HGF gene expression was found to be high in freshly isolated OSE but low in freshly isolated stroma. Levels of HGF gene expression after culture of stroma increased. Observations indicate that normal OSE express high levels of HGF in vivo and in vitro. Expression of HGF by normal epithelial cells versus stromal cells was unexpected and suggests that HGF may be important in an autocrine regulation

关键词：细胞分裂/药物作用细胞膜/代谢细胞培养的上皮细胞/代谢基因表达调控肿瘤肝细胞生长因子/遗传学肝细胞生长因子/代谢肝细胞生长因子/药理学卵巢肿瘤/代谢卵巢/细胞学卵巢/药物作用卵巢/生理学逆转录聚合酶链反应间质细胞/代谢动物牛女(雌)性人类

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Experimental study of the effects of deletion variant of hepatocyte growth factor on hepatic ischaemia-reperfusion injury

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BRITISH JOURNAL OF SURGERY 2000年第1期87卷 59-64页

作者： Ikegami, T Nishizaki, T Uchiyama, H Hashimoto, K Yanaga, K Sugimachi, K Kyushu Univ Dept Surg 2 Fukuoka 8128582 Japan

Background: Hepatic ischaemia-reperfusion (IR) injury is still a serious complication following liver surgery. The effect of the deletion variant of hepatocyte growth factor (dHGF) on hepatic IR injury was examined in rats. Methods: Male Wistar rats were divided into two groups after 90 min of partial liver ischaemia: the dHGF group which was given dHGF 0.5 mg/kg intravenously immediately after reperfusion, followed by 0.5 mg/kg every 12 h, and the control group, which received vehicle buffer only. Serum chemistry, histopathological findings and liver weights were compared between the groups. Results: In the dHGF group, the increase in serum alanine transaminase and hyaluronic acid levels was significantly reduced, and the serum albumin level increased after reperfusion. The extent of hepatic necrosis 24 h after reperfusion was decreased in the dHGF group. Moreover, the proportion of terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick end labelling-positive hepatocytes 6 h after reperfusion was reduced in the dHGF group. The non-ischaemic-, ischaemic- and whole-liver weight : body-weight ratio significantly increased in the dHGF group after reperfusion. The proportion of proliferating cell nuclear antigen-positive hepatocytes in the dHGF group markedly increased after 6 h after reperfusion in the non-ischaemic lobes, while in the ischaemic lobes it increased 24 h after reperfusion. Conclusion: These data suggest that dHGF not only improves recovery from IR injury, but also accelerates recovery from these injuries. dHGF may be an effective pharmacological agent for prevention and treatment of hepatic IR injury.

关键词：细胞凋亡/生理学药物评价临床前肝细胞生长因子/遗传学肝细胞生长因子/药理学肝疾病/病理学肝疾病/预防和控制坏死大鼠 Wistar 再灌注损伤/病理学再灌注损伤/预防和控制动物男(雄)性大鼠

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The tyrosine phosphatase SHP-2 is required for sustained activation of extracellular signal-regulated kinase and epithelial morphogenesis downstream from the Met receptor tyrosine kinase

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MOLECULAR AND CELLULAR BIOLOGY 2000年第22期20卷 8513-8525页

作者： Maroun, CR Naujokas, MA Holgado-Madruga, M Wong, AJ Park, M Royal Victoria Hosp Mol Oncol Grp Montreal PQ H3A 1A1 Canada McGill Univ Dept Med Montreal PQ H3A 1A1 Canada McGill Univ Dept Oncol Montreal PQ H3A 1A1 Canada McGill Univ Dept Biochem Montreal PQ H3A 1A1 Canada Kimmel Canc Inst Dept Microbiol & Immunol Philadelphia PA 19107 USA Kimmel Canc Inst Dept Pharmacol Philadelphia PA 19107 USA

Epithelial morphogenesis is critical during development and wound healing, and alterations in this program contribute to neoplasia. Met, the hepatocyte growth factor (HGF) receptor, promotes a morphogenic program in epithelial cell lines in matrix cultures. Previous studies have identified Gab1, the major phosphorylated protein following Met activation, as important for the morphogenic response. Gab1 is a docking protein that couples the Met receptor with multiple signaling proteins, including phosphatidylinositol-3 kinase, phospholipase C gamma, the adapter protein Crk, and the tyrosine specific phosphatase SHP-2. HGF induces sustained phosphorylation of Gab1 and sustained activation of extracellular signal-regulated kinase (Erk) in epithelial Madin-Darby canine kidney cells. In contrast, epidermal growth factor fails to promote a morphogenic program and induces transient Gab1 phosphorylation and Erk activation. To elucidate the Gab1-dependent signals required for epithelial morphogenesis, we undertook a structure-function approach and demonstrate that association of Gab1 with the tyrosine phosphatase SHP-2 is required for sustained Erk activation and for epithelial morphogenesis downstream from the Met receptor. Epithelial cells expressing a Gab1 mutant protein unable to recruit SHP-2 elicit a transient activation of Erk in response to HGF. Moreover, SHP-2 catalytic activity is required, since the expression of a catalytically inactive SHP-2 mutant, C/S, abrogates sustained activation of Erk and epithelial morphogenesis by the Met receptor. These data identify SHP-2 as a positive modulator of Erk activity and epithelial morphogenesis downstream from the Met receptor.

关键词：细胞系/药物作用细胞系/超微结构酶激活/药物作用上皮细胞/生理学肝细胞生长因子/药理学细胞内信号肽和蛋白质类微管/代谢丝裂原激活蛋白激酶类/代谢突变磷蛋白类/遗传学磷蛋白类/代谢磷酰化蛋白质酪氨酸磷酸酶非受体11型蛋白酪氨酸磷酸酶非受体6型蛋白质酪氨酸磷酸酶类/遗传学蛋白质酪氨酸磷酸酶类/代谢原癌基因蛋白质c-met/遗传学原癌基因蛋白质c-met/代谢动物狗

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The relationship between differentiation and proliferation in late gestation fetal rat hepatocytes

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PEDIATRIC RESEARCH 1999年第1期46卷 14-19页

作者： Gruppuso, PA Bienieki, TC Faris, RA Rhode Isl Hosp Div Pediat Endocrinol Providence RI 02903 USA Brown Univ Providence RI 02903 USA

Hepatocyte proliferation and differentiation occur simultaneously during late mammalian gestation, We hypothesized that regulation of hepatocyte growth and differentiation would be coordinated in late gestation fetal hepatocyte cultures such that proliferation would be most active in a population of less well-differentiated cells. Cultured fetal hepatocytes (embryonic d 19 and 21;E19 and E21) were studied using double staining immunofluorescent microscopy. Differentiation was assessed as staining for cw-fetoprotein (AFP), three markers of enzymic differentiation (glucokinase [GK], phosphoenolpyruvate carboxykinase [PEPCK], and carbamoyl phosphate synthase [CPS]), and a hepatocyte cell-cell adhesion molecule (C-CAM). Proliferation was assessed using immunocytochemical detection of proliferating cell nuclear antigen (PCNA) or 5-bromo-2'-deoxy-uridine (BrdU) incorporation into DNA. Fetal hepatocyte cultures consisted of a heterogeneous population of cells, slightly more than half of which were proliferative under defined, growth factor-free conditions. These cultures were heterogeneous for AFP expression. There was no correlation between the expression of AFP and PCNA or AFP and S-phase entry (BrdU staining) during the first 48 h in culture. Similar results were obtained in staining for the enzymic differentiation markers and C-CAM. In addition, the differentiation status of cultured fetal hepatocytes was unrelated to a presumed indicator of mature growth regulation, mitogenic responsiveness to transforming growth factor alpha (TGF alpha), and hepatocyte growth factor (HGF). Finally, absence of any correlation between proliferation and differentiated phenotype was supported by in vivo studies using staining for PCNA, AFP, CPS, and PEPCK in liver sections. These results indicate that the developmental program governing differentiation of late gestation fetal rat hepatocytes is independent from mechanisms controlling proliferation.

关键词：动物新生生物学标记/分析细胞黏附分子/分析细胞分化/药物作用细胞分裂/药物作用细胞培养的 DNA/生物合成胎儿孕龄葡糖激酶/分析肝细胞生长因子/药理学肝/细胞学肝/药物作用肝/胚胎学磷酸烯醇丙酮酸羧激酶(GTP)/分析转化生长因子α/药理学甲胎蛋白类/分析动物大鼠

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