Oncostatin M and hepatocyte growth factor induce hepatic maturation via distinct signaling pathways

Kamiya, Akihide; Kinoshita, Taisei; Miyajima, Atsushi

doi:10.1016/s0014-5793(01)02140-8

Cited by 179 publications

(161 citation statements)

References 30 publications

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“…147,148 Studies using a hepatoblast culture system have shown that oncostatin M, which is secreted from hematopoietic cells within the fetal liver, contributes to control late stages of hepatocyte differentiation, possibly by increasing HNF4␣ expression. [149][150][151] Furthermore, mice lacking the gp130 subunit of the oncostatin M receptor fail to accumulate normal levels of glycogen, which is consistent with a requirement for oncostatin M in completion of hepatocyte maturation. 152 Not only do hematopoietic cells contribute to development of the liver parenchyma but, conversely, differentiation of the hematopoietic cells is also influenced by the hepatocytes.…”

Section: What Governs the Establishment Of Hepatic Architecture And Msupporting

confidence: 57%

Embryonic development of the liver†

2005

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Section: What Governs the Establishment Of Hepatic Architecture And Msupporting

confidence: 57%

Embryonic development of the liver†

2005

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“…46 Additionally, in situ hybridization has demonstrated LIF, LIF receptor (LIFR) and glycoprotein (gp)130 mRNA expression in oval cells, with weak expression in parenchymal cells. Oncostatin M has recently been implicated in the maturation of fetal hepatocytes in vitro and in vivo , 47 and it may have a similar role in the hepatic differentiation of oval cells.…”

Section: Role Of Inflammatory Cytokinesmentioning

confidence: 99%

Oval cell‐mediated liver regeneration: Role of cytokines and growth factors

Lowes

Croager

Olynyk

et al. 2002

J of Gastro and Hepatol

154

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In experimental models, which induce liver damage and simultaneously block hepatocyte proliferation, the recruitment of a hepatic progenitor cell population comprised of oval cells is invariably observed. There is a substantial body of evidence to suggest that oval cells are involved in liver regeneration, as they differentiate into hepatocytes and biliary cells. Recently, bone marrow cells were shown to be a source of a stem cells with the capacity to repopulate the liver. Presently, the relationship between bone marrow cells and oval cells is unclear. Investigations will be greatly assisted by the availability of in vitro models based on a knowledge of cytokines that affect oval cells. While the cytokines, which regulate the different hematopoietic lineages, are well characterized, there is relatively little information regarding those that influence oval cells. This review outlines recent developments in the field of oval cell research and focuses on cytokines and growth factors that have been implicated in regulating oval cell proliferation and differentiation.

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“…Disruption of the regulatory system that controls G 1 -phase progression is a common event in human hepatocarcinogenesis (Hui et al, 1998), and p27 Kip1 has been associated with differentiation, invasiveness, and metastasis of hepatocellular carcinoma tumors (Zhou et al, 2003). Recent evidence indicate that OSM signaling plays a prominent role in liver development (Kamiya et al, 1999(Kamiya et al, , 2001Kojima et al, 2000;Kinoshita and Miyajima, 2002;Matsui et al, 2002;Chagraoui et al, 2003;Hanada et al, 2003;Lazaro et al, 2003). OSM stimulates hepatocyte nuclear factor-4 ( Kamiya et al, 2003), which may integrate the genetic programs of liver-specific gene expression and epithelial morphogenesis (Spath and Weiss, 1998).…”

Section: Introductionmentioning

confidence: 99%

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics

IJzendoorn

Théard

Wouden

et al. 2004

MBoC

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Oncostatin M regulates membrane traffic and stimulates apicalization of the cell surface in hepatoma cells in a protein kinase A-dependent manner. Here, we show that oncostatin M enhances the expression of the cyclin-dependent kinase (cdk)2 inhibitor p27 Kip1 , which inhibits G 1 -S phase progression. Forced G 1 -S-phase transition effectively renders presynchronized cells insensitive to the apicalization-stimulating effect of oncostatin M. G 1 -S-phase transition prevents oncostatin M-mediated recruitment of protein kinase A to the centrosomal region and precludes the oncostatin M-mediated activation of a protein kinase A-dependent transport route to the apical surface, which exits the subapical compartment (SAC). This transport route has previously been shown to be crucial for apical plasma membrane biogenesis. Together, our data indicate that oncostatin M-stimulated apicalization of the cell surface is critically dependent on the ability of oncostatin M to control p27 Kip1 /cdk2-mediated G 1 -S-phase progression and suggest that the regulation of apical plasma membrane-directed traffic from SAC is coupled to centrosome-associated signaling pathways. INTRODUCTIONThe establishment and maintenance of apical and basolateral plasma membrane (PM) domains in epithelia require a careful orchestration of extra-and intracellular signals, triggering crucial cytoskeleton-, organelle-, and membrane traffic-linked machineries, as partly elucidated in systems as diverse as yeast, Drosophila, and mammalian cells (Lecuit and Pilot, 2003;Mostov et al., 2003;Baas et al., 2004). Impairment of these events may cause a loss of apical-basolateral asymmetry and may lead to deranged cell growth (Bilder et al., 2000;Vermeer et al., 2003;Baas et al., 2004) or spindle misorientation . Recent studies have reported an evolutionary conserved genetic program that may link the process of polarity development and proliferation (Bilder et al., 2000;Humbert et al., 2003;Rolls et al., 2003;Klezovitch et al., 2004). However, many aspects of such a link remain unclear, e.g., the extent to which cell proliferation can directly affect epithelial cell organization or vice versa. Indeed, epithelial cell proliferation and apical-basolateral polarity may be controlled by different signaling pathways (Liu et al., 2004).Signaling cascades stimulated by interleukin-6 family cytokines, including oncostatin M (OSM), elicit multiple responses in the cell. Originally, as its name indicates, oncostatin M was primarily recognized to inhibit the proliferation of tumor cells (Tanaka and Miyajima, 2003), presumably by modulating cell cycle regulatory proteins, including the cyclin-dependent kinase (cdk)2-inhibitor p27 Kip1 (Kortylewski et al., 1999;Klausen et al., 2000;Li et al., 2001). Disruption of the regulatory system that controls G 1 -phase progression is a common event in human hepatocarcinogenesis (Hui et al., 1998), and p27 Kip1 has been associated with differentiation, invasiveness, and metastasis of hepatocellular carcinoma tumors (Zhou et al., 2003). ...

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Oncostatin M and hepatocyte growth factor induce hepatic maturation via distinct signaling pathways

Cited by 179 publications

References 30 publications

Embryonic development of the liver†

Embryonic development of the liver†

Oval cell‐mediated liver regeneration: Role of cytokines and growth factors

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics

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Oncostatin M and hepatocyte growth factor induce hepatic maturation via distinct signaling pathways

Cited by 179 publications

References 30 publications

Embryonic development of the liver†

Embryonic development of the liver†

Oval cell‐mediated liver regeneration: Role of cytokines and growth factors

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27Kip1-Regulated Cell Cycle Dynamics

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Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics