Purification of a lipoprotein lipase-inhibiting protein produced by a melanoma cell line associated with cancer cachexia

Mori, Mitsuo; Yamaguchi, Ken; Abe, Kaoru

doi:10.1016/s0006-291x(89)80114-7

Cited by 152 publications

(44 citation statements)

References 13 publications

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“…The addition of leukemia inhibitory factor (LIF) to the culture medium suppressed the ability of the epiblast-derived hepatocytes to accumulate and secrete lipid (manuscript submitted, Talbot et al, 1994; unpublished observation). Because LIF was demonstrated to inhibit lipoprotein lipase activity in adipocytes (Mori et al, 1989), it is possible that lipoprotein lipase is being similarly affected in the fetal pig hepatocyte cultures. This would also suggest that the lipid accumulation by the fetal pig hepatocytes is a sequestration and processing of lipid components in the culture medium (Guyton, 1986).…”

Section: Discussionmentioning

confidence: 99%

Colony isolation and secondary culture of fetal porcine hepatocytes on STO feeder cells

Talbot

Pursel

Rexroad

et al. 1994

In Vitro Cell Dev Biol - Animal

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SUMMARYThe secondary culture of non-transformed parenchymal hepatocytes has not been possible. STO feeder cell-dependent secondary cultures of fetal pig hepatocytes were established by colony isolation from primary cultures of 26-d fetal livers. The liver cells had the typical polygonal morphology of parenchymal hepatocytes. They also spontaneously differentiated to form small biliary canaliculi between individual cells or progressed further to large multicellular duct-like structures or cells undergoing gross lipid accumulation and secretion. The secondary hepatocyte cultures expressed alpha-fetoprotein (AFP), albumin, and f-fibrinogen mRNA, and conditioned medium from the cells contained elevated levels of transferrin and albumin. STO feeder cell co-culture may be useful for the sustainable culture of hepatocytes from other species.

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Section: Discussionmentioning

confidence: 99%

Colony isolation and secondary culture of fetal porcine hepatocytes on STO feeder cells

Talbot

Pursel

Rexroad

et al. 1994

In Vitro Cell Dev Biol - Animal

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“…A number of reports have implicated the IL-6 family in adipogenesis, though their results were somewhat controversial, e.g. IL-6 was reported to inhibit adipocyte differentiation of 3T3-L1 cells (10,11); LIF was purified as a lipoprotein lipase-inhibiting protein (12), but another study reported that LIF stimulated adipogenesis of 3T3-F442A and Ob1771 preadipocytes, whereas it had only a modest effect on 3T3-L1 cells (13); IL-11 was found as an inhibitor of the adipogenesis of 3T3-L1 cells (14) and bone marrow stroma cells (15); and CT-1 and CNTF did not affect adipogenesis, though they induced signals in 3T3-L1 cells (16,17). Because these studies were conducted mostly by using cultured cells, the controversy could be due to the developmental stage of cells and tissues used by different investigators.…”

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confidence: 99%

Oncostatin M Inhibits Adipogenesis through the RAS/ERK and STAT5 Signaling Pathways

Miyaoka

Tanaka

Naiki

et al. 2006

Journal of Biological Chemistry

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Adipocytes are a major energy reservoir, storing excess energy as lipids and releasing it on demand. In addition, adipocytes constitute an endocrine system by secreting soluble mediators known as adipokines, which regulate not only peripheral tissues such as muscles and adipose tissues but also the central nervous system (1). Disorders in adipose tissues are a major cause of the development of the metabolic syndrome, a common basis of type 2 diabetes and atherosclerotic vascular diseases (2). It is therefore important to understand the nature of adipocytes and the mechanism of adipocyte differentiation.

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“…1) Other humoral factors such as cachectin, tumor-necrosis factor, interleukin (IL)-1, IL-6, interferon (IFN)-γ, leukemia-inhibitory factor (LIF), and lipid-mobilizing factor have also been reported to act as mediators inducing cancer cachexia. [2][3][4] We purified an anemiainducing substance (AIS) that depresses erythrocyte and immunocompetent cell functions, as reported in our previous papers, 5,6) and AIS has been recently shown to have another biological action, i.e., lipolytic activity. As stated above, many substances have been reported to be causative agents of cancer cachexia, and at present it is difficult to discuss the etiology of this condition in a coherent fashion.…”

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confidence: 99%

Apoptosis of Muscle Cells Causes Weight Loss Prior to Impairment of DNA Synthesis in Tumor‐bearing Rabbits

Ishiko¹,

Sumi²,

Hirai³

et al. 2001

Japanese Journal of Cancer Research

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The mechanism of weight loss induced by the growth of malignant tumors is still unknown. We investigated it by focusing on apoptosis of skeletal muscle. VX2-tumor was implanted into rabbits and the apoptotic index (AI) of skeletal muscle was measured by in situ end-labeling assay. Plasma of the tumor-bearing rabbits was perfused repeatedly through non-coated charcoal resin. The AI reached 54.6% early after tumor implantation, when weight loss amounted to an 18% decrease in lean body mass (LBM) without change in muscle DNA synthesis or urinary 3-methylhistidine/ creatinine ratio (3-MH/Cr). When the decrease of LBM reached 30%, DNA synthesis was decreased by 48% and 3-MH/Cr was increased by 104%, whereas AI was only 4.7%. The plasma perfusion did not prevent apoptosis in muscle, but improved LBM, DNA synthesis, and 3-MH/Cr. There may be two mechanisms of muscle depletion during the tumor growth: apoptosis in the early stage and metabolic abnormalities in muscle in the late stage.Key words: Muscle cell -Apoptosis -DNA synthesis -Weightloss -Plasma perfusion The weight loss induced by the progression of malignant tumors is the symptom that has attracted the greatest attention among investigators attempting to identify the etiology of cancer cachexia, a condition that gives rise to a variety of symptoms. Cancer cachexia is generally considered to be characterized metabolically by proteolysis and lipolysis rates that exceed protein synthesis and lipogenesis, but no conclusion has been reached concerning how these metabolic abnormalities occur. Todorov et al. succeeded in purifying a cancer cachectic factor that induces skeletal muscle catabolism from mice transplanted with MAC16 tumors. 1) Other humoral factors such as cachectin, tumor-necrosis factor, interleukin (IL)-1, IL-6, interferon (IFN)-γ, leukemia-inhibitory factor (LIF), and lipid-mobilizing factor have also been reported to act as mediators inducing cancer cachexia.2-4) We purified an anemiainducing substance (AIS) that depresses erythrocyte and immunocompetent cell functions, as reported in our previous papers, 5,6) and AIS has been recently shown to have another biological action, i.e., lipolytic activity. As stated above, many substances have been reported to be causative agents of cancer cachexia, and at present it is difficult to discuss the etiology of this condition in a coherent fashion.In the present study using tumor-bearing rabbits, we examined the relationship between weight loss induced during the progression of malignant tumors and the morphological and energy metabolism changes in muscle tissue. MATERIALS AND METHODSExperimental animals Male Japanese White rabbits implanted with VX2-carcinoma 7) in the muscles of their right thigh were supplied by Tsukuba Animal Research Laboratories Co. (Tsukuba) and fed essential CR-3 (Clea, Tokyo) and water. When the VX2-carcinoma in the right thigh of the rabbits grew to more than 5 cm in diameter, it was resected, and cell suspensions (1×10 5 cells in 1 ml of 0.15 M NaCl) were injected intramuscularly in...

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Purification of a lipoprotein lipase-inhibiting protein produced by a melanoma cell line associated with cancer cachexia

Cited by 152 publications

References 13 publications

Colony isolation and secondary culture of fetal porcine hepatocytes on STO feeder cells

Colony isolation and secondary culture of fetal porcine hepatocytes on STO feeder cells

Oncostatin M Inhibits Adipogenesis through the RAS/ERK and STAT5 Signaling Pathways

Apoptosis of Muscle Cells Causes Weight Loss Prior to Impairment of DNA Synthesis in Tumor‐bearing Rabbits

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