Transforming growth factor‐β1 rapidly activates phosphorylase in a calcium‐dependent manner in rat hepatocytes

Hahm, Sung−Ho; Cooper, Ronald H.

doi:10.1016/0014-5793(92)81361-o

Cited by 7 publications

(4 citation statements)

References 35 publications

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“…In culture, prostate carcinoma cells (PC-3U) retain the ability to respond to a stimulation with TGF-β with signs of an apoptosis initiation, displaying both a calcium transient and mitochondria depolarization [ 91 ]. This finding of calcium-transient induction is consistent with TGF-β effects on other cell types, such as hepatocytes [ 92 ] and renal mesangial cells [ 93 ], as well as on primary pulmonary fibroblasts [ 94 ], which exhibited calcium waves, and on osteoblasts [ 95 ], which display oscillations. In other epithelial cells, the evidence for the involvement of calcium in inhibitory TGF-β signaling comes from experiments on keratinocytes, in which nucleolin-mediated nuclear translocation of the S100C/A11 calcium-binding protein is a shared feature of the response to calcium elevation and TGF-β [ 96 , 97 , 98 ].…”

Section: Resistance To Growth Inhibitionsupporting

confidence: 77%

Fatty Acids and Calcium Regulation in Prostate Cancer

Maly

Hofmann

2018

Nutrients

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Prostate cancer is a widespread malignancy characterized by a comparative ease of primary diagnosis and difficulty in choosing the individualized course of treatment. Management of prostate cancer would benefit from a clearer understanding of the molecular mechanisms behind the transition to the lethal, late-stage forms of the disease, which could potentially yield new biomarkers for differential prognosis and treatment prioritization in addition to possible new therapeutic targets. Epidemiological research has uncovered a significant correlation of prostate cancer incidence and progression with the intake (and often co-intake) of fatty acids and calcium. Additionally, there is evidence of the impact of these nutrients on intracellular signaling, including the mechanisms mediated by the calcium ion as a second messenger. The present review surveys the recent literature on the molecular mechanisms associated with the critical steps in the prostate cancer progression, with special attention paid to the regulation of these processes by fatty acids and calcium homeostasis. Testable hypotheses are put forward that integrate some of the recent results in a more unified picture of these phenomena at the interface of cell signaling and metabolism.

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Section: Resistance To Growth Inhibitionsupporting

confidence: 77%

Fatty Acids and Calcium Regulation in Prostate Cancer

Maly

Hofmann

2018

Nutrients

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“…It is possible that TGF-p1 binds to receptors and that subsequent gene transcription leads to a modulation of Ca2+ channel activity by way of production of stimulatory factors or reduction of inhibitory factors. In rat hepatocytes, TGF-p 1 increases [Ca2+li (32); however, the mechanism of this phenomenon remains to be clarified.…”

Section: Evaluation Of the Na +Lca2+ Exchange Mechanismmentioning

confidence: 97%

Hepatic ito cells contain calcium channels: Increases with transforming growth factor-β 1

Oide

Thurman

1994

Hepatology

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Ito cells (fat-storing cells) have been implicated in mechanisms of liver fibrosis, and transforming growth factor-beta 1 is a key factor that stimulates collagen production by Ito cells. Moreover, Ito cells are reported to possess contractile proteins and to contract with ligands. We recently reported the presence of L-type voltage-operated Ca2+ channels in Kupffer cells. In this study, we examined whether Ito cells contain Ca2+ channels and also evaluated the effect of transforming growth factor-beta 1 on Ca2+ channels. Cytosolic free calcium concentration was measured in individual cultured Ito cells with the fluorescent Ca2+ indicator dye fura-2. Partial replacement of extracellular Na+ with K+ caused an increase in cytosolic free calcium, presumably as a result of transmembrane Ca2+ influx. Basal cytosolic free calcium levels were around 40 to 50 nmol/L in both control and transforming growth factor-beta 1-treated cells. In transforming growth factor-beta 1-treated cells, cytosolic free calcium increased in response to K+ at values as low as 10 mmol/L, whereas untreated cells did not respond. Half-maximal increases in cytosolic free calcium in transforming growth factor-beta 1-treated cells were observed with 63 +/- 6 mmol/L K+. With 100 mmol/L K+, intracellular free calcium increased around fourfold above basal values in transforming growth factor-beta 1-treated cells but was only increased about twofold in untreated controls. We conclude that this increase in cytosolic free calcium occurs by way of voltage-operated calcium channels; it did not occur in the absence of extracellular calcium and cannot be explained by Na+/Ca2+ exchange mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…The Smad complex binds to DNA directly or indirectly via interaction with other proteins, recruiting coactivators to mediate the transcription of genes involved in a variety of pathways (28). In addition, TGF-b1 signals through a variety of diverse, Smad-independent pathways that modulate [Ca 21 ] i levels (29,30), ras homolog gene family, member A (RhoA)/rho-associated protein kinase (ROCK) (31), MAPK, and ERK pathways (32,33). Both Smad-independent and Smad-dependent pathways may mediate airway remodeling and AHR.…”

Section: Tgf-b1 Signalingmentioning

confidence: 99%

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Ojiaku

Yoo

Panettieri

2017

Am J Respir Cell Mol Biol

100

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The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and epithelial cells, mediate all three aspects of asthma pathogenesis. Although studies show a connection between airway remodeling and changes in bronchomotor tone, the relationship between the two remains unclear. Transforming growth factor b1 (TGF-b1), a growth factor elevated in the airway of patients with asthma, plays a role in airway remodeling and in the shortening of various airway structural cells. However, the role of TGF-b1 in mediating airway hyperresponsiveness remains unclear. In this review, we summarize the literature addressing the role of TGF-b1 in airway remodeling and shortening. Through our review, we aim to further elucidate the role of TGF-b1 in asthma pathogenesis and the link between airway remodeling and airway hyperresponsiveness in asthma and to define TGF-b1 as a potential therapeutic target for reducing asthma morbidity and mortality.

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Transforming growth factor‐β1 rapidly activates phosphorylase in a calcium‐dependent manner in rat hepatocytes

Cited by 7 publications

References 35 publications

Fatty Acids and Calcium Regulation in Prostate Cancer

Fatty Acids and Calcium Regulation in Prostate Cancer

Hepatic ito cells contain calcium channels: Increases with transforming growth factor-β 1

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

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