Activation of phospholipase D activity in transforming growth factor-beta-induced cell growth inhibition

Bin, Zhou; Chen, Jun Song; Chai, Ming Qiang; Zhao, Sheng; Liang, Jun; Chen, He Hua; Song, Jian

doi:10.1038/sj.cr.7290043

Cited by 5 publications

(4 citation statements)

References 27 publications

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“…Interestingly, TGFβ1 could induce the expression of arachidonic acid synthase PLA2G4A and PLCG2 , although arachidonic acid could not induce the expression of TGFβ1 in Eph4 cells. The similar phenomenon was also observed in other cell lines [36, 37]. TGFβ1 activates the PLA2 in cultured rat costochondral chondrocytes [36].…”

Section: Discussionsupporting

confidence: 82%

“…TGFβ1 activates the PLA2 in cultured rat costochondral chondrocytes [36]. TGFβ1 also activates phospholipase D activity and increases the production of arachidonic acid precursor, diacyl-glycerol (DAG), in lung and kidney epithelial cells [37]. Those results indicate that TGFβ1 signalling pathway may stimulate the arachidonic acid synthesis during the involution period.…”

Section: Discussionmentioning

confidence: 99%

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Decrease of lactogenic hormones induce epithelial-mesenchymal transition via TGFβ1 and arachidonic acid during mammary gland involution

Zhang

Liu

Weng

et al. 2017

Journal of Reproduction and Development

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During mammary gland involution, the epithelial mesenchymal transition (EMT) process plays an important role in tissue remodelling and in the termination of milk production. Transforming growth factor β (TGFβ) has been known as a central inducer to EMT and contributor to the mammary gland involution. However, the whole mechanism has accomplished the EMT process in mammary gland is still unclear. Here, we show that arachidonic acid, one of the major products in milk, is new player to control the EMT together with TGFβ during mammary gland involution. Firstly, we observed decrease in CDH1 (epithelial marker gene) expression and increases in VIM and TWIST1 (mesenchymal marker genes), TGFB1, and PLCG2 (arachidonic acid synthesis gene) at involution. In epithelial cells culture experiments, depletion of lactogenic hormones to mimic the involution induced TGFβ1 and PLCG2 expressions. Treatment with arachidonic acid in epithelial cells increased VIM and TWIST1 expressions without decrease of CDH1 expression, while TGFβ1 decreased CDH1 and increased VIM and TWIST1; more importantly, TGFβ1 induced the expression of PLCG2, but arachidonic acid did not induce the expression of TGFB1. Finally, arachidonic acid accelerated the TGFβ1 increasing VIM and TWIST1 expressions, meanwhile arachidonic acid synthase inhibitor partially blocked the TGFβ1 increasing VIM and TWIST1 expressions. In conclusion, TGFβ1 stimulates arachidonic acid synthesis and the arachidonic acid has a function to postulate the EMT process together with TGFβ1 during mammary gland involution.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Decrease of lactogenic hormones induce epithelial-mesenchymal transition via TGFβ1 and arachidonic acid during mammary gland involution

Zhang

Liu

Weng

et al. 2017

Journal of Reproduction and Development

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“…Investigating the signaling pathways induced by TGF-β is important for the understanding of the mechanism that underlies the various biological events mediated by TGF-β. It was demonstrated that increased PLD activity are involved in TGF-β-induced growth inhibition of several types of epithelial cell lines [3]. TGF-β can induce apoptosis in normal hepatocytes [4][5][6][7] and hepatoma cells [8], [9].…”

Section: Introductionmentioning

confidence: 99%

The involvement of p38 MAPK in transforming growth factor β1-induced apoptosis in murine hepatocytes

et al. 2001

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We reported in this manuscript that TGF-β1 induces apoptosis in AML12 murine hepatocytes, which is associated with the activation of p38 MAPK signaling pathway. SB202190, a specific inhibitor of p38 MAPK, strongly inhibited the TGF-β1-induced apoptosis and PAI-1 promoter activity. Treatment of cells with TGF-β1 activates p38. Furthermore, over-expression of dominant negative mutant p38 also reduced the TGF-β1-induced apoptosis. The data indicate that the activation of p38 is involved in TGF-β1-mediated gene expression and apoptosis.

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“…Aberrant PLD activity has been identified in chronic inflammatory autoimmune disorders and in allergic asthma (Choi et al., 2015, Kang et al., 2013). Moreover, TGF-β1 increases PLD activity and increases the levels of PA and PA-related metabolites in epithelial cell lines (Zhou et al., 2000). We sought to establish whether there is a link between PLD and the TGF-β1 suppression of GC activity.…”

Section: Discussionmentioning

confidence: 99%

A Non-canonical Pathway with Potential for Safer Modulation of Transforming Growth Factor-β1 in Steroid-Resistant Airway Diseases

Keenan

López–Campos

et al. 2019

iScience

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SummaryImpaired therapeutic responses to anti-inflammatory glucocorticoids (GC) in chronic respiratory diseases are partly attributable to interleukins and transforming growth factor β1 (TGF-β1). However, previous efforts to prevent induction of GC insensitivity by targeting established canonical and non-canonical TGF-β1 pathways have been unsuccessful. Here we elucidate a TGF-β1 signaling pathway modulating GC activity that involves LIM domain kinase 2-mediated phosphorylation of cofilin1. Severe, steroid-resistant asthmatic airway epithelium showed increased levels of immunoreactive phospho-cofilin1. Phospho-cofilin1 was implicated in the activation of phospholipase D (PLD) to generate the effector(s) (lyso)phosphatidic acid, which mimics the TGF-β1-induced GC insensitivity. TGF-β1 induction of the nuclear hormone receptor corepressor, SMRT (NCOR2), was dependent on cofilin1 and PLD activities. Depletion of SMRT prevented GC insensitivity. This pathway for GC insensitivity offers several promising drug targets that potentially enable a safer approach to the modulation of TGF-β1 in chronic inflammatory diseases than is afforded by global TGF-β1 inhibition.

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Activation of phospholipase D activity in transforming growth factor-beta-induced cell growth inhibition

Abstract: The data presented suggest that PLD activation is involved in the TGF-β 1 -induced cell growth inhibition.

Cited by 5 publications

References 27 publications

Decrease of lactogenic hormones induce epithelial-mesenchymal transition via TGFβ1 and arachidonic acid during mammary gland involution

Decrease of lactogenic hormones induce epithelial-mesenchymal transition via TGFβ1 and arachidonic acid during mammary gland involution

The involvement of p38 MAPK in transforming growth factor β1-induced apoptosis in murine hepatocytes

A Non-canonical Pathway with Potential for Safer Modulation of Transforming Growth Factor-β1 in Steroid-Resistant Airway Diseases

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