The Mitotic and Metabolic Effects of Phosphatidic Acid in the Primary Muscle Cells of Turbot (Scophthalmus maximus)

Wang, Tingting; Wang, Xuan; Zhou, Huihui; Jiang, Haowen; Mai, Kangsen; He, Gang

doi:10.3389/fendo.2018.00221

Cited by 20 publications

(20 citation statements)

References 106 publications

(119 reference statements)

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“…All full-length PLA1 transcripts revealed in this study are likely to be secretory with most having highly fish-specific expression profiles. Importantly, PLA1A and Lipase H release the lipid mediators lysophosphatidylserine (LPS) and lysophosphatidic acid (LPA) that induce cell proliferation and chronic disease pathology 52 , 53 . It is, therefore, tantalizing to speculate that such lipid mediators may drive PKD pathology.…”

Section: Discussionmentioning

confidence: 99%

Comparative transcriptomics and host-specific parasite gene expression profiles inform on drivers of proliferative kidney disease

Faber

Shaw

Yoon

et al. 2021

Sci Rep

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The myxozoan parasite, Tetracapsuloidesbryosalmonae has a two-host life cycle alternating between freshwater bryozoans and salmonid fish. Infected fish can develop Proliferative Kidney Disease, characterised by a gross lymphoid-driven kidney pathology in wild and farmed salmonids. To facilitate an in-depth understanding of T.bryosalmonae-host interactions, we have used a two-host parasite transcriptome sequencing approach in generating two parasite transcriptome assemblies; the first derived from parasite spore sacs isolated from infected bryozoans and the second from infected fish kidney tissues. This approach was adopted to minimize host contamination in the absence of a complete T.bryosalmonae genome. Parasite contigs common to both infected hosts (the intersect transcriptome; 7362 contigs) were typically AT-rich (60–75% AT). 5432 contigs within the intersect were annotated. 1930 unannotated contigs encoded for unknown transcripts. We have focused on transcripts encoding proteins involved in; nutrient acquisition, host–parasite interactions, development, cell-to-cell communication and proteins of unknown function, establishing their potential importance in each host by RT-qPCR. Host-specific expression profiles were evident, particularly in transcripts encoding proteases and proteins involved in lipid metabolism, cell adhesion, and development. We confirm for the first time the presence of homeobox proteins and a frizzled homologue in myxozoan parasites. The novel insights into myxozoan biology that this study reveals will help to focus research in developing future disease control strategies.

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Section: Discussionmentioning

confidence: 99%

Comparative transcriptomics and host-specific parasite gene expression profiles inform on drivers of proliferative kidney disease

Faber

Shaw

Yoon

et al. 2021

Sci Rep

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“…PA is a component of the other pathway of TAG synthesis, and there is evidence that PA has mitogenic effects that play a role in liver regeneration. (28,30,48) PA stimulates cell proliferation through activation of the mammalian target of rapamycin pathway (49,50) and inhibition of PA synthesis impairs liver regeneration following acetaminophen toxicity. (28) Though it is not yet clear why PA content was reduced with Mogat1 ASO, it is possible that impaired PA-mediated signaling and proliferation pathways may lead to a defective regenerative response.…”

Section: Original Article | 131mentioning

confidence: 99%

Monoacylglycerol Acyltransferase 1 Knockdown Exacerbates Hepatic Ischemia/Reperfusion Injury in Mice With Hepatic Steatosis

Liss¹,

Lutkewitte

et al. 2020

Liver Transpl.

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Nonalcoholic fatty liver disease (NAFLD) is becoming the most common indication for liver transplantation. The growing prevalence of NAFLD not only increases the demand for liver transplantation, but it also limits the supply of available organs because steatosis predisposes grafts to ischemia/reperfusion injury (IRI) and many steatotic grafts are discarded. We have shown that monoacylglycerol acyltransferase (MGAT) 1, an enzyme that converts monoacylglycerol to diacylglycerol, is highly induced in animal models and patients with NAFLD and is an important mediator in NAFLD-related insulin resistance. Herein, we sought to determine whether Mogat1 (the gene encoding MGAT1) knockdown in mice with hepatic steatosis would reduce liver injury and improve liver regeneration following experimental IRI. Antisense oligonucleotides (ASO) were used to knockdown the expression of Mogat1 in a mouse model of NAFLD. Mice then underwent surgery to induce IRI. We found that Mogat1 knockdown reduced hepatic triacylglycerol accumulation, but it unexpectedly exacerbated liver injury and mortality following experimental ischemia/reperfusion surgery in mice on a high-fat diet. The increased liver injury was associated with robust effects on the hepatic transcriptome following IRI including enhanced expression of proinflammatory cytokines and chemokines and suppression of enzymes involved in intermediary metabolism. These transcriptional changes were accompanied by increased signs of oxidative stress and an impaired regenerative response. We have shown that Mogat1 knockdown in a mouse model of NAFLD exacerbates IRI and inflammation and prolongs injury resolution, suggesting that Mogat1 may be necessary for liver regeneration following IRI and that targeting this metabolic enzyme will not be an effective treatment to reduce steatosis-associated graft dysfunction or failure.

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“…These findings are consistent with the PA myogenic stimulation of mTOR, which is downstream of Akt or ERK1-2, in different cell types or tissues, including skeletal muscle [ 13 , 18 , 33 , 34 ]. In a recent report, PA has also been demonstrated to stimulate cell proliferation and promote G1/S phase transition through the activation of mTOR in primary muscle cells of the fish turbot ( Scophthalmus maximus ) [ 35 ], which, given the disparate growth pattern compared to mammals, suggests a well conserved action of PA through evolution.…”

Section: Discussionmentioning

confidence: 99%

Phosphatidic Acid Stimulates Myoblast Proliferation through Interaction with LPA1 and LPA2 Receptors

Gómez-Larrauri

Gangoiti

Presa

et al. 2021

IJMS

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Phosphatidic acid (PA) is a bioactive phospholipid capable of regulating key biological functions, including neutrophil respiratory burst, chemotaxis, or cell growth and differentiation. However, the mechanisms whereby PA exerts these actions are not completely understood. In this work, we show that PA stimulates myoblast proliferation, as determined by measuring the incorporation of [3H]thymidine into DNA and by staining the cells with crystal violet. PA induced the rapid phosphorylation of Akt and ERK1/2, and pretreatment of the cells with specific small interferin RNA (siRNA) to silence the genes encoding these kinases, or with selective pharmacologic inhibitors, blocked PA-stimulated myoblast proliferation. The mitogenic effects of PA were abolished by the preincubation of the myoblasts with pertussis toxin, a Gi protein inhibitor, suggesting the implication of Gi protein-coupled receptors in this action. Although some of the effects of PA have been associated with its possible conversion to lysoPA (LPA), treatment of the myoblasts with PA for up to 60 min did not produce any significant amount of LPA in these cells. Of interest, pharmacological blockade of the LPA receptors 1 and 2, or specific siRNA to silence the genes encoding these receptors, abolished PA-stimulated myoblast proliferation. Moreover, PA was able to compete with LPA for binding to LPA receptors, suggesting that PA can act as a ligand of LPA receptors. It can be concluded that PA stimulates myoblast proliferation through interaction with LPA1 and LPA2 receptors and the subsequent activation of the PI3K/Akt and MEK/ERK1-2 pathways, independently of LPA formation.

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The Mitotic and Metabolic Effects of Phosphatidic Acid in the Primary Muscle Cells of Turbot (Scophthalmus maximus)

Cited by 20 publications

References 106 publications

Comparative transcriptomics and host-specific parasite gene expression profiles inform on drivers of proliferative kidney disease

Comparative transcriptomics and host-specific parasite gene expression profiles inform on drivers of proliferative kidney disease

Monoacylglycerol Acyltransferase 1 Knockdown Exacerbates Hepatic Ischemia/Reperfusion Injury in Mice With Hepatic Steatosis

Phosphatidic Acid Stimulates Myoblast Proliferation through Interaction with LPA1 and LPA2 Receptors

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