Diacylglycerol kinase activity in purified basolateral membranes of kidney tubules

Nogaroli, Luciana; Silva, Osman F.; Bonilha, Thais Alcantra; Moreno, Pilar A.; Bernardo, Robson Roney; Vieyra, Adalberto; Einicker‐Lamas, Marcelo

doi:10.1016/j.biocel.2004.05.020

Cited by 8 publications

(7 citation statements)

References 48 publications

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“…#857130, 2017) in a known concentration was used, which allowed to perform the densitometry after the thin layer chromatography (TLC). The extraction procedure began with the addition of 5 ml chloroform: methanol: HCl (2:1:0.075, v/v) to the samples as previously described (Horwitz & Perlman, 1987;Nogaroli et al, 2005). The resulting organic phase was dried with N 2 gas and reconstituted in 90 µL chloroform:methanol:H2O (7.5:2.5:0.2, v/v).…”

Section: Lipid Extraction and Analysis In Microglia (Mg Cm) And Gbmmentioning

confidence: 99%

Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA₁ receptor

Amaral

Geraldo

Einicker‐Lamas

et al. 2020

Journal of Neurochemistry

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Glioblastomas (GBMs) are highly aggressive primary brain tumors characterized by cellular heterogeneity, insensitivity to chemotherapy and poor patient survival. Lysophosphatidic acid (LPA) is a lysophospholipid that acts as a bioactive signaling molecule and plays important roles in diverse biological events during development and disease, including several cancer types. Microglial cells, the resident macrophages of the central nervous system, express high levels of Autotaxin (ATX,Enpp2), an enzyme that synthetizes LPA. Our study aimed to investigate the role of LPA on tumor growth and invasion in the context of microglia-GBM interaction. First, through bioinformatics studies, patient data analysis demonstrated that more aggressive GBM expressed higher levels of ENPP2, which was also associated with worse patient prognosis with proneural GBM. Using GBM-microglia co-culture system we then demonstrated that GBM secreted factors were able to increase LPA 1 and ATX in microglia, which could be further enhanced by hypoxia. On the other hand, interaction with microglial cells also increased ATX expression in GBM. Furthermore, microglialinduced GBM proliferation and migration could be inhibited by pharmacological inhibition of LPA 1 , suggesting that microglial-derived LPA could support tumor growth and invasion. Finally, increased LPA 1 expression was observed in GBM comparing with other gliomas and could be also associated with worse patient survival. These results show for the first time a microglia-GBM interaction through the LPA pathway with relevant implications for tumor progression. A better understanding of this interaction can lead to the development of new therapeutic strategies setting LPA as a potential target for GBM treatment.

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Section: Lipid Extraction and Analysis In Microglia (Mg Cm) And Gbmmentioning

confidence: 99%

Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA₁ receptor

Amaral

Geraldo

Einicker‐Lamas

et al. 2020

Journal of Neurochemistry

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“…The assay allowed the detection of the phosphorylated lipids, such as S1P, in the reaction medium through the incorporation of [𝛾- 32 Pi] from [𝛾-32 P]-ATP (10 8 cpm/experimental group), as previously described by the authors' group. [39,40] For total lipid analysis, 35 μCi of [𝛾-32 P]-Pi/experimental condition was added shortly after the withdrawal of the ischemic buffer (HBSS and AA) and medium exchange for 24 h of reoxygenation. Immediately after reoxygenation in these two different experimental analyses, total lipids were extracted as described elsewhere.…”

Section: Methodsmentioning

confidence: 99%

Sphingosine 1‐Phosphate Prevents Human Embryonic Stem Cell Death Following Ischemic Injury

Assis

Fernandes

Aniceto

et al. 2022

Euro J Lipid Sci & Tech

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Cell therapy based on humanembryonic stem cells (hESCs) is a potential treatment for several human diseases caused by ischemic processes. Efficiency and feasibility of these therapies rely on understanding stem cell biology and the interaction and survival of these cells within the injured tissue. hESCs are an important source of diffusible bioactive paracrine modulators and the targets for different signaling molecules that prime cellular tissue repair. Notably, sphingosine 1-phosphate (S1P) is an emerging bioactive lipid that activates G protein-coupled receptors, known as S1P receptors (S1PR1-5), promoting cell survival, differentiation, and migration. It is shown that S1P increases cell viability and prevents death in about 50% after the ischemic insult. S1P-mediated protectiveeffect is attributed to the modulation of S1PR3 and S1PR4 expression, which have been associated with the reperfusion injury salvage kinase/survivoractivating factor enhancement (RISK/SAFE) pathway. Involvement of the SAFE pathway is further verified by applying Janus Kinase (JAK2) and signal transducer and activation of transcription 3 pathway inhibitors, which prevents the S1P protective effect. An increase in sphingosine kinase (SphK) activity is also observed after S1P pretreatment. These results provide evidence for an S1P-dependent, SphK positive feedback that stimulates hESCs to deliver large amounts of S1P. Thus, S1P protects hESC under ischemic conditions through the different receptors. Practical Applications: It is considered that S1P can be used as an adjuvant to pretreat hESCs prior to the administration in cell therapy-based protocols for different diseases.

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“…In the last fifteen years, our group has been studying the ability of bioactive lipids to modulate some of the main ion transporters and other cell signaling pathways present in the basolateral membranes (BLM) from kidney proximal tubules [18,[24][25][26][27][28][29]. Here, we extend our efforts to bring new insights into the role of C1P within the renal tissue, with C1P the bioactive lipid less studied in the sphingolipid rheostate scenario, thus illustrating the need to identify intracellular target molecules/pathways and intracellular mechanism(s) for C1P, and also uncover any crosstalk with other bioactive lipids [30].…”

Section: Introductionmentioning

confidence: 99%

Ceramide-1-Phosphate as a Potential Regulator of the Second Sodium Pump from Kidney Proximal Tubules by Triggering Distinct Protein Kinase Pathways in a Hierarchic Way

Cabral

Almeida

Grelle

et al. 2022

CIMB

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Kidney proximal tubules are a key segment in the reabsorption of solutes and water from the glomerular ultrafiltrate, an essential process for maintaining homeostasis in body fluid compartments. The abundant content of Na+ in the extracellular fluid determines its importance in the regulation of extracellular fluid volume, which is particularly important for different physiological processes including blood pressure control. Basolateral membranes of proximal tubule cells have the classic Na+ + K+-ATPase and the ouabain-insensitive, K+-insensitive, and furosemide-sensitive Na+-ATPase, which participate in the active Na+ reabsorption. Here, we show that nanomolar concentrations of ceramide-1 phosphate (C1P), a bioactive sphingolipid derived in biological membranes from different metabolic pathways, promotes a strong inhibitory effect on the Na+-ATPase activity (C1P50 ≈ 10 nM), leading to a 72% inhibition of the second sodium pump in the basolateral membranes. Ceramide-1-phosphate directly modulates protein kinase A and protein kinase C, which are known to be involved in the modulation of ion transporters including the renal Na+-ATPase. Conversely, we did not observe any effect on the Na+ + K+-ATPase even at a broad C1P concentration range. The significant effect of ceramide-1-phosphate revealed a new potent physiological and pathophysiological modulator for the Na+-ATPase, participating in the regulatory network involving glycero- and sphingolipids present in the basolateral membranes of kidney tubule cells.

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Diacylglycerol kinase activity in purified basolateral membranes of kidney tubules

Cited by 8 publications

References 48 publications

Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA₁ receptor

Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA₁ receptor

Sphingosine 1‐Phosphate Prevents Human Embryonic Stem Cell Death Following Ischemic Injury

Ceramide-1-Phosphate as a Potential Regulator of the Second Sodium Pump from Kidney Proximal Tubules by Triggering Distinct Protein Kinase Pathways in a Hierarchic Way

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Diacylglycerol kinase activity in purified basolateral membranes of kidney tubules

Cited by 8 publications

References 48 publications

Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA1 receptor

Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA1 receptor

Sphingosine 1‐Phosphate Prevents Human Embryonic Stem Cell Death Following Ischemic Injury

Ceramide-1-Phosphate as a Potential Regulator of the Second Sodium Pump from Kidney Proximal Tubules by Triggering Distinct Protein Kinase Pathways in a Hierarchic Way

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Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA₁ receptor

Microglial lysophosphatidic acid promotes glioblastoma proliferation and migration via LPA₁ receptor