New Members of the Mammalian Glycerophosphodiester Phosphodiesterase Family

Ohshima, Noriyasu; Kudo, Takahiro; Yamashita, Yosuke; Mariggiò, Stefania; Araki, Mari; Honda, Ayako; Nagano, Tomomi; Isaji, Chiaki; Katô, Norihisa; Corda, Daniela; Izumi, Tohru; Yanaka, Noriyuki

doi:10.1074/jbc.m114.614537

Cited by 43 publications

(26 citation statements)

References 50 publications

(38 reference statements)

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“…The first involves the conversion of NAPE by phospholipase A2 to form N-arachidonyl lysophosphatidylethanolamine followed by lysophospholipase D-catalyzed release of AEA (see steps 1A and 1B in Fig. 1) (15, 16). NAPE may also be directly converted to AEA by NAPE-specific phospholipase D (step 2) (14) .…”

Section: Regional and Cellular Distribution Of Aea In The Kidneymentioning

confidence: 99%

“…Mice carrying NAPE-PLD gene knockouts have been generated, but no data have been reported regarding the effect of this knockout on renal AEA. In regard to the third pathway, recently a member of the glycerophosphodiester phosphodiesterase family, GDE4, having lysophospholipase D activity with the ability to liberate AEA from N-arachidonyl lysophosphatidylethanolamine has been identified in the kidney (16, 17). …”

Section: Regional and Cellular Distribution Of Aea In The Kidneymentioning

confidence: 99%

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Anandamide and its metabolites what are their roles in the kidney

Ritter

Xia

et al. 2016

Front Biosci

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Anandamide (AEA) is the N-acyl ethanolamide of arachidonic acid, an agonist of cannabinoid and non-cannabinoid receptors in the body. The kidneys are enriched in AEA and in enzymes that metabolize AEA, but the roles of AEA and its metabolites in the kidney remain poorly understood. This system likely is involved in the regulation of renal blood flow and hemodynamics and of tubular sodium and fluid reabsorption. It may act as a neuromodulator of the renal sympathetic nervous system. AEA and its cyclooxygenase-2 metabolites, the prostamides, in the renal medulla may represent a unique antihypertensive system involved in the long-term control of blood pressure. AEA and its metabolites are also implicated as modulators of inflammation and mediators of signaling in inflammation. AEA and its metabolites may be influential in chronic kidney disease states associated with inflammation and cardiovascular diseases associated with hyperhomocysteinemia. The current knowledge of the roles of AEA and its derivatives highlights the need for further research to define and potentially exploit the role of this endocannabinoid system in the kidney.

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Section: Regional and Cellular Distribution Of Aea In The Kidneymentioning

confidence: 99%

Section: Regional and Cellular Distribution Of Aea In The Kidneymentioning

confidence: 99%

Anandamide and its metabolites what are their roles in the kidney

Ritter

Xia

et al. 2016

Front Biosci

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“…Extract 1 mainly included water-soluble molecules in aqueous culture medium, meaning polar molecules including cAMP, Ca ion and peptides. Extract 2, which was extracted by the Bligh & Dyer lipid extraction method [46,47], contained non-polar molecules, including lipids. As a result, in both Extraction 1 and Extraction2 assay, molecules extracted from different cell stages induced the difference of matrix mineralization on Day 12.…”

Section: Discussionmentioning

confidence: 99%

“…To test this, we collected culture medium from undifferentiated, early and middle stage MC3T3-E1 cells that had been incubated for 6h under normal conditions. We extracted non-protein molecules from the culture media by first performing a 100 ˚C, 5 min heat denaturation step, followed by centrifugation at 4 ˚C and 15,000 rpm for 15 min, or via the Bligh-Dyer extraction method, which is widely used in lipid research [46,47]; the former method isolates including mainly polar molecules and peptides that are dissolved in the culture medium (Extract 1), and the latter method only isolates mainly non-polar molecules (Extract 2).…”

Section: Non-protein Molecules Secreted By Mc3t3-e1 Cells Regulate Acmentioning

confidence: 99%

Extracellular matrix mineralization in the mouse osteoblast-like cell line MC3T3-E1 is regulated by actin cytoskeleton reorganization and non-protein molecules secreted from the cells themselves

Suzuki

Tatei

Ohshima

et al. 2019

Preprint

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Bone tissue constantly undergoes turnover via bone formation by osteoblasts and bone resorption by osteoclasts. This process enables bone to maintain its overall shape while altering its local structure. However, the detailed mechanism of how osteoblast cell-signaling systems induce various structural changes in bone tissue have not yet been completely elucidated. In this study, we focused on the actin cytoskeleton as a regulatory system for bone formation and constructed an in vitro experimental system using the mouse osteoblast-like cell line MC3T3-E1. We found that, in MC3T3-E1 cells, the actin cytoskeleton had an important role in matrix mineralization via activation of specific developmental pathways and it was regulated by non-protein molecules secreted from MC3T3-E1 cells themselves. In MC3T3-E1 cells, we observed changes of actin cytoskeleton reorganization and accumulation of PIP 2 related to actin filament convergences during cell differentiation, in the undifferentiated, early, middle and late stage. Actin cytoskeleton disruption with Cyto D, polymerization inhibitor of actin filament, in early and middle stage cells induced significant increase of osteocalcin mRNA expression normally expressed only in late stage, decrease of Alkaline phosphatase mRNA expression after 24h and abnormal matrix mineralization in MC3T3-E1 cells. Inhibition of Giα with PTX known to regulate actin cytoskeleton in middle stage induced changes in the actin cytoskeleton and PIP 2 accumulation and suppression of matrix mineralization after 5 days. Furthermore, addition of non-protein molecules from culture medium of cells at various differentiation stage induced difference of PIP 2 accumulation after 5 min, actin cytoskeleton in 20 min, and matrix mineralization after 5 days. These results not only provide new knowledge about the actin cytoskeleton function in bone-forming cells, but also suggest that cell signaling via non-protein molecules such as lipids plays important roles in bone formation.

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“…However, the substrate specificity and specific enzymatic activity, as well as the physiological functions of proteins encoded by this gene family are not well understood. As recombinant proteins, both Gdpd3 (Gde7) and Gdpd1 (Gde4; Gdpd3’s closest relative) have been shown to have lysoPLD activity that catalyzes the formation of LPA and choline ( 44, 45 ). LysoPLD activity of Gdpd3 makes it plausible that low Gdpd3 expression in Hip1 deficient mice led to perturbations in choline-related metabolites as discussed in the results section.…”

Section: Discussionmentioning

confidence: 99%

Deficiency of the Endocytic ProteinHip1Leads to DecreasedGdpd3expression, Low Phosphocholine, and Kypholordosis

Wijayatunge

Holmstrom

Foley

et al. 2018

Preprint

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47Deficiency of huntingtin interacting protein 1 (Hip1) results in degenerative phenotypes. 48Here we generated a Hip1 deficiency allele where a floxed transcriptional stop-cassette 49 and a human HIP1 cDNA were knocked-in to intron 1 of mouse Hip1 locus. CMV-Cre-50 mediated germline excision of the stop-cassette resulted in expression of HIP1 and rescue 51 of the Hip1 knockout phenotype. Mx1-Cre-mediated excision led to HIP1 expression in 52 spleen, kidney and liver, and also rescued the phenotype. In contrast, GFAP-Cre-53 mediated HIP1 expression in brain did not rescue the phenotype. Metabolomics and 54 microarrays of several Hip1 knockout tissues identified low phosphocholine (PC) levels 55 and low Glycerophosphodiester Phosphodiesterase Domain Containing 3 (Gdpd3) 56 expression. Since Gdpd3 has lysophospholipase D activity that results in the formation of 57 choline, a precursor of PC, Gdpd3 downregulation could lead to the low PC levels. To 58 test if Gdpd3 contributes to the Hip1 deficiency phenotype, we generated Gdpd3 59 knockout mice. Double knockout of Gdpd3 and Hip1 worsened the Hip1 phenotype. This 60 suggests that Gdpd3 compensates for Hip1 loss. More detailed knowledge of how Hip1 61 deficiency leads to low PC will improve our understanding of HIP1 in choline 62 metabolism in normal and disease states. 63 64 65 amplified from pcDNA3-hHip1 plasmid. The IRES (~0.6 kb) and eGFP (~0.9 kb) 128 sequences were amplified from pIRES2-AcGFP1 and pEGFP-N1 plasmid, respectively. 129The final vector was obtained by standard molecular cloning. Aside from the 130 homology arms, the final vector also contains a Lox-Stop-Lox cassette (~1.5 kb), mHip1 131 partial intron1+ partial exon 2, hHip1 cDNA, IRES, EGFP + polyA, Frt sequences flanking 132 the Neo expression cassette (the neo cassette was used for positive selection of the 133 electroporated ES cells), and a DTA expression cassette (for negative selection of the ES 134

show abstract

New Members of the Mammalian Glycerophosphodiester Phosphodiesterase Family

Cited by 43 publications

References 50 publications

Anandamide and its metabolites what are their roles in the kidney

Anandamide and its metabolites what are their roles in the kidney

Extracellular matrix mineralization in the mouse osteoblast-like cell line MC3T3-E1 is regulated by actin cytoskeleton reorganization and non-protein molecules secreted from the cells themselves

Deficiency of the Endocytic ProteinHip1Leads to DecreasedGdpd3expression, Low Phosphocholine, and Kypholordosis

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