Transcriptome of a mouse kidney cortical collecting duct cell line: Effects of aldosterone and vasopressin

Robert-Nicoud, Maya; Flahaut, Marjorie; Elalouf, Jean‐Marc; Nicod, M; Salinas, Miguel; Bens, Marcelle; Doucet, Alain; Wincker, Patrick; Artiguenave, François; Horisberger, Jean‐Daniel; Vandewalle, Alain; Rossier, Bernard C.; Firsov, Dmitri

doi:10.1073/pnas.051603198

Cited by 198 publications

(171 citation statements)

References 37 publications

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“…24,31 Our results indicate a strong increase, of up to 6%, in ex vivo thymic apoptosis, as evaluated by TUNEL, in TG mice, which was associated with an augmented activation of the caspase-8/caspase-3 pathway. This rise in apoptosis apparently contrasts with reports, indicating that GILZ inhibits apoptosis induced by anti-CD3 stimulation 13,20 or IL-2 withdrawal. 32 However, some molecules are known to play opposing roles in apoptosis.…”

Section: Discussioncontrasting

confidence: 52%

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Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice

Delfino

Agostini

Spinicelli

et al. 2004

Blood

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Glucocorticoids promote thymocyte apoptosis and modulate transcription of numerous genes. GILZ (glucocorticoidinduced leucine zipper), being one of them, is strongly up-regulated in the thymus. To elucidate its function we generated transgenic mice overexpressing it specifically in the T-cell lineage and characterized its influence on thymus function. In young adult transgenic mice CD4 ؉ CD8 ؉ thymocyte number was significantly decreased and ex vivo thymocyte apoptosis was increased. Apoptotic pathway analysis detected reduced antiapoptotic B-cell leukemia XL (Bcl-xL) expression and increased activation of caspase-8 and caspase-3. Time-course experiments showed that in wild-type (WT) thymocytes GILZ up-regulation was followed by sequential Bcl-xL decreased expression and activation of caspase-8 and of caspase-3. Moreover, GILZ delivered inside WT thymocytes by a fusion protein with the transactivator of transcription (TAT) peptide decreased Bcl-xL and promoted their apoptosis. In aged mice perturbation of thymic subset numbers was amplified over time, as demonstrated by a further decrease in CD4 ؉ CD8 ؉ cells and increases in CD4 ؉ CD8 ؊ , CD4 ؊ CD8 ؊ , and CD8 ؉ CD4 ؊ cell counts. These results support the hypothesis that GILZ participates in the regulation of thymocyte apoptosis by glucocorticoids. IntroductionGlucocorticoids (GCs) are hormones and drugs that express their functions by binding and activating their specific intracellular receptor (GR), thus acting through genomic and nongenomic mechanisms. The thymus, one of their target organs, promotes thymocyte maturation to functional CD4 ϩ or CD8 ϩ single positive (SP) T lymphocytes that are ready to migrate to the periphery. T-cell development in the thymus is ordered by sequential steps that involve waves of cell proliferation and apoptosis. Apoptosis is a key process in thymus physiology and is triggered in 3 well-known ways: (1) negative selection, involving 5% of all thymocytes, eliminates autoreactive T-cell clones at the level of CD4 ϩ CD8 ϩ double-positive (DP) cells; (2) death by neglect involves 90% of DP thymocytes that are neither positively nor negatively selected; and (3) stress-induced cell death. 1 GCs promote apoptosis of DP thymocytes 2 but are not involved in apoptosis by negative selection. 3 Their role in apoptosis by neglect is uncertain, but they certainly mediate stress-induced apoptosis. 1 The apoptotic signaling pathway triggered by the synthetic GC dexamethasone (DEX) in thymocytes has recently been clarified to some extent. The GC receptor coordinates activation of gene transcription and caspase-8, -9, and -3 in a sequence that leads to thymocyte apoptosis. [4][5][6][7] Additionally, GC-mediated thymic apoptosis is regulated by many different molecules, and the B-cell leukemia 2 (Bcl-2) family of proteins is a critical regulator of apoptosis. 8 The family is subdivided into antiapoptotic members such as Bcl-2 and Bcl-xL, and proapoptotic members such as Bcl-2-associated X protein (Bax) and BCL-2 homologous antagonist/killer (Ba...

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Section: Discussioncontrasting

confidence: 52%

“…Its expression is up-regulated prominently in lymphoid organs. 12 Interestingly, GILZ expression is reported to be induced in the kidney, 13 in pluripotent mesenchymal cells, 14,15 and by GCs in erythroid progenitors, 16 thus suggesting GILZ plays a role not only in the immune system but also in several other physiologic systems.…”

Section: Introductionmentioning

confidence: 99%

Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice

Delfino

Agostini

Spinicelli

et al. 2004

Blood

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“…The major advantages of SAGE in comparison to microarray analyses are that absolute values (tag counts) are obtained which can be easily compared with other SAGE libraries, and that SAGE yields very extensive transcriptome information whereas microarray studies are restricted by the number of DNAs spotted onto the arrays. The SAGE method has been used extensively to characterize 3 differences in gene expression profiles of cancer versus normal cells [14,17], and has proven to be an appropriate tool for the analysis of complete transcriptomes [15,18,19]. Currently, no global gene expression data for cardiac fibroblasts is available.…”

Section: Introductionmentioning

confidence: 99%

Quantitative analysis of the cardiac fibroblast transcriptome—implications for NO/cGMP signaling

et al. 2004

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SummaryCardiac fibroblasts regulate tissue repair and remodeling in the heart. To quantify transcript levels in these cells we performed a comprehensive gene expression study using serial analysis of gene expression (SAGE). Among 110,169 sequenced tags we could identify 30,507 unique transcripts. A comparison of SAGE data from cardiac fibroblasts with data derived from total mouse heart revealed a number of fibroblast-specific genes. Cardiac fibroblasts expressed a specific collection of collagens, matrix proteins and metalloproteinases, growth factors, and components of signalling pathways. The NO/cGMP signalling pathway was represented by the mRNAs for α 1 and β 1 subunits of guanylyl cyclase, cGMP-dependent protein kinase type I (cGK I) and interestingly the G-kinase anchoring protein GKAP42. The expression of cGK I was verified by RT-PCR and Western Blot. To establish a functional role for cGK I in cardiac fibroblasts we studied its effect on cell proliferation. Selective activation of cGK I with a cGMP-analog inhibited the proliferation of serum-stimulated cardiac fibroblasts which express cGK I, but not higher passage fibroblasts which contain no detectable cGK I. Currently, our data suggest that cGK I mediates the inhibitory effects of the NO/cGMP pathway on cardiac fibroblast growth.Furthermore the SAGE library of transcripts expressed in cardiac fibroblasts provides a basis for future investigations into the pathological regulatory mechanisms underlying cardiac fibrosis.

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“…We used forskolin and IBMX to examine the effect of cAMP elevation in H441 and M-1 cells. We also examined the effect of corticosteroids on VIT32 gene expression because in the original analysis both aldosterone and AVP were reported to increase the abundance of this transcript (27). In M-1 cells, cAMP increased vit32 gene expression by 2 h with a peak effect by 4 h and the effect was persistent even at 24 h (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…To identify genes that may be important for the AVP effect on collecting duct Na ϩ transport, Robert-Nicoud et al (27) screened mpkCCD14 by serial analysis of gene expression (SAGE) library analysis and identified 48 vasopressin-induced transcripts (VIT). One of these, vit32 or PP5395 or Esau, is highly conserved across mammalian species and reduces Na ϩ transport when coexpressed with ENaC in Xenopus laevis oocytes (26).…”

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confidence: 99%

AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5′-flanking region of the VIT32 gene

Thomas

Loftus

Liu

2004

American Journal of Physiology-Renal Physiology

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. AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5Ј-flanking region of the VIT32 gene. Am J Physiol Renal Physiol 287: F460 -F468, 2004. First published May 12, 2004 10.1152/ajprenal.00107.2004.-VIT32, a vasopressin-induced transcript, inhibits Na ϩ transport when coexpressed with the epithelial sodium channel in Xenopus laevis oocytes (EMBO J 21: 5109 -5117, 2002). To understand the mechanism of VIT32 gene regulation, we examined the effect of DDAVP and cAMP stimulation on VIT32 expression in M-1 mouse collecting duct cells and in H441 human airway epithelial cells. Elevation of cAMP with forskolin and IBMX increased VIT32 gene expression with a peak effect at 2 h. The increase in gene expression was abolished by H89 and by actinomycin D, suggesting that cAMP stimulates VIT32 mRNA expression by a PKA-mediated increase in gene transcription. An ϳ1.5-kb fragment of the 5Ј-flanking region of VIT32 was cloned and was able to confer cAMP-stimulated reporter gene activity when transfected into M-1 and H441 cells. By deletion analysis and sitedirected mutagenesis, a cAMP response element (CRE) was identified within the proximal promoter region that was sufficient to account for the increase in VIT32 gene expression seen with DDAVP and elevation of cAMP. Furthermore, DDAVP-stimulated VIT32 promoterreporter activity was inhibited by H89 and by a dominant negative CREB construct. Finally, we were able to identify CREB as a nuclear protein that bound to the VIT32 CRE in gel mobility shift assays. In summary, DDAVP stimulates transcription of VIT32 via a CRE within the proximal promoter region of the VIT32 gene.PP5395; epithelial sodium channel; sodium transport; airway epithelia; adenosine 3Ј,5Ј-cyclic monophosphate response element binding protein IN THE COLLECTING duct, AVP binds the V2 receptor and regulates water homeostasis by activation of the water channel, aquaporin-2 (34). AVP also regulates Na ϩ handling in the distal nephron by its effects on Na ϩ transporters (30). The principal effect is a stimulation of benzamil-sensitive Na ϩ transport, which has been noted in the toad bladder, in the isolated rat cortical collecting duct, in primary cultures of collecting duct cells, and in many distal nephron cell lines. The early effects of AVP may be mediated by cAMP and result in an increase in surface expression of the epithelial Na ϩ channel (ENaC) (24,31,35). Others have reported an increase in Na ϩ -K ϩ -ATPase activity in microdissected mouse and rat collecting ducts and in a mouse collecting duct cell line, mpkCCD14 (6,8,13). In A6 cells, an amphibian cell line used as a model of collecting duct epithelia, the early effects of AVP effect on Na ϩ transport appear to require phosphatidylinositol-3 kinase and be mediated by the regulatory kinase sgk1 (2,11,12).Although the earliest effects of AVP on Na ϩ transport are independent of transcription, chronic effects are likely to require the transcription of target genes (18). DDAVP, a selective V2 receptor agoni...

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Transcriptome of a mouse kidney cortical collecting duct cell line: Effects of aldosterone and vasopressin

Cited by 198 publications

References 37 publications

Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice

Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice

Quantitative analysis of the cardiac fibroblast transcriptome—implications for NO/cGMP signaling

AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5′-flanking region of the VIT32 gene

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