Differential Regulation of the Carbonic Anhydrase II Gene Expression by Hormonal Nuclear Receptors in Monocytic Cells: Identification of the Retinoic Acid Response Element

Quélo, Isabelle; Jurdic, Pierre

doi:10.1006/bbrc.2000.2654

Cited by 13 publications

(7 citation statements)

References 39 publications

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“…However, the Akap12β RARE is only weakly (∼2-fold) activated with atRA stimulation (Figure 3B). This level of activation is comparable to that seen with carbonic anhydrase ( Ca2 ), a known retinoid responsive target gene containing a similar DR-2 RARE as that seen in the Akap12β RARE [30] (Figure 3B). Mutagenesis experiments failed to reveal a clear-cut dependence on the DR-2 RARE (data not shown), likely because of the weak level of induction.…”

Section: Resultssupporting

confidence: 66%

“…We provide evidence here for a conserved RARE in the upstream Akap12β promoter region that is weakly responsive to retinoids. The DR-2 RARE in the Akap12β promoter is very similar to that of the known retinoid-response gene Ca2 [30], which similarly exhibits weak activation with atRA stimulation (Figure 3B). Although we could not show consistent binding of a retinoic acid receptor to the RARE containing region, several lines of evidence suggest that retinoid receptors target this or perhaps a more distal Akap12β promoter region.…”

Section: Discussionmentioning

confidence: 76%

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Retinoid-Induced Expression and Activity of an Immediate Early Tumor Suppressor Gene in Vascular Smooth Muscle Cells

et al. 2011

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Retinoids are used clinically to treat a number of hyper-proliferative disorders and have been shown in experimental animals to attenuate vascular occlusive diseases, presumably through nuclear receptors bound to retinoic acid response elements (RARE) located in target genes. Here, we show that natural or synthetic retinoids rapidly induce mRNA and protein expression of a specific isoform of A-Kinase Anchoring Protein 12 (AKAP12β) in cultured smooth muscle cells (SMC) as well as the intact vessel wall. Expression kinetics and actinomycin D studies indicate Akap12β is a retinoid-induced, immediate-early gene. Akap12β promoter analyses reveal a conserved RARE mildly induced with atRA in a region that exhibits hyper-acetylation. Immunofluorescence microscopy and protein kinase A (PKA) regulatory subunit overlay assays in SMC suggest a physical association between AKAP12β and PKA following retinoid treatment. Consistent with its designation as a tumor suppressor, inducible expression of AKAP12β attenuates SMC growth in vitro. Further, immunohistochemistry studies establish marked decreases in AKAP12 expression in experimentally-injured vessels of mice as well as atheromatous lesions in humans. Collectively, these results demonstrate a novel role for retinoids in the induction of an AKAP tumor suppressor that blocks vascular SMC growth thus providing new molecular insight into how retiniods may exert their anti-proliferative effects in the injured vessel wall.

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Section: Resultssupporting

confidence: 66%

Section: Discussionmentioning

confidence: 76%

Retinoid-Induced Expression and Activity of an Immediate Early Tumor Suppressor Gene in Vascular Smooth Muscle Cells

et al. 2011

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“…Both inhibitory [MacDonald et al, 1993;Haussler et al, 1997] and stimulatory [Kato et al, 1995;Li et al, 1997;Sneddon et al, 1998;Zhao et al, 1999] actions of 9-cisRA on calcitriol-induced gene expression have been reported. Further, in some cases, 9-cisRA had no effect on calcitriolinduced gene expression [Ferrara et al, 1994;Quelo and Jurdic, 2000]. In this study, we used quantitative PCR method to show that, in human osteoblastic cells, 9-cisRA efficiently accelerates osteocalcin mRNA production induced by calcitriol or KH1060.…”

Section: Discussionmentioning

confidence: 80%

9‐cis retinoic acid accelerates calcitriol‐induced osteocalcin production and promotes degradation of both vitamin D receptor and retinoid X receptor in human osteoblastic cells

Jääskeläinen

Ryhänen

Mäenpää

2003

J of Cellular Biochemistry

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vitamin D receptor (VDR) and retinoid X receptor (RXR) heterodimerize to mediate the genomic actions of 1alpha,25-dihydroxyvitamin D(3) (1alpha,25(OH)(2)D(3), calcitriol), the biologically active form of vitamin D(3). In this study, we show that 9-cis retinoic acid (9-cisRA), the ligand for RXR, accelerates calcitriol-induced expression of osteocalcin gene, the marker for mature osteoblasts. Calcitriol and its synthetic analog KH1060 (1 nM) induced osteocalcin secretion after a 96-h incubation period as detected by radioimmunoassay. When these compounds were used together with 9-cisRA, osteocalcin protein secretion was, however, detected already after 72 and 48 h, respectively. Detection of osteocalcin mRNA with quantitative PCR revealed elevated mRNA levels already after a 4-h treatment of the cells with calcitriol, KH1060, or 9-cisRA compared with untreated cells. In combination treatments, 9-cisRA rapidly stimulated osteocalcin mRNA synthesis induced by the different vitamin D(3) compounds. In MG-63 cells treated with calcitriol or KH1060, the stimulation was maximal after the first 4 h and diminished thereafter. In fact, after the 48-h incubation 9-cisRA reduced osteocalcin mRNA levels in KH1060-treated cells, the amount of mRNA being only 44% of the levels obtained with KH1060 alone. The reduction was accompanied by an increased degradation rate of both VDR and RXRbeta in the presence of 9-cisRA. Furthermore, 9-cisRA increased the formation of RXRbeta-VDR-VDRE complex on the osteocalcin gene VDRE. These results suggest that 9-cisRA accelerates calcitriol-induced osteocalcin production in human osteoblastic cells through increased formation of transcriptionally active chromatin complexes and, subsequently, promotes degradation of the heterodimeric complex of VDR and RXR.

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“…CAs, although ubiquitously expressed, are highly regulated enzymes, and, in some tissues, CAII expression changes during development, differentiation, or in the presence of hormones and growth factors (Disela et al, 1991;Buono et al, 1992;Quelo and Jurdic, 2000). The variables that determine the spatiotemporal changes in CAI and/or CAII expression and CO 2 chemosensitivity in the AM remain to be determined.…”

Section: Discussionmentioning

confidence: 99%

Rat Adrenal Chromaffin Cells Are Neonatal CO₂Sensors

Muñoz-Cabello¹,

Toledo‐Aral²,

López‐Barneo³

et al. 2005

J. Neurosci.

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We studied the participation of adrenal medulla (AM) chromaffin cells in hypercapnic chemotransduction. Using amperometric recordings, we measured catecholamine (CAT) secretion from cells in AM slices of neonatal and adult rats perfused with solutions bubbled with different concentrations of CO 2 . The secretory activity augmented from 1.74 Ϯ 0.19 pC/min at 5% CO 2 to 6.36 Ϯ 0.77 pC/min at 10% CO 2 . This response to CO 2 was dose dependent and appeared without changes in extracellular pH, although it was paralleled by a drop in intracellular pH. Responsiveness to hypercapnia was higher in neonatal than in adult slices. The secretory response to hypercapnia required extracellular Ca 2ϩ influx. Both the CO 2 -induced internal pH drop and increase in CAT secretion were markedly diminished by methazolamide (2 M), a membrane-permeant carbonic anhydrase (CA) inhibitor. We detected the presence of two CA isoforms (CAI and CAII) in neonatal AM slices by in situ hybridization and real-time PCR. The expression of these enzymes decreased in adult AM together with the disappearance of responsiveness to CO 2 . In patch-clamped chromaffin cells, hypercapnia elicited a depolarizing receptor potential, which led to action potential firing, extracellular Ca 2ϩ influx, and CAT secretion. This receptor potential (inhibited by methazolamide) was primarily attributable to activation of a resting cationic conductance. In addition, voltage-gated K ϩ current amplitude was also decreased by high CO 2 . The CO 2 -sensing properties of chromaffin cells may be of physiologic relevance, particularly for the adaptation of neonates to extrauterine life, before complete maturation of peripheral and central chemoreceptors.

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Differential Regulation of the Carbonic Anhydrase II Gene Expression by Hormonal Nuclear Receptors in Monocytic Cells: Identification of the Retinoic Acid Response Element

Cited by 13 publications

References 39 publications

Retinoid-Induced Expression and Activity of an Immediate Early Tumor Suppressor Gene in Vascular Smooth Muscle Cells

Retinoid-Induced Expression and Activity of an Immediate Early Tumor Suppressor Gene in Vascular Smooth Muscle Cells

9‐cis retinoic acid accelerates calcitriol‐induced osteocalcin production and promotes degradation of both vitamin D receptor and retinoid X receptor in human osteoblastic cells

Rat Adrenal Chromaffin Cells Are Neonatal CO₂Sensors

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Differential Regulation of the Carbonic Anhydrase II Gene Expression by Hormonal Nuclear Receptors in Monocytic Cells: Identification of the Retinoic Acid Response Element

Cited by 13 publications

References 39 publications

Retinoid-Induced Expression and Activity of an Immediate Early Tumor Suppressor Gene in Vascular Smooth Muscle Cells

Retinoid-Induced Expression and Activity of an Immediate Early Tumor Suppressor Gene in Vascular Smooth Muscle Cells

9‐cis retinoic acid accelerates calcitriol‐induced osteocalcin production and promotes degradation of both vitamin D receptor and retinoid X receptor in human osteoblastic cells

Rat Adrenal Chromaffin Cells Are Neonatal CO2Sensors

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Rat Adrenal Chromaffin Cells Are Neonatal CO₂Sensors