scholarly journals A retinoic acid-inducible skin-specific gene (RIS-1/psoriasin): molecular cloning and analysis of gene expression in human skinin vivo and cultured skin cellsin vitro

1994 ◽  
Vol 20 (2) ◽  
pp. 75-83 ◽  
Author(s):  
Amir Tavakkol ◽  
Christos C. Zouboulis ◽  
Elizabeth A. Duell ◽  
John J. Voorhees
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Molecular Cloning ◽  
Specific Gene ◽  
Cultured Skin

scholarly journals microRNA-138 modulates cardiac patterning during embryonic development

2008 ◽  
Vol 105 (46) ◽  
pp. 17830-17835 ◽  
Author(s):  
Sarah U. Morton ◽  
Paul J. Scherz ◽  
Kimberly R. Cordes ◽  
Kathryn N. Ivey ◽  
Didier Y. R. Stainier ◽  
...  
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Embryonic Development ◽  
Expression Patterns ◽  
Acid Synthesis ◽  
Specific Gene ◽  
Protein Activity ◽  
Gene Encoding ◽  
Small Noncoding Rnas ◽  
Discrete Domains

Organ patterning during embryonic development requires precise temporal and spatial regulation of protein activity. microRNAs (miRNAs), small noncoding RNAs that typically inhibit protein expression, are broadly important for proper development, but their individual functions during organogenesis are largely unknown. We report that miR-138 is expressed in specific domains in the zebrafish heart and is required to establish appropriate chamber-specific gene expression patterns. Disruption of miR-138 function led to ventricular expansion of gene expression normally restricted to the atrio-ventricular valve region and, ultimately, to disrupted ventricular cardiomyocyte morphology and cardiac function. Temporal-specific knockdown of miR-138 by antagomiRs showed miR-138 function was required during a discrete developmental window, 24–34 h post-fertilization (hpf). miR-138 functioned partially by repressing the retinoic acid synthesis enzyme, aldehyde dehydrogenase-1a2, in the ventricle. This activity was complemented by miR-138-mediated ventricular repression of the gene encoding versican (cspg2), which was positively regulated by retinoic-acid signaling. Our findings demonstrate that miR-138 helps establish discrete domains of gene expression during cardiac morphogenesis by targeting multiple members of a common pathway, and also establish the use of antagomiRs in fish for temporal knockdown of miRNA function.

scholarly journals Overexpression of the cellular retinoic acid binding protein-I (CRABP-I) results in a reduction in differentiation-specific gene expression in F9 teratocarcinoma cells.

1991 ◽  
Vol 112 (5) ◽  
pp. 965-979 ◽  
Author(s):  
J F Boylan ◽  
L J Gudas
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Binding Protein ◽  
Expression Vectors ◽  
Specific Gene ◽  
Specific Gene Expression ◽  
Acid Binding Protein ◽  
Retinoic Acid Response Element ◽  
Crabp I ◽  
F9 Teratocarcinoma

Treatment of F9 teratocarcinoma stem cells with retinoic acid (RA) causes their irreversible differentiation into extraembryonic endoderm. To elucidate the role of the cellular retinoic acid binding protein-I (CRABP-I) in this differentiation process, we have generated several different stably transfected F9 stem cell lines expressing either elevated or reduced levels of functional CRABP-I protein. Stably transfected lines expressing elevated levels of CRABP-I exhibit an 80-90% reduction in the RA induced expression of retinoic acid receptor (RAR) beta, laminin B1, and collagen type IV (alpha 1) mRNAs at low exogenous RA concentrations, but this reduction is eliminated at higher RA concentrations. Thus, greater expression of CRABP-I reduces the potency of RA in this differentiation system. Moreover, transfection of a CRABP-I expression vector into F9 cells resulted in five- and threefold decreases in the activation of the laminin B1 RARE (retinoic acid response element) and the RAR beta RARE, respectively, as measured from RARE/CAT expression vectors in transient transfection assays. These results support the idea that CRABP-I sequesters RA within the cell and thereby prevents RA from acting to regulate differentiation specific gene expression. Our data suggest a mechanism whereby the level of CRABP-I can regulate responsiveness to RA during development.

A retinoic acid-inducible transgenic marker of sino-atrial development in the mouse heart

Development ◽  
1999 ◽  
Vol 126 (12) ◽  
pp. 2677-2687 ◽  
Author(s):  
J. Xavier-Neto ◽  
C.M. Neville ◽  
M.D. Shapiro ◽  
L. Houghton ◽  
G.F. Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alkaline Phosphatase ◽  
Retinoic Acid ◽  
Transgenic Mice ◽  
Transgene Expression ◽  
Single Pulse ◽  
Transgenic Animals ◽  
Specific Gene ◽  
Mouse Heart ◽  
Pregnant Mice

To study the specification of inflow structures in the heart we generated transgenic animals harboring the human alkaline phosphatase (HAP) gene driven by the proximal 840 bp of a quail SMyHC3 promoter. In transgenic mice, the SMyHC3-HAP reporter was expressed in posterior heart precursors at 8.25 dpc, in sinus venosa and in the atrium at 8.5 and 9.0 dpc, and in the atria from 10.5 dpc onwards. SMyHC3-HAP transgene expression overlapped synthesis and endogenous response to retinoic acid (RA) in the heart, as determined by antibodies directed against a key RA synthetic enzyme and by staining of RAREhsplacZ transgenic animals. A single pulse of all-trans RA administered to pregnant mice at 7.5, but not after 8.5, dpc induced cardiac dismorphology, ranging from complete absence of outflow tract and ventricles to hearts with reduced ventricles expressing both SMyHC3-HAP and ventricular markers. Blockade of RA synthesis with disulfiram inhibited RA-induced transcription and produced hearts lacking the atrial chamber. This study defines a novel marker for atrial-restricted transcription in the developing mouse heart. It also suggests that atrial-specific gene expression is controlled by localized synthesis of RA, and that exclusion of RA from ventricular precursors is essential for correct specification of the ventricles.

Stimulatory effect of retinoic acid on GH gene expression: the interaction of retinoic acid and tri-iodothyronine in rat pituitary cells

1990 ◽  
Vol 125 (2) ◽  
pp. 251-256 ◽  
Author(s):  
S. Morita ◽  
K. Matsuo ◽  
M. Tsuruta ◽  
S. Leng ◽  
S. Yamashita ◽  
...  
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Specific Gene ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Gh Gene ◽  
Rat Pituitary Cells

ABSTRACT We have previously demonstrated that retinoic acid (RA) as well as thyroid hormone stimulates GH gene expression. To clarify the relationship between the action of RA and thyroid hormone, pituitary-specific gene expression was investigated further in rat pituitary cells. Rat clonal pituitary cells, GH3, were treated with RA with or without tri-iodothyronine (T3) for up to 3 days. After treatment with 10–1000 nmol RA/1 with or without 0·1–10 nmol T3/1, medium was collected for radioimmunoassay and cells were subjected to RNA extraction, and GH and prolactin gene expression was analysed using 32P-labelled rat GH and rat prolactin cDNA probes respectively. The data demonstrated the dose–responsive manner of the stimulatory effects of RA and T3 on GH secretion with T3-depleted media. The action of RA was additive to that of T3 for GH secretion when maximum effective doses of RA or T3 were used. Using dot blot and Northern gel analysis, it was shown that RA increased GH mRNA levels in T3-depleted media, and that this action of RA was additive to that of T3 on the induction of GH mRNA levels. In contrast, neither RA nor T3 stimulated the secretion of prolactin and prolactin mRNA levels in these cells. Our results indicate that RA stimulates GH mRNA increment and GH secretion in T3-depleted media, and that the stimulatory effect of RA is additive to the maximum effective dose of T3. Journal of Endocrinology (1990) 125, 251–256

scholarly journals Retinoic acid-induced gene expression in normal and leukemic myeloid cells.

1986 ◽  
Vol 163 (5) ◽  
pp. 1325-1330 ◽  
Author(s):  
M P Murtaugh ◽  
O Dennison ◽  
J P Stein ◽  
P J Davies
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Tissue Transglutaminase ◽  
Myeloid Cells ◽  
Peritoneal Macrophages ◽  
Promyelocytic Leukemia ◽  
Specific Gene ◽  
Mrna Levels ◽  
Specific Gene Expression

Retinoic acid has been shown to induce large accumulations of tissue transglutaminase in cultured myeloid cells. Addition of retinoic acid to mouse resident peritoneal macrophages increased the level of tissue transglutaminase mRNA within 30-60 min. Retinoic acid also increased tissue transglutaminase mRNA levels in human promyelocytic leukemia (HL-60) cells. These studies show that retinoic acid can induce acute alterations in specific gene expression in both normal and leukemic myeloid cells.

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