Regulation of ferredoxin gene in steroidogenic and nonsteroidogenic cells

Yeh, Jing-Ruey Joanna; Huang, Cory; Wu, Du An; Guo, Ing-Cherng; Rainey, William E.; Chung, Bon Chu

doi:10.1016/0960-0760(95)00020-z

Cited by 6 publications

(4 citation statements)

References 12 publications

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“…Cycloheximide prevents adrenodoxin mRNA induction in bovine adrenocortical cells observed 24 h after stimulation with ACTH or cAMP (48). Moreover, in H295 cells cycloheximide abolishes the forskolin-induced adrenodoxin mRNA accumulation (95). Costimulation with cAMP and cycloheximide causes adrenodoxin mRNA superinduction in Y-1 cells after 24 h (62), although the ACTH-induced increases in adrenodoxin mRNA levels are completely blocked by cycloheximide in this cell line (3).…”

Section: Discussionmentioning

confidence: 90%

“…Adrenodoxin mRNA is also regulated in Y-1 mouse adrenocortical cells by cAMP (3,62) and the calcium ionophore A23187 (95). Forskolin upregulates adrenodoxin mRNA in H295 cells (95). Adrenodoxin mRNA expression in our H295R cells is rapidly and transiently induced by ANG II.…”

Section: Discussionmentioning

confidence: 90%

“…ACTH increases adrenodoxin mRNA levels severalfold in bovine adrenal zona fasciculata-reticularis cells (66). Adrenodoxin mRNA is also regulated in Y-1 mouse adrenocortical cells by cAMP (3,62) and the calcium ionophore A23187 (95). Forskolin upregulates adrenodoxin mRNA in H295 cells (95).…”

Section: Discussionmentioning

confidence: 99%

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Angiotensin II early regulated genes in H295R human adrenocortical cells

Romero

Plonczynski

Vergara

et al. 2004

Physiological Genomics

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Evidence for the dysregulation of aldosterone synthesis in cardiovascular pathophysiology has renewed interest in the control of its production. Cellular mechanisms by which angiotensin II (ANG II) stimulates aldosterone synthesis in the adrenal zona glomerulosa are incompletely understood. To elucidate the mechanism of intracellular signaling by ANG II stimulation in the adrenal, we have studied immediate-early regulated genes in human adrenal H295R cells using cDNA microarrays. H295R cells were stimulated with ANG II for 3 h. Gene expression was analyzed by microarray technology and validated by real-time RT-PCR. Eleven genes were found to be upregulated by ANG II. These encode the proteins for ferredoxin, Nor1, Nurr1, c6orf37, CAT-1, A20, MBLL, M-Ras, RhoB, GADD45alpha, and a novel protein designated FLJ45273. Maximum expression levels for all genes occurred 3-6 h after ANG II stimulation. This increase was dose dependent and preceded maximal aldosterone production. Other aldosterone secretagogues, K+ and endothelin-1 (ET-1), also induced the expression of these genes with variable efficiency depending on the gene and with lower potency than ANG II. ACTH had negligible effect on gene expression except for the CAT-1 and Nurr1 genes. These ANG II-stimulated genes are involved in several cellular functions and are good candidate effectors and regulators of ANG II-mediated effects in adrenal zona glomerulosa.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 90%

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Angiotensin II early regulated genes in H295R human adrenocortical cells

Romero

Plonczynski

Vergara

et al. 2004

Physiological Genomics

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“…Collectively, Sp1 seems to cooperate with steroidogenic transcription factors to enhance the basal and cAMP-inducible activities of CYP11A1 promoter. Similarly, the transcription of ferredoxin, a partner of CYP11A1, is also controlled by two Sp1 sites proximal to RNA initiation site [36,37]. Sp1 is a protein family consists of many members [38].…”

Section: Role Of Sp1 In Cyp11a1 Promotermentioning

confidence: 98%

Transcriptional regulation of human CYP11A1 in gonads and adrenals

et al. 2007

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The CYP11A1 gene encodes the cholesterol side-chain cleavage enzyme, also termed cytochrome P450scc, which catalyzes the conversion of cholesterol to pregnenolone in the first step of steroid biosynthesis in mitochondria. The adrenal- and gonad-selective, hormonally and developmentally regulated expression of CYP11A1 is principally driven by its 2.3 kb promoter. Multiple trans-acting factors like SF-1, Sp1, AP-2, TReP-132, LBP-1b, LBP-9, AP-1, NF-1, and Ets control CYP11A1 transcription either through DNA-protein interaction with their specific cis-acting elements or through protein-protein interaction between each other, wherein SF-1 plays a central role in adrenals and testes. In addition to binding with its proximal and upstream motifs, SF-1 also physically interacts with TFIIB, CBP/p300, TReP-132, and c-Jun/AP-1 to specifically transmit the regulatory signals of cAMP. Other factors like Sp1 family members, AP-2, and LBP-1b/LBP-9 may be other factors that play a role in CYP11A1 transcription, particularly in placental cells. The TATA sequence could also contribute to tissue-specificity and hormonal regulation of CYP11A1 transcription. This article reviews recent studies focusing on adrenals and gonads.

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