A Sp1 Binding Site in the GC-Rich Region Is Essential for a Core Promoter Activity of the Human Endothelial Nitric Oxide Synthase Gene

Wariishi, Seiichiro; Miyahara, Katsunori; Toda, Katsumi; Ogoshi, Shohei; Doi, Yoshiharu; Ohnishi, Shunsuke; Mitsui, Y.; Yui, Y.; Chie, Kawai; Shizuta, Yutaka

doi:10.1006/bbrc.1995.2682

Cited by 39 publications

(29 citation statements)

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“…At the level of transcription, this is exemplified by the numerous cis-elements for binding of various transcription factors in the human NOS3 promoter. It is apparent that, similar to the human one (Wariishi et al, 1995;Zhang et al, 1995), the sheep NOS3 promoter also contains a consensus AP-1 site and seven half-estrogen receptor binding sites as well as many others (Fig. 1).…”

Section: Disscussionmentioning

confidence: 79%

“…In addition, a potential site for the binding of the NF-1 transcription factor (TGGNNNNNNNCCA), a sterol regulatory element (SRE-1, CACCCCAC), 3 acute-phase response (APR) elements (CTGGGA or TCCCAG), 3 shear stress-responsive element (SSRE, GGTCTC), 26 Ets (GGAA/T or A/ TTCC, not included) were also identified. Five Sp1 binding sites (GGGCGG or CCGCCC) were identified, 4 of which were present in the so-called "positive regulatory domain" (Karantzoulis-Fegaras et al, 1999;Wariishi et al, 1995;Zhang et al, 1995), which also contained a p53 half site (GGGCTAGTTC), a Ets/Elf site, 1 myc-associated zine-finger protein (MAZ, CCCTCCC), 1 Ying Yang (CCATT, YY1), one PAX (GTTCC), and a Ets family transcription factor PEA3 (CCCTTCCT) (Fleming and Busse, 2003;KarantzoulisFegaras et al, 1999). Of note, the AP-1 site was conserved in the NOS3 promoter of all species surveyed (Fig.…”

Section: Cloning and Analysis Of Sheep Nos3 Promoter Sequencementioning

confidence: 99%

“…Further deletion of the next 121 bases containing the AP-1 site did not result in additional decrease in the promoter activity. However, the deletion of two tightly clustered so called "positive regulatory domains" I and II proximal to the promoter (−104/−95 and −144/−115 relative to the transcription initiation) characterized in the human NOS3 promoter (Wariishi et al, 1995;Zhang et al, 1995) resulted in complete loss of the promoter activity. Thus, it is apparent that common mechanisms in the basal transcriptional control of NOS3 expression exist in the UAEC.…”

Section: Disscussionmentioning

confidence: 99%

“…We have recently isolated a 1305-bp sheep NOS3 promoter sequence. Sequence analysis revealed that sheep NOS3 promoter also possesses a consensus AP-1 binding site (5′-TGAGTCA-3′, −682 to −676) and many other cis-regulatory sequences similar to these of the human and bovine NOS3 promoters (Venema et al, 1994;Wariishi et al, 1995;Zhang et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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Transcriptional regulation of endothelial nitric oxide synthase expression in uterine artery endothelial cells by c-Jun/AP-1

Qian¹,

Mata‐Greenwood²,

Wu³

et al. 2007

Molecular and Cellular Endocrinology

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Despite extensive studies have shown that increased endothelial nitric oxide synthase (NOS3) expression in the uterine artery endothelial cells (UAEC) plays a key role in uterine vasodilatation, the molecular mechanism controlling NOS3 expression in UAEC is unknown. According to the sheep NOS3 promoter sequence isolated in our laboratory, we hypothesize that the activator protein-1 (AP-1) site in the proximal sheep NOS3 promoter (TGAGTCA, -682 to -676) is important for NOS3 expression. We developed a c-Jun adenoviral expression system to overexpress c-Jun protein into UAEC to investigate the effects of c-Jun/AP-1 on NOS3 expression. Basal levels of c-Jun protein and mRNA were detected in UAEC. C-Jun protein was overexpressed in a concentration and timedependent fashion in UAEC infected with sense c-Jun (S-c-Jun), but not sham and antisense c-Jun (A-c-Jun) adenoviruses. Infection with S-c-Jun adenovirus (25 MOI, multiplicity of infection) resulted in efficient c-Jun protein overexpression in UAEC up to 3 days. In S-c-Jun, but not sham and A-c-Jun adenovirus infected UAEC, NOS3 mRNA and protein levels were increased (P<0.05) compared to noninfected controls. Increased NOS3 expression was associated with increased total NOS activity. Transient transfections showed that c-Jun overexpression augmented the transactivation of the sheep NOS3 promoter-driven luciferase/reporter constructs with the AP-1 site but not of deletion constructs without the AP-1 site. When the AP-1 site was mutated, c-Jun failed to trans-activate the sheep NOS3 promoter. AP-1 DNA binding activity also increased in c-Jun overexpressed UAEC. Lastly, the pharmacological AP-1 activator phorbol myristate acetate increased AP-1 binding, trans-activated the wild-type but not the AP-1 mutant NOS3 promoter and dose-dependently stimulated UAEC NOS3 and c-Jun protein expression. Hence, our data show that c-Jun/AP-1 regulates NOS3 transcription involving the proximal AP-1 site in the 5′-regulatory region of the sheep NOS3 gene. Keywordsc-Jun/AP-1; endothelial nitric oxide synthase expression; uterine artery endothelial cells

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Section: Disscussionmentioning

confidence: 79%

Section: Cloning and Analysis Of Sheep Nos3 Promoter Sequencementioning

confidence: 99%

Section: Disscussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Transcriptional regulation of endothelial nitric oxide synthase expression in uterine artery endothelial cells by c-Jun/AP-1

Qian¹,

Mata‐Greenwood²,

Wu³

et al. 2007

Molecular and Cellular Endocrinology

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show abstract

“…Consistently, these promoters often depend on a functional Sp1 site, which can interact with TATA-binding protein, TBP, as well as TBP-associated factor, TAF110, to help mediate recruitment of the basal transcription machinery [20]. Several studies have shown that elimination of Sp1 binding sites destroys promoter activity [21][22][23][24][25][26][27], implicating an important function of Sp1 sites in TATA-less promoters. It has been demonstrated that Sp1 can act as an initiator of transcription in genes lacking a TATA-box by directing the preinitiation complex to a region 40-100 bp downstream its binding site [28], and therefore our finding of a consensus Sp1 binding site 40 bp uptream the putative initiation site suggests that it may function as an initiator in the MYADM promoter.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the Mouse Myeloid-associated Differentiation Marker (Myadm) Gene: Promoter Analysis and Protein Localization

2005

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Shear stress induction of the endothelial nitric oxide synthase gene is calcium-dependent but not calcium-activated

Xiao¹,

Zhang²,

Diamond³

1997

J. Cell. Physiol.

102

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Arterial levels of shear stress (25 dynes/cm2) can elevate constitutive endothelial nitric oxide synthase (eNOS) gene expression in cultured endothelial cells (Ranjan et al., 1995). By PhosphorImaging of Northern blots, we report that the eNOS/glyceraldehyde 3-phosphate dehydrogenase (GAPDH) messenger RNA (mRNA) ratio in bovine aortic endothelial cells (BAEC) increased by 4.8- and 7.95-fold after 6-hr shear stress exposure of 4 and 25 dynes/cm2, respectively. Incubation of BAEC with dexamethasone (1 microM) had no effect on shear stress induction of eNOS mRNA. Buffering of intracellular calcium in BAEC with bis-(o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid, tetra(acetoxymethyl)-ester (BAPTA/AM) reduced shear stress induction of eNOS mRNA by 70%. Yet, stimulation of BAEC with ionomycin (0.1-1.0 microM) for 6-24 hr to elevate intracellular calcium had no effect on eNOS mRNA. These studies indicated that the shear stress induction of eNOS mRNA was a calcium-dependent, but not calcium-activated, process. Shear stress was a very potent and rapid inducer of the eNOS mRNA, which could not be mimicked with phorbol myristrate acetate or endotoxin. Inhibition of tyrosine kinases with genistein (10 microM) or tyrphostin B46 (10 microM) or inhibition of G-protein signaling with guanosine 5'-O-(2-thiodiphosphate) (GDP-betaS) (600 microM, 6-hr preincubation) did not block the shear stress elevation of eNOS mRNA.

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A Sp1 Binding Site in the GC-Rich Region Is Essential for a Core Promoter Activity of the Human Endothelial Nitric Oxide Synthase Gene

Cited by 39 publications

References 0 publications

Transcriptional regulation of endothelial nitric oxide synthase expression in uterine artery endothelial cells by c-Jun/AP-1

Transcriptional regulation of endothelial nitric oxide synthase expression in uterine artery endothelial cells by c-Jun/AP-1

Characterization of the Mouse Myeloid-associated Differentiation Marker (Myadm) Gene: Promoter Analysis and Protein Localization

Shear stress induction of the endothelial nitric oxide synthase gene is calcium-dependent but not calcium-activated

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