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Early growth response-2 expression in uterine leiomyoma cells: regulation and function
Oleh:
Yin, Ping
;
Navarro, Antonia
;
Fang, Feng
;
Xie, Anna
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 96 no. 02 (Aug. 2011)
,
page 439-444.
Topik:
Collagen
;
c-myc
;
dermatopontin
;
Egr-2
;
leiomyomata
;
PCNA
;
TGF-ß3
Ketersediaan
Perpustakaan FK
Nomor Panggil:
F02.K.2011.04
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
Objective To investigate the regulation of early growth response-2 (Egr-2) by transforming growth factor ß3 (TGF-ß3) and its functions in cultured human uterine leiomyoma smooth muscle cells. Design Laboratory research. Setting Academic medical center. Patient(s) Primary leiomyoma cells from patients with symptomatic leiomyomata. Intervention(s) Tissue culture followed by RNA and protein analysis. Main Outcome Measure(s) Cell proliferation, alteration in extracellular matrix component expression. Result(s) In vivo mRNA levels of Egr-2 were statistically significantly higher in leiomyoma tissues compared with matched myometrial tissues, and showed a statistically significant correlation with TGF-ß3 messenger RNA (mRNA) levels in leiomyoma tissues. In primary leiomyoma smooth muscle cells, TGF-ß3 statistically significantly induced Egr-2 gene expression in a dose-dependent and time-dependent manner. Small interfering RNA (siRNA) knockdown of Egr-2 markedly increased the level of the proliferation marker proliferating cell nuclear antigen and the expression of proto-oncogene c-myc. On the other hand, ablation of Egr-2 stimulated collagen-1A1 and collagen-3A1 transcription and inhibited dermatopontin gene expression. However, the mRNA levels of a-smooth muscle actin and fibronectin were not affected by Egr-2 knockdown. Conclusion(s) We demonstrated that TGF-ß3 regulated Egr-2 gene expression and presented evidence that Egr-2 decreases collagen production and stimulates dermatopontin gene expression.
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