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- 저자 : ( Hyun Jung Jade Lim ) (검색결과 2 건)
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( Hyun Gwoo Lee ),( Ae Jin Choi ),( Gum Yong Kang ),( Hyung Soon Park ),( Hyung Chan Kim ),( Hyun Jung Jade Lim ),( Hye Won Chung ) 생화학분자생물학회 2014 BMB Reports Vol.47 No.5
Age-related macular degeneration (AMD) is the leading causeof blindness in the world. Evidence indicates that thesuppression of the ubiquitin-proteasome system (UPS) contributesto the accumulation of toxic proteins and inflammation inretinal pigment epithelium (RPE), the functional abnormalitiesand/or the degeneration of which are believed to be theinitiators and major pathologies of AMD. To identify newprotein associations with the altered UPS in AMD, we usedLC-ESI-MS/MS to perform a proteomic analysis of the aqueoushumor (AH) of AMD patients and matched control subjects. SixUPS-related proteins were present in the AH of the patients andcontrol subjects. Four of the proteins, including 26S proteasomenon-ATPase regulatory subunit 1 (Rpn2), were increasedin patients, according to semi-quantitative proteomic profiling. An LC-MRM assay revealed a significant increase of Rpn2 in 15AMD patients compared to the control subjects, suggesting thatthis protein could be a biomarker for AMD.[BMB Reports 2014; 47(5): 292-297]
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Kim, Hye‐,Ryun,Kim, Yeon Sun,Yoon, Jung Ah,Yang, Seung Chel,Park, Mira,Seol, Dong‐,Won,Lyu, Sang Woo,Jun, Jin Hyun,Lim, Hyunjung Jade,Lee, Dong Ryul,Song, Haengseok Federation of American Society for Experimental Bi 2018 The FASEB Journal Vol.32 No.3
<P>The harmonized actions of ovarian E-2 and progesterone (P-4) regulate the proliferation and differentiation of uterine cells in a spatiotemporal manner. Imbalances between these hormones often lead to infertility and gynecologic diseases. Whereas numerous factors that are involved in P-4 signaling have been identified, few local factors that mediate E-2 actions in the uterus have been revealed. Here, we demonstrate that estrogen induces the transcription factor, early growth response 1 (Egr1), to fine-tune its actions in uterine epithelial cells (ECs) that are responsible for uterine receptivity for embryo implantation. In the presence of exogenous gonadotrophins, ovulation, fertilization, and embryonic development normally occur in Egr1(-/-) mice, but these animals experience the complete failure of embryo implantation with reduced artificial decidualization. Although serum levels of E-2 and P-4 were comparable between Egr1(+/+) and Egr1(-/-) mice on d 4 of pregnancy, aberrantly reduced levels of progesterone receptor in Egr1(-/-) uterine ECs caused enhanced E-2 activity and impaired P-4 response. Ultrastructural analyses revealed that Egr1(-/-) ECs are not fully able to provide proper uterine receptivity. Uterine mRNA landscapes in Egr1(-/-) mice revealed that EGR1 controls the expression of a subset of E-2-regulated genes. In addition, P-4 signaling was unable to modulate estrogen actions, including those that are involved in cell-cycle progression, in ECs that were deficient in EGR1. Furthermore, primary coculture of Egr1(-/-) ECs with Egr1(+/+) stromal cells, and vice versa, supported the notion that Egr1 is required tomodulate E-2 actions on ECs to prepare the uterine environment for embryo implantation. In contrast to its role in ECs, loss of Egr1 in stroma significantly reduced stromal cell proliferation. Collectively, our results demonstrate that E-2 induces EGR1 to streamline its actions for the preparation of uterine receptivity for embryo implantation in mice.</P>
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