12 results on '"Zhao, Lijia"'
Search Results
2. Bmal1 promotes prostaglandin E2 synthesis by upregulating Ptgs2 transcription in response to increasing estradiol levels in day 4 pregnant mice
- Author
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Zhao, Lijia, primary, Yang, Luda, additional, Zhang, Jing, additional, Xiao, Yaoyao, additional, Wu, Meina, additional, Ma, Tiantian, additional, Wang, Xiaoyu, additional, Zhang, Linlin, additional, Jiang, Haizhen, additional, Chao, Hsu-Wen, additional, Wang, Aihua, additional, Jin, Yaping, additional, and Chen, Huatao, additional
- Published
- 2021
- Full Text
- View/download PDF
3. Removal of Rev-erbα inhibition contributes to the prostaglandin G/H synthase 2 expression in rat endometrial stromal cells
- Author
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Isayama, Keishiro, primary, Zhao, Lijia, additional, Chen, Huatao, additional, Yamauchi, Nobuhiko, additional, Shigeyoshi, Yasufumi, additional, Hashimoto, Seiichi, additional, and Hattori, Masa-aki, additional
- Published
- 2015
- Full Text
- View/download PDF
4. Inhibitory role of REV-ERBα in the expression of bone morphogenetic protein gene family in rat uterus endometrium stromal cells
- Author
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Tasaki, Hirotaka, primary, Zhao, Lijia, additional, Isayama, Keishiro, additional, Chen, Huatao, additional, Yamauchi, Nobuhiko, additional, Shigeyoshi, Yasufumi, additional, Hashimoto, Seiichi, additional, and Hattori, Masa-aki, additional
- Published
- 2015
- Full Text
- View/download PDF
5. Downregulation of core clock gene Bmal1 attenuates expression of progesterone and prostaglandin biosynthesis-related genes in rat luteinizing granulosa cells
- Author
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Chen, Huatao, primary, Zhao, Lijia, additional, Kumazawa, Makoto, additional, Yamauchi, Nobuhiko, additional, Shigeyoshi, Yasufumi, additional, Hashimoto, Seiichi, additional, and Hattori, Masa-aki, additional
- Published
- 2013
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- View/download PDF
6. FSH induces the development of circadian clockwork in rat granulosa cells via a gap junction protein Cx43-dependent pathway
- Author
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Chen, Huatao, primary, Zhao, Lijia, additional, Chu, Guiyan, additional, Kito, Gakushi, additional, Yamauchi, Nobuhiko, additional, Shigeyoshi, Yasufumi, additional, Hashimoto, Seiichi, additional, and Hattori, Masa-aki, additional
- Published
- 2013
- Full Text
- View/download PDF
7. Circadian clock regulates granulosa cell autophagy through NR1D1-mediated inhibition of ATG5.
- Author
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Zhang J, Zhao L, Li Y, Dong H, Zhang H, Zhang Y, Ma T, Yang L, Gao D, Wang X, Jiang H, Li C, Wang A, Jin Y, and Chen H
- Subjects
- Animals, Autophagy-Related Protein 5 antagonists & inhibitors, Autophagy-Related Protein 5 genetics, Cells, Cultured, Circadian Rhythm Signaling Peptides and Proteins biosynthesis, Circadian Rhythm Signaling Peptides and Proteins genetics, Female, Granulosa Cells pathology, HEK293 Cells, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Nuclear Receptor Subfamily 1, Group D, Member 1 genetics, Autophagy physiology, Autophagy-Related Protein 5 biosynthesis, Circadian Clocks physiology, Circadian Rhythm physiology, Granulosa Cells metabolism, Nuclear Receptor Subfamily 1, Group D, Member 1 biosynthesis
- Abstract
Autophagy of granulosa cells (GCs) is involved in follicular atresia, which occurs repeatedly during the ovarian development cycle. Several circadian clock genes are rhythmically expressed in both rodent ovarian tissues and GCs. Nuclear receptor subfamily 1 group D member 1 (NR1D1), an important component of the circadian clock system, is involved in the autophagy process through the regulation of autophagy-related genes. However, there are no reports illustrating the role of the circadian clock system in mouse GC autophagy. In the present study, we found that core circadian clock genes ( Bmal1 , Per2 , Nr1d1 , and Dbp ) and an autophagy-related gene ( Atg5 ) exhibited rhythmic expression patterns across 24 h in mouse ovaries and primary GCs. Treatment with SR9009, an agonist of NR1D1, significantly reduced the expression of Bmal1 , Per2 , and Dbp in mouse GCs. ATG5 expression was significantly attenuated by SR9009 treatment in mouse GCs. Conversely, Nr1d1 knockdown increased ATG5 expression in mouse GCs. Decreased NR1D1 expression at both the mRNA and protein levels was detected in the ovaries of Bmal1
-/- mice, along with elevated expression of ATG5. Dual-luciferase reporter assay and electrophoretic mobility shift assay showed that NR1D1 inhibited Atg5 transcription by binding to two putative retinoic acid-related orphan receptor response elements within the promoter. In addition, rapamycin-induced autophagy and ATG5 expression were partially reversed by SR9009 treatment in mouse GCs. Taken together, our current data demonstrated that the circadian clock regulates GC autophagy through NR1D1-mediated inhibition of ATG5 expression, and thus, plays a role in maintaining autophagy homeostasis in GCs.- Published
- 2022
- Full Text
- View/download PDF
8. Bmal1 promotes prostaglandin E 2 synthesis by upregulating Ptgs2 transcription in response to increasing estradiol levels in day 4 pregnant mice.
- Author
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Zhao L, Yang L, Zhang J, Xiao Y, Wu M, Ma T, Wang X, Zhang L, Jiang H, Chao HW, Wang A, Jin Y, and Chen H
- Subjects
- ARNTL Transcription Factors genetics, Animals, Cells, Cultured, Cyclooxygenase 2 metabolism, Estradiol pharmacology, Female, Gestational Age, Male, Mice, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Pregnancy, Progesterone pharmacology, Transcriptional Activation drug effects, Uterus drug effects, Uterus metabolism, ARNTL Transcription Factors physiology, Cyclooxygenase 2 genetics, Dinoprostone biosynthesis, Estradiol blood
- Abstract
Prostaglandin G/H synthase 2 (PTGS2) is a rate-limiting enzyme in prostaglandin synthesis. The present study assessed the role of the uterine circadian clock on Ptgs2 transcription in response to steroid hormones during early pregnancy. We demonstrated that the core clock genes ( Bmal1 , Per2 , Nr1d1 , and Dbp ), Vegf , and Ptgs2, and their encoded proteins, have rhythmic expression in the mouse uterus from days 3.5 to 4.5 ( D3.5-4.5 ) of pregnancy. Progesterone (P
4 ) treatment of cultured uterus endometrial stromal cells (UESCs) isolated from mPer2Luciferase reporter gene knock-in mice on D4 induced a phase shift in PER2::LUCIFERASE oscillations. This P4 -induced phase shift of PER2::LUCIFERASE oscillations was significantly attenuated by the P4 antagonist RU486. Additionally, the amplitude of PER2::LUCIFERASE oscillations was increased by estradiol (E2 ) treatment in the presence of P4 . Consistently, the mRNA levels of clock genes ( Bmal1 and Per2 ), Vegf , and Ptgs2 were markedly increased by E2 treatment of UESCs in the presence of P4 . Treatment with E2 also promoted prostaglandin E2 (PGE2 ) synthesis by UESCs. Depletion of Bmal1 in UESCs by small-interfering RNA (siRNA) decreased the transcript levels of clock genes ( Nr1d1 and Dbp ), Vegf , and Ptgs2 compared with nonsilencing siRNA treatment. Bmal1 knockdown also inhibited PGE2 synthesis. Moreover, the mRNA expression levels of clock genes ( Nr1d1 and Dbp ), Vegf , and Ptgs2 , and their respective proteins were significantly decreased in the uterus of Bmal1-/- mice. Thus, these data suggest that Bmal1 in mice promotes PGE2 synthesis by upregulating Ptgs2 in response to increases in E2 on D4 of pregnancy. NEW & NOTEWORTHY Rhythmic expression of Bmal1 and Ptgs2 was observed in the uterus isolated from D3.5-4.5 of pregnant mice. E2 increased the expression of Bmal1 and Ptg2 in UESCs isolated from mice on D4. The expression of Ptgs2 was significantly decreased in Bmal1-siRNA treated UESCs. Bmal1 knockdown also inhibited PGE2 synthesis. Thus, these data suggest that Bmal1 in mice promotes PGE2 synthesis by upregulating Ptgs2 in response to increases in E2 on D4 of pregnancy.- Published
- 2021
- Full Text
- View/download PDF
9. Removal of Rev-erbα inhibition contributes to the prostaglandin G/H synthase 2 expression in rat endometrial stromal cells.
- Author
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Isayama K, Zhao L, Chen H, Yamauchi N, Shigeyoshi Y, Hashimoto S, and Hattori MA
- Subjects
- 5' Untranslated Regions, ARNTL Transcription Factors antagonists & inhibitors, ARNTL Transcription Factors genetics, ARNTL Transcription Factors metabolism, Animals, Cells, Cultured, Cyclooxygenase 2 genetics, Endometrium cytology, Endometrium enzymology, Female, Nuclear Receptor Subfamily 1, Group D, Member 1 antagonists & inhibitors, Nuclear Receptor Subfamily 1, Group D, Member 1 genetics, Nuclear Receptor Subfamily 1, Group F, Member 1 genetics, Nuclear Receptor Subfamily 1, Group F, Member 1 metabolism, Pregnancy, Prolactin analogs & derivatives, Prolactin genetics, Prolactin metabolism, RNA Interference, RNA, Small Interfering, Rats, Rats, Transgenic, Response Elements, Stromal Cells cytology, Stromal Cells enzymology, Circadian Clocks, Cyclooxygenase 2 metabolism, Endometrium metabolism, Gene Expression Regulation, Enzymologic, Nuclear Receptor Subfamily 1, Group D, Member 1 metabolism, Placentation, Stromal Cells metabolism
- Abstract
The rhythmic expression of clock genes in the uterus is attenuated during decidualization. This study focused on Ptgs2, which is essential for decidualization, as a putative clock-controlled gene, and aimed to reveal the functions of clock genes in relation to Ptgs2 during decidualization. We compared the transcript levels of clock genes in the rat uterus on days 4.5 (D4.5) and 6.5 of pregnancy. The transcript levels of clock genes (Per2, Bmal1, Rorα, and Rev-erbα) had decreased at implantation sites on day 6.5 (D6.5e) compared with those on D4.5, whereas Ptgs2 transcripts had increased on D6.5e. Similar observations of Rev-erbα and Ptgs2 were also obtained in the endometrium on D6.5e by immunohistochemistry. In the decidual cells induced by medroxyprogesterone and 2-O-dibutyryl-cAMP, the rhythmic expression levels of clock genes were attenuated, whereas Ptgs2 transcription was induced. These results indicate that decidualization causes the attenuation of clock genes and the induction of Ptgs2. Furthermore, in the experiment of Bmal1 siRNA, the rhythmic expression of clock genes and Ptgs2 was attenuated by the siRNA. Transcript levels of Ptgs2 and prostaglandin (PG)E₂ production were increased by treatment with the Rev-erbα antagonist, suggesting the contribution of the nuclear receptor Rev-erbα to Ptgs2 expression. Moreover, Rev-erbα knockdown enhanced the induction of Ptgs2 transcription and PGE₂ production by forskolin. Chromatin immunoprecipitation-PCR analysis revealed that Rev-erbα could directly bind to a proximal RORE site of Ptgs2. Collectively, this study demonstrates that the attenuation of the circadian clock, especially its core component Rev-erbα, contributes to the induction of Ptgs2 during decidualization., (Copyright © 2015 the American Physiological Society.)
- Published
- 2015
- Full Text
- View/download PDF
10. Inhibitory role of REV-ERBα in the expression of bone morphogenetic protein gene family in rat uterus endometrium stromal cells.
- Author
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Tasaki H, Zhao L, Isayama K, Chen H, Yamauchi N, Shigeyoshi Y, Hashimoto S, and Hattori MA
- Subjects
- Animals, Cells, Cultured, Female, Gene Expression Regulation, Pregnancy, Rats, Rats, Transgenic, Stromal Cells metabolism, Uterus cytology, Uterus metabolism, Bone Morphogenetic Proteins antagonists & inhibitors, Bone Morphogenetic Proteins biosynthesis, Endometrium cytology, Endometrium metabolism, Nuclear Receptor Subfamily 1, Group D, Member 1 biosynthesis
- Abstract
Uterus circadian rhythms have been implicated in the gestation processes of mammals through entraining of the clock proteins to numerous downstream genes. Bone morphogenetic proteins (BMPs), having clock-controlled regulatory sites in their gene promoters, are expressed in the uterus during decidualization, but the regulation of the Bmp gene expression is poorly understood. The present study was designed to dissect the physiological roles of the uterus oscillators in the Bmp expression using the uterus endometrial stromal cells (UESCs) isolated from Per2-dLuc transgenic rats on day 4.5 of gestation. The in vitro decidualization of UESCs was induced by medroxyprogesterone acetate and 2-O-dibutyryl cAMP. A significant decline of Per2-dLuc bioluminescence activity was induced in decidual cells, and concomitantly, the expression of canonical clock genes was downregulated. Conversely, the expression of the core Bmp genes Bmp2, Bmp4, Bmp6, and Bmp7 was upregulated. In UESCs transfected with Bmal1-specific siRNA, in which Rev-erbα expression was downregulated, Bmp genes, such as Bmp2, Bmp4, and Bmp6 were upregulated. However, Bmp1, Bmp7, and Bmp8a were not significantly affected by Bmal1 silencing. The expression of all Bmp genes was enhanced after treatment with the REV-ERBα antagonist (SR8278), although their rhythmic profiles were differed from each other. The binding of REV-ERBα to the proximal regions of the Bmp2 and Bmp4 promoters was revealed by chromatin immunoprecipitation-PCR analysis. Collectively, these results indicate that the Bmp genes are upregulated by the attenuation of the cellular circadian clock; in particular, its core component REV-ERBα functions as a transcriptional silencer in the Bmp gene family., (Copyright © 2015 the American Physiological Society.)
- Published
- 2015
- Full Text
- View/download PDF
11. Downregulation of core clock gene Bmal1 attenuates expression of progesterone and prostaglandin biosynthesis-related genes in rat luteinizing granulosa cells.
- Author
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Chen H, Zhao L, Kumazawa M, Yamauchi N, Shigeyoshi Y, Hashimoto S, and Hattori MA
- Subjects
- ARNTL Transcription Factors biosynthesis, ARNTL Transcription Factors genetics, Animals, CLOCK Proteins antagonists & inhibitors, CLOCK Proteins biosynthesis, Cells, Cultured, Female, Gene Expression Regulation, Mice, Progesterone biosynthesis, Progesterone genetics, Prostaglandins biosynthesis, Rats, Rats, Transgenic, ARNTL Transcription Factors antagonists & inhibitors, CLOCK Proteins genetics, Down-Regulation genetics, Luteal Cells metabolism, Progesterone antagonists & inhibitors, Prostaglandins genetics
- Abstract
Ovarian circadian oscillators have been implicated in the reproductive processes of mammals. However, there are few reports regarding the detection of ovarian clock-controlled genes (CCGs). The present study was designed to unravel the mechanisms through which CCG ovarian circadian oscillators regulate fertility, primarily using quantitative RT-PCR and RNA interference against Bmal1 in rat granulosa cells. Mature granulosa cells were prepared from mouse Per2-destabilized luciferase (dLuc) reporter gene transgenic rats. A real-time monitoring system of Per2 promoter activity was employed to detect Per2-dLuc oscillations. The cells exposed to luteinizing hormone (LH) displayed clear Per2-dLuc oscillations and a rhythmic expression of clock genes (Bmal1, Per1, Per2, Rev-erbα, and Dbp). Meanwhile, the examined ovarian genes (Star, Cyp19a1, Cyp11a1, Ptgs2, Lhcgr, and p53) showed rhythmic transcript profiles except for Hsd3b2, indicating that these rhythmic expression genes may be CCGs. Notably, Bmal1 small interfering (si)RNA treatment significantly decreased both the amplitude of Per2-dLuc oscillations and Bmal1 mRNA levels compared with nonsilencing RNA treatment in luteinizing granulosa cells. Depletion of Bmal1 by siRNA decreased the transcript levels of clock genes (Per1, Per2, Rev-erbα, and Dbp) and examined ovarian genes (Star, Cyp19a1, Cyp11a1, Ptgs2, Hsd3b2, and Lhcgr). Accordingly, knockdown of Bmal1 also inhibited the synthesis of progesterone and prostaglandin E2, which are associated with crucial reproductive processes. Collectively, these data suggest that ovarian circadian oscillators regulate the synthesis of steroid hormones and prostaglandins through ovarian-specific CCGs in response to LH stimuli. The present study provides new insights into the physiologic significance of Bmal1 related to fertility in ovarian circadian oscillators.
- Published
- 2013
- Full Text
- View/download PDF
12. FSH induces the development of circadian clockwork in rat granulosa cells via a gap junction protein Cx43-dependent pathway.
- Author
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Chen H, Zhao L, Chu G, Kito G, Yamauchi N, Shigeyoshi Y, Hashimoto S, and Hattori MA
- Subjects
- Animals, Cell Differentiation drug effects, Cells, Cultured, Chorionic Gonadotropin metabolism, Circadian Rhythm Signaling Peptides and Proteins biosynthesis, Circadian Rhythm Signaling Peptides and Proteins genetics, Circadian Rhythm Signaling Peptides and Proteins metabolism, Connexin 43 antagonists & inhibitors, Connexin 43 genetics, Dexamethasone pharmacology, Female, GABA-A Receptor Antagonists pharmacology, Gap Junctions drug effects, Genes, Reporter drug effects, Glucocorticoids pharmacology, Granulosa Cells cytology, Granulosa Cells drug effects, Membrane Transport Modulators pharmacology, Mice, Period Circadian Proteins biosynthesis, Period Circadian Proteins genetics, Period Circadian Proteins metabolism, Rats, Rats, Transgenic, Receptors, LH biosynthesis, Receptors, LH genetics, Receptors, LH metabolism, Circadian Clocks drug effects, Connexin 43 metabolism, Follicle Stimulating Hormone metabolism, Gap Junctions metabolism, Granulosa Cells metabolism, Up-Regulation drug effects
- Abstract
The present study was designed to assess the relationship between gap junctions and the maturation of a clock system in rat granulosa cells stimulated by follicle-stimulating hormone (FSH). Immature and mature granulosa cells were prepared by puncturing the ovaries of diethylstilbestrol- and equine chorionic gonadotropin (eCG)-treated mouse Period2 (Per2)-dLuc reporter gene transgenic rats, respectively. Mature granulosa cells exposed to dexamethasone (DXM) synchronization displayed several Per2-dLuc oscillations and a rhythmic expression of clock genes. Intriguingly, we observed clear evidence that the FSH stimulation significantly increased the amplitude of Per2 oscillations in the granulosa cells, which was confirmed by the elevation of the Per2 and Rev-erbα (Nr1d1) mRNA levels. FSH also induced a major phase-advance shift of Per2 oscillations. The mature granulosa cells cultured for 2 days with FSH expressed higher mRNA levels of Per2, Rev-erbα, Bmal1 (Arnt1), Lhcgr, and connexin (Cx) 43 (Gja1) compared with the immature granulosa cells. Consistently, our immunofluorescence results revealed abundant Cx43 protein in antral follicles stimulated with eCG and weak or no fluorescence signal of Cx43 in primary and preantral follicles. Similar results were confirmed by Western blotting analysis. Two gap junction blockers, lindane and carbenoxolone (CBX), significantly decreased the amplitude of Per2 oscillations, which further adhered significant decreases in Per2 and Rev-erbα transcript levels. In addition, both lindane and CBX induced a clear phase-delay shift of Per2 oscillations. These findings suggest that FSH induces the development of the clock system by increasing the expression of Cx43.
- Published
- 2013
- Full Text
- View/download PDF
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