• Title/Summary/Keyword: ANGPT1

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Angiopoietin-1 and -2 and vascular endothelial growth factor expression in ovarian grafts after cryopreservation using two methods

  • Cho, In Ae;Lee, Yeon Jee;Lee, Hee Jung;Choi, In Young;Shin, Jeong Kyu;Lee, Soon Ae;Lee, Jong Hak;Choi, Won Jun
    • Clinical and Experimental Reproductive Medicine
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    • v.45 no.3
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    • pp.143-148
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    • 2018
  • Objective: The favored method of preserving fertility in young female cancer survivors is cryopreservation and autotransplantation of ovarian tissue. Reducing hypoxia until angiogenesis takes place is essential for the survival of transplanted ovarian tissue. The aim of this study was to investigate the role of angiopoietin-1 (Angpt-1), angiopoietin-2 (Angpt-2), and vascular endothelial growth factor (VEGF) in ovarian tissue grafts that were cryopreserved using two methods. Methods: Ovarian tissues harvested from ICR mice were divided into three groups: group I (control), no cryopreservation; group II, vitrification in EFS (ethylene-glycol, ficoll, and sucrose solution)-40; and group III, slow freezing in dimethyl sulfoxide. We extracted mRNA for VEGF, Angpt-1, and Angpt-2 from ovarian tissue 1 week following cryopreservation and again 2 weeks after autotransplantation. We used reverse transcriptase-polymerase chain reaction to quantify the levels of VEGF, Angpt-1, and Angpt-2 in the tissue. Results: Angpt-1 and Angpt-2 expression decreased after cryopreservation in groups II and III. After autotransplantation, Angpt-1 and Angpt-2 expression in ovarian tissue showed different trends. Angpt-1 expression in groups II and III was lower than in group I, but Angpt-2 in groups II and III showed no significant difference from group I. The vitrified ovarian tissues had higher expression of VEGF and Angpt-2 than the slow-frozen ovarian tissues, but the difference was not statistically significant. Conclusion: Our results indicate that Angpt-2 may play an important role in ovarian tissue transplantation after cryopreservation although further studies are needed to understand its exact function.

Transcriptional repression of ANGPT1 by histone H3K9 demethylase KDM3B

  • Han, Arim;Chae, Yun-Cheol;Park, Jin Woo;Kim, Kee-Beom;Kim, Ji-Young;Seo, Sang-Beom
    • BMB Reports
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    • v.48 no.7
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    • pp.401-406
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    • 2015
  • Here we report that the H3K9 demethylase KDM3B represses transcription of the angiogenesis regulatory gene, ANGPT1. Negative regulation of ANGPT1 by KDM3B is independent of its Jumonji (JmjC) domain-mediated H3K9 demethylase activity. We demonstrate that KDM3B downregulates ANGPT1 via interaction with SMRT, and suggest that the repressor complex is formed at the promoter area of ANGPT1. Using MTT and wound healing assays, depletion of KDM3B was found to increase cell proliferation and cell motility, indicating that KDM3B has a role in angiogenesis. [BMB Reports 2015; 48(7): 401-406]

Microarray Analysis of Extracranial Arteriovenous Malformation Endothelial Cells

  • Lee, Joon Seok;Oh, Eun Jung;Kim, Hyun Mi;Kwak, Suin;Lee, Seok-Jong;Lee, Jongmin;Huh, Seung;Kim, Ji Yoon;Chung, Ho Yun
    • Journal of Interdisciplinary Genomics
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    • v.4 no.2
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    • pp.31-34
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    • 2022
  • Background: Arteriovenous malformations (AVMs) are rare diseases comprising abnormally dilated arteries and veins with an absence of a capillary network. Since these diseases are intractable after diagnosis, various treatment strategies have been examined, with continuous efforts to identify target genes. Here, we report relevant new target genes selected via gene microarray. Methods: Endothelial cells were isolated from samples collected from three patients with AVM and three healthy individuals, followed by microarray analysis. Additionally, quantitative PCR was performed to select genes highly relevant to AVM. Results: In the vascular endothelial cells derived from the tissues of patients with AVM, the expression of ANGPT1, ANGPT2, DLL4, IL6, NRG1, TGFBR1, and VEGFA was typically higher compared to those derived from normal tissues. Conclusion: Seven candidate genes were selected to analyze the pathophysiological mechanism of AVM. These results may aid in future directions of diagnosis and treatment.