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  • Open Access

    ARTICLE

    Reversal of maternal obesity attenuates hypoxia and improves placental development in the preeclamptic-like BPH/5 mouse model

    DANIELLA M. ADAMS1, KALIE F. BECKERS1, JULIET P. FLANAGAN1, VIVIANE C. L. GOMES1,#, CHIN-CHI LIU1, JENNY L. SONES1,2,*

    BIOCELL, Vol.47, No.9, pp. 2051-2058, 2023, DOI:10.32604/biocell.2023.029644 - 28 September 2023

    Abstract Background: Women with obesity have higher risk of adverse pregnancy outcomes, including preeclampsia (PE). Late-gestational hypertension, aberrant fetoplacental development, and fetal growth restriction (FGR), hallmarks of PE, are observed spontaneously in BPH/5 mice. Similar to obese preeclamptic women, BPH/5 mice have higher visceral white adipose tissue (WAT) and circulating leptin. We hypothesized that attenuation of maternal obesity and serum leptin in pregnant BPH/5 mice will improve fetoplacental development by decreasing hypoxia markers and leptin expression at the maternal-fetal interface. Methods: To test this hypothesis, BPH/5 mice were fed ad libitum (lib) and pair-fed (PF) to C57… More >

  • Open Access

    ARTICLE

    In Silico Disulfide Bond Engineering to Improve Human LEPTIN Stability

    Bahram Barati1, Fatemeh Fazeli Zafar1, Shuanhu Hu1, Najmeh Fani2, Sajjad Eshtiaghi3, Shuang Wang1,*

    Journal of Renewable Materials, Vol.9, No.11, pp. 1843-1857, 2021, DOI:10.32604/jrm.2021.016301 - 04 June 2021

    Abstract Enhancing the stability of biomolecules is one of the hot topics in industry. In this study, we enhanced the stability of an important protein called LEPTIN. LEPTIN is a hormone secreted by fat cells playing an essential role in body weight and composition, and its deficiency can result in several disorders. The treatment of related LEPTIN dysfunctions is often available in the form of injection. To decrease the cost and the frequency of its applications can be achieved by increasing its lifetime through engineering LEPTIN. In this study, to engineer LEPTIN, we have introduced disulfide… More > Graphic Abstract

    <i>In Silico</i> Disulfide Bond Engineering to Improve Human LEPTIN Stability

  • Open Access

    ARTICLE

    Leptin promotes proliferation and invasion of osteosarcoma cells by upregulating the expression of SIRT1

    HELIN FENG1,2, XIAOCHONG ZHANG3, QIANQIAN ZHANG4, ZE LI5, LILI ZHAO1,6,*

    BIOCELL, Vol.44, No.3, pp. 443-450, 2020, DOI:10.32604/biocell.2020.010705 - 22 September 2020

    Abstract Osteosarcoma (OS) is a primary high-grade malignant bone neoplasm, and the prognosis of OS remains poor due to early metastasis. Leptin plays an essential role in tumorigenesis, but the role of leptin in the development of OS is still not fully understood. In this study, we used a human osteosarcoma MG-63 cell line as an experimental model. MG-63 cells were treated with leptin, and cell proliferation, apoptosis, adhesion, invasion, and gene expression, were evaluated. The results showed that leptin promoted proliferation, decreased adhesion, suppressed apoptosis, and promoted invasion, of MG-63 cells. Moreover, the expression of More >

  • Open Access

    ARTICLE

    Interleukin-1β regulates metalloproteinase activity and leptin secretion in a cytotrophoblast model

    VANINA ANDREA FONTANA1, MELISA SANCHEZ1, ELISA CEBRAL2 AND JUAN CARLOS CALVO1,3*

    BIOCELL, Vol.34, No.1, pp. 37-44, 2010, DOI:10.32604/biocell.2010.34.037

    Abstract Implantation is one of the most regulated processes in human reproduction, by endocrine and immunological systems. Cytokines are involved in embryo-maternal communication and an impaired balance could result in pregnancy loss. Here we investigated the effect of interleukin 1-β on the activity of two important metalloproteinases (MMP-2 and MMP-9) that are involved in extracellular matrix remodeling as well as the secretion of leptin, one of the reproductive hormones actively regulating their activity and secretion. We found that IL-1β activates matrix metalloproteinase activity as well as increases leptin secretion. We propose that this interleukin, through the More >

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