组织胚胎学-文献订阅-三峡大学图书馆

摘要： The Liver is constantly subjected to mechanical, chemical and pathological insults throughout life, as a result of which there is a common occurrence of various liver diseases. Due to the complex nature of liver architecture, it is not possible to mimic the in-vivo conditions beyond a certain limit. Hence, the development of in-vitro and ex-vivo models to study various liver diseases has gained more importance over the last few decades. The present study aims to develop a semi-perfused liver explant model to give an extended lifetime for studying liver pathology and treatment options. Caprine liver tissue explants were sliced, weighed (25 mg) and placed on the area vasculosa of fertilized chicken eggs. Unfertilized eggs were used as controls. After varying time intervals of incubation on area vasculosa of fertilized chicken eggs, the liver slices were subjected to cell viability assay, lactate dehydrogenase assay and Serum glutamic pyruvic transaminase assays. The results indicate that the viability and functional properties of such semi-perfused liver tissue explants holds good up to 6 h. Finally, the liver tissue explants were pre-treated with FBS, with and without anti-fibrotic drugs, and placed on chick embryo area vasculosa up to 6 h. The anti-fibrotic drug-treated semi perfused liver tissue explant showed a decrease in collagen formation as confirmed by histology and western blot. We deem that the use of extra-embryonic vasculature of chicken bed for extending the life of tissue explants will serve as a cost-effective alternative to animal models to understand disease mechanisms under drug treatments.

The NuRD chromatin-remodeling complex enzyme CHD4 prevents hypoxia-induced endothelial Ripk3 transcription and murine embryonic vascular rupture

Colijn, Sarah Gao, Siqi Ingram, Kyle G. Menendez, Matthew Muthukumar, Vijay Silasi-Mansat, Robert Chmielewska, Joanna J. Hinsdale, Myron Lupu, Florea Griffin, Courtney T.

Oklahoma Med Res Fdn Cardiovasc Biol Res Program 825 NE 13th St Oklahoma City OK 73104 USAUniv Oklahoma Hlth Sci Ctr Dept Cell Biol Oklahoma City OK 73190 USAOklahoma State Univ Dept Physiol Sci Stillwater OK 74078 USAStowers Inst Med Res Kansas City MO 64110 USAJackson Lab 600 Main St Bar Harbor ME 04609 USAUniv Warsaw Ctr New Technol PL-02097 Warsaw Poland

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关键词： Chromatin remodelling Development Gene expression

摘要： Physiological hypoxia can trigger transcriptional events that influence many developmental processes during mammalian embryogenesis. One way that hypoxia affects transcription is by engaging chromatin-remodeling complexes. We now report that chromodomain helicase DNA binding protein 4 (CHD4), an enzyme belonging to the nucleosome remodeling and deacetylase (NuRD) chromatin-remodeling complex, is required for transcriptional repression of the receptor-interacting protein kinase 3 (Ripk3)-a critical executor of the necroptosis cell death program-in hypoxic murine embryonic endothelial cells. Genetic deletion of Chd4 in murine embryonic endothelial cells in vivo results in upregulation of Ripk3 transcripts and protein prior to vascular rupture and lethality at midgestation, and concomitant deletion of Ripk3 partially rescues these phenotypes. In addition, CHD4 binds to and prevents acetylation of the Ripk3 promoter in cultured endothelial cells grown under hypoxic conditions to prevent excessive Ripk3 transcription. These data demonstrate that excessive RIPK3 is detrimental to embryonic vascular integrity and indicate that CHD4 suppresses Ripk3 transcription when the embryonic environment is particularly hypoxic prior to the establishment of fetal-placental circulation at midgestation. Altogether, this research provides new insights into regulators of Ripk3 transcription and encourages future studies into the mechanism by which excessive RIPK3 damages embryonic blood vessels.

高职组织学与胚胎学信息化教学设计探讨

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人体解剖学与组织胚胎学课程整合的初步探索

董文亚赵茹茹

商丘工学院医学院河南商丘 476000

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