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Effects of LPS on the accumulation of lipid droplets, proliferation, and steroidogenesis in goat luteinized granulosa cells.

08:00 EDT 1st April 2019 | BioPortfolio

Summary of "Effects of LPS on the accumulation of lipid droplets, proliferation, and steroidogenesis in goat luteinized granulosa cells."

Lipopolysaccharide (LPS) can cause ovarian dysfunction and infertility in mammals. The purpose of this study was to investigate the effects of LPS on the accumulation of lipid droplets (LDs), proliferation, and steroidogenesis in goat luteinized granulosa cells (LGCs). GCs isolated from the ovarian follicles were spontaneously luteinized under media with fetal bovine serum, resulting in increased progesterone and shifted shape from spherical to star with multiple prolongations. Then, LGCs were treated with LPS (0-10 μg/mL) for 0-48 hours. Oil Red O staining was performed to observe LDs accumulation and commercial kit was applied to detect intracellular triglyceride (TG) content. The cell proliferation were detected by cell counting kit-8. Expressions of cell-cycle-related genes were determined by real-time polymerase chain reaction. Estradiol (E ) and progesterone (P ) from cell supernatants were determined by enzyme-linked immunosorbent assay, and expressions of STAR, P450scc, 3β-hydroxysteroid dehydrogenase (3β-HSD) and CYP19A1 were detected by Western blot. Results showed that LPS treatment significantly increased LDs accumulation after 24 hours, and 5 μg/mL LPS increased TG content ( P < 0.05). LPS treatment for 24 hours stimulated the LGCs activities ( P<0.05), which was confirmed by the increases in the expressions of proliferating cell nuclear antigen (PCNA), cyclinB1 and cyclinD1, while 48 hours treatment had no effect. LPS treatment suppressed E and P output of LGCs ( P < 0.05). Western blot results showed that 10 μg/mL LPS decreased the protein expression of 3β-HSD in LGCs ( P < 0.05). In conclusion, LPS increased LDs accumulation and cell proliferation, and LPS-mediated P reduction could be attributed to the decreased 3β-HSD protein expression, which provide new information for the regulation of ovarian function in goats.

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Journal Details

This article was published in the following journal.

Name: Journal of biochemical and molecular toxicology
ISSN: 1099-0461
Pages: e22329

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A perilipin that localizes to LIPID DROPLETS; CYTOPLASM; ENDOSOMES; and PLASMA MEMBRANE, especially in MACROPHAGES. It functions as a transporter of free fatty acids to lipid droplets to promote their biogenesis and growth. It is also required for the transport of the MANNOSE-6-PHOSPHATE RECEPTOR from endosomes to the TRANS-GOLGI NETWORK. Its structure consists of four helix bundles that interact with the hydrophobic lipid droplet surface.

Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.

A perilipin that is expressed by many different cell types. It binds FATTY ACIDS and CHOLESTEROL, stabilizes TRIGLYCERIDES, and localizes to both the surface and hydrophobic core of LIPID DROPLETS, as well as the ENDOPLASMIC RECTICULUM and PLASMA MEMBRANE in MACROPHAGES. It also plays a central role in the biogenesis of lipid droplets and FOAM CELLS and is highly expressed by macrophages at atherosclerotic lesions in human arteries along with the INFLAMMATION markers TNF-ALPHA; MCP-1 RECEPTOR; and IL-6.

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Proteins, such as PERILIPINS, that localize to LIPID DROPLETS either transiently or constitutively.

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