AI Article Synopsis
- The corpus luteum (CL) survives in low-oxygen conditions by developing a complex blood vessel network, with hypoxia playing a key role.
- Hypoxia-inducible factor-1 (HIF-1) is crucial for cellular responses to low oxygen, regulating genes that help the CL function and develop.
- This review highlights the specific genes (like VEGFA and FGF-2) that are activated in luteal cells due to hypoxia, which are important for the formation of new blood vessels in the CL.
Article Abstract
The hypoxic microenvironment that occurs in fast-growing tissue such as the corpus luteum (CL) is a major contributor to its ability to survive via the induction of an intricate vascular network. Cellular responses to hypoxia are mediated by hypoxia-inducible factor-1 (HIF-1), an oxygen-regulated transcriptional activator. HIF-1, a heterodimer consisting of a constitutively-expressed β subunit and an oxygen-regulated α subunit, binds to the hypoxia responsive element (HRE) present in the promoter regions of responsive genes. This review summarises evidence for the involvement of hypoxia and HIF-1α in CL development and function. Special emphasis is given to hypoxia-induced, luteal cell-specific expression of multiple genes (vascular endothelial growth factor A (VEGFA), fibroblast growth factor 2 (FGF-2), prokineticin receptor 2 (PK-R2), stanniocalcin 1 (STC-1) and endothelin 2 (EDN-2) that participate in the angiogenic process during CL formation.
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| http://dx.doi.org/10.1071/RD12139 | DOI Listing |
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