TY - JOUR
T1 - Ever-changing cell interactions during the life span of the corpus luteum
T2 - Relevance to luteal regression
AU - Smith, George W.
AU - Meidan, Rina
PY - 2014/4
Y1 - 2014/4
N2 - The corpus luteum (CL) undergoes dramatic morphological and functional changes throughout its lifespan. It initially develops from cells that remain in the follicle following ovulation. Eventually the mature CL is composed of multiple, distinctive cell types including steroidogenic cells (small and large luteal cells) and other cell types (endothelial cells, pericytes, fibroblasts, and immune cells). Robust angiogenesis accompanies CL formation, establishing an elaborate blood vessel network at mid cycle. In the absence of embryonic signals, the CL will regress in a process triggered by prostaglandin F2α (PG). Luteal demise in the responsive gland is characterized by cessation of steroid production, angio-regression, and apoptotic cell death, brought about by leukocyte infiltration, inflammatory responses, and diminished angiogenic support. However, the young immature CL is resistant or refractory to the luteolytic actions of PG. Evidence based on functional genomics and other studies highlight the roles played by endothelial, immune, and steroidogenic luteal cells and their interactions in the PG-responsive vs. PG-refractory CL.
AB - The corpus luteum (CL) undergoes dramatic morphological and functional changes throughout its lifespan. It initially develops from cells that remain in the follicle following ovulation. Eventually the mature CL is composed of multiple, distinctive cell types including steroidogenic cells (small and large luteal cells) and other cell types (endothelial cells, pericytes, fibroblasts, and immune cells). Robust angiogenesis accompanies CL formation, establishing an elaborate blood vessel network at mid cycle. In the absence of embryonic signals, the CL will regress in a process triggered by prostaglandin F2α (PG). Luteal demise in the responsive gland is characterized by cessation of steroid production, angio-regression, and apoptotic cell death, brought about by leukocyte infiltration, inflammatory responses, and diminished angiogenic support. However, the young immature CL is resistant or refractory to the luteolytic actions of PG. Evidence based on functional genomics and other studies highlight the roles played by endothelial, immune, and steroidogenic luteal cells and their interactions in the PG-responsive vs. PG-refractory CL.
KW - Angiogenesis
KW - Endothelial cells
KW - Immune cells
KW - Luteolysis
KW - Prostaglandin F2α
UR - http://www.scopus.com/inward/record.url?scp=84901239797&partnerID=8YFLogxK
U2 - 10.1016/j.repbio.2013.12.004
DO - 10.1016/j.repbio.2013.12.004
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C2 - 24856465
AN - SCOPUS:84901239797
SN - 1642-431X
VL - 14
SP - 75
EP - 82
JO - Reproductive Biology
JF - Reproductive Biology
IS - 2
ER -