Impaired granulosa cells promote self-damage by regulating the generation of macrophage in polycystic ovary syndrome

Granulosa cell is one of the most important somatic cell in ovary, abnormality of its proliferation or apoptosis plays key role in the development of polycystic ovary syndrome ( PCOS). However, the molecular mechanism of it in PCOS is still unclear. In this study, we find that many inflammation genes including CD163, Fas are upregulated in PCOS granulosa cells by comparing the mRNA profile data in normal and PCOS granulosa cells. Further experiments demonstrate that granulosa cells have a faint CD163 expression, while supernatant from granulosa cells especially impaired granulosa cells can elevate the expression of CD163 in monocyte which represents the generation of macrophage. Besides, monocyte can markedly promote cellular apoptosis, reactive oxygen production and Fas protein expression. This alteration is also observed in KGN cells treated with THP1 derived macrophage. This study proposes a new mechanism of macrophage and granulosa cell impairment in PCOS which will help us better understand the formation of PCOS.