Background
This study aims at investigating the effect of growth hormone (GH) on the growth of human endometrial glandular cells (hEGCs) and preliminary exploring its mechanism.
Conclusions
GH promoted hEGCs proliferation and motion, which is GHR-JAK-STAT3/5 signaling pathway-dependent. These findings reveal the essential roles of GH in the hEGCs growth and provide evidence for potential GH therapy in intrauterine adhesion (IUA) treatment.
Methods
HEGCs were isolated from the endometrial biopsies and exposed to different dose of GH (0, 50, 100, and 200 ng/mL). Cell proliferation and cell cycle assay, migration assay was performed to investigate the growth and motivation of hEGCs, respectively. Reverse transcription-polymerase chain reaction (RT-PCR), immunocytochemistry (ICC), and western blot (WB) were processed to investigate its related gene or protein expression.
Results
The results revealed that GH administration promoted the proliferation, cell cycle, migration, and growth hormone receptors (GHRs) expression of the hEGC. We further inhibited GHRs with AG490, and the inhibitor reversed the effects of GH on cell growth, motion, and the activation of GHR and STAT3/5. Conclusions: GH promoted hEGCs proliferation and motion, which is GHR-JAK-STAT3/5 signaling pathway-dependent. These findings reveal the essential roles of GH in the hEGCs growth and provide evidence for potential GH therapy in intrauterine adhesion (IUA) treatment.