Abstract
ObjectiveDuring early pregnancy, the proliferation placental cells is crucial for proper implantation and formation of maternal–fetal circulation. Platelet-derived growth factor-AA (PDGF-AA) has been detected in placenta during early pregnancy; however, the role of PDGF-AA in placental cell growth has not been studied extensively. Primary cilium, a centrosome-based cellular protrusion, is an signaling hub for regulating development and differentiation. Importantly, the receptor of PDGF-AA (Pdgfr-α) is detected in the primary cilium and primary cilia-mediated PDGF-AA signaling regulates development and differentiation. Here we would like to investigate whether PDGF-AA regulates placental cell growth and whether primary cilia play roles in this process. Materials and methodsHuman placental choriocarcinoma JAR cells were treated with PDGF-AA followed by examining cell growth. Primary cilia and subcellular localization of Pdgfr-α were observed by immunofluorescence staining. Manipulation of primary cilia was performed by treating cells with roscovitine or by transfecting cells with siRNA against IFT88. ResultsHere we showed that PDGF-AA induced JAR cell proliferation. In addition, JAR cells grew primary cilia where Pdgfr-α was detected. More importantly, pharmacological inhibition of primary cilia formation or depletion of cilia-related gene, IFT88, alleviated PDGF-AA induced JAR cell proliferation. ConclusionThus, our study show that PDGF-AA facilitates human placental choriocarcinomaJARcell growth via primary cilia.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.