International Journal of Stem Cells : eISSN 2005-5447

Fig. 5.

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Fig. 5. cAMP/PKA signaling pathway is involved in regulating the proliferation effect of PTHrP in patient-derived GSCs. Three patient-derived GSCs (GSC-01, GSC-02, and GSC-03) were transfected with siNC or siPTHrP. The siPTHrP cells were randomly allocated into two groups. One group was treated with 10 μM forskolin, the other just add an equal volume of the medium. (A) After culturing for three days, cell proliferation was analyzed using BrdU incorporation. Scale bar=100 μm. (B) The value represents the mean±standard deviation of three independent experiments (n=3). *p<0.05 versus siNC group; ###p<0.001 versus siPTHrP group. (C) The illustration depicts the mechanism that PTHrP regulates the proliferation of patient-derived GSCs. PTHrP is secreted by GSCs to the extracellular environment. A high level of PTHrP significantly increases cAMP concentration via autocrine or paracrine routes. The PKA is activated due to a high level of cAMP, eventually promoting the proliferation of patient-derived GSCs. PTHR1: parathyroid hormone 1 receptor, PTHR2: parathyroid hormone 2 receptor, AC: adenylyl cyclase.
International Journal of Stem Cells 2023;16:315-25 https://doi.org/10.15283/ijsc22097
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