Mitochondrial transfer is a naturally occurring cellular phenomenon involving the intercellular transport of functional mitochondria from donor cells to recipient cells with impaired mitochondrial function. If appropriately regulated, this phenomenon may serve as a therapeutic strategy for disorders associated with mitochondrial dysfunction. However, the underlying mechanisms governing mitochondrial transfer remain largely unknown, primarily due to difficulties in long-term, precise mitochondrial labeling. In particular, the molecular cues "help-me signals" released by metabolically stressed recipient cells that trigger mitochondrial donation from donor cells are not well understood. We previously reported a method to detect mitochondrial transfer using precise fluorescent labeling with a red fluorescent protein, turbo RFP. We demonstrated that human amniotic epithelial cells (hAECs), a type of placental stem cell possessing pluripotent stem cell-like differentiation potential, immunomodulatory, and anti-inflammatory properties, can transfer their healthy mitochondria to recipient cells. Here, we hypothesized that recipient cells with damaged mitochondria release the molecular cues initiating mitochondrial transfer. To gain insights, we first performed live-cell imaging to observe mitochondrial transfer processes. We used hAECs with fluorescently labeled mitochondria (tRFPmit-hAECs) as donor cells and HEK293T cells, whose mitochondrial function was impaired by mild hydrogen peroxide treatment, as recipient cells. Additionally, we established a ρ⁰ derivative of the HLE cell line, which lacks functional mitochondria, and performed co-culture experiments with donor tRFPmit-hAECs. Comprehensive gene expression analyses were performed to compare the transcriptomic profiles of recipient cells with and without uptake of fluorescently labeled mitochondria. In results, the gene ontology analyses revealed that the mitochondria received recipient cells differentially expressed genes including mitochondrial respiratory functions and genes associated with the "help-me signals". Our results indicate that recipient cells of mitochondrial transfer exhibit a unique gene expression profile. These findings lay the groundwork for further investigations into the detailed analysis of the molecular cues "help-me signals", which may facilitate the identifying small molecules to precisely regulating this process, ultimately facilitating its therapeutic application.