Since the human lifespan has been extended in the past decades, age-related diseases have become a significant societal problem. Thus, life science research is increasingly attempting to develop approaches to delay or attenuate aging and age-related diseases. These attempts target mostly cell-autonomous factors. However, it has been shown that during aging cell populations become increasingly heterogenous, with some cells still young and functional and others damaged or dying. This has raised an interest in the role of non-cell-autonomous factors in aging, i.e. how cells with different phenotypes affect each other. In this study I tested the hypothesis of cellular parabiosis, which states that the cellular damage may be phenotypically supressed by intercellular communication with the surrounding healthy cells. Cellular damage was induced in the immortalized hamster lung fibroblasts by staurosporine - an inducer of apoptosis. Sublethal dose of staurosporine that allows recovery of the cells after removal of the treatment was determined using a cell viability assay. Mammalian cells were then treated with such dose of staurosporine, and grown either in the monoculture or in the co-culture with healthy cells. Comparison of the numbers of surviving cells between the two conditions was performed by flow cytometry. The results showed that the recovery of the damaged cells was significantly higher in co-culture with the healthy cells compared to the monoculture conditions. Next, I tested the involvement of the tunneling nanotube-mediated intercellular communication in this recovery. The same experiment was performed in the presence or absence of the actin polymerization inhibitor latrunculin B, which also inhibits the formation of the tunneling nanotubes. The efficiency and lack of toxicity of latrunculin B was confirmed by imaging the actin cytoskeleton using fluorescent microscopy and by the cell viability assay, respectively. Comparing the results obtained in the presence or absence of latrunculin B showed that latrunculin B partially inhibited the recovery of the damaged cells in co-culture, suggesting the involvement of the tunneling nanotubes in the process. These results support the initial hypothesis of cellular parabiosis, as well as the importance of non-cell-autonomous factors in damaged phenotype supression.