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Psoriasis is a multifactorial disease and the mechanisms involved in its pathogenesis remain to be elucidated. FOS-like antigen 1 (Fra-1) is a proto-oncogene. It is a negative inhibitor of activator protein-1 activity and possesses transforming activity. The effect of and possible mechanisms underlying Fra-1 in psoriasis remain to be elucidated. In the present study, western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) techniques were used to identify differentially expressed Fra-1 in psoriatic and in normal control tissues. Compared with the control samples, the expression of normalized Fra-1 genes in psoriasis was 12.6 times higher. Western blot analysis was used to assess the protein levels of Fra-1. The results demonstrated that the protein expression of Fra-1 was high in tissues affected by psoriasis. This also corresponded with the results of RT-qPCR. Fra-1-stable expressing HaCaT/Fra-1 or control HaCaT/vector cell lines were then generated to elucidate the function of Fra-1 in the growth of HaCaT cells. The results demonstrated that Fra-1 promoted the growth of HaCaT cells in vitro by arresting the cell cycle and inhibiting cell apoptosis. These results suggested that Fra-1 may be important in psoriasis. [ABSTRACT FROM AUTHOR]

Cerebral palsy (CP) is a condition resulting from perinatal brain injury and can lead to physical disabilities. Exosomes derived from human amniotic mesenchymal stromal cells (hAMSC-Exos) hold promise as potential therapeutic options. This study aimed to investigate the impact of hAMSC-Exos on neuronal cells and their role in regulating apoptosis both in vitro and in vivo. hAMSC-Exos were isolated via ultracentrifugation and characterized via transmission electron microscopy, particle size analysis, and flow cytometry. In vitro, neuronal damage was induced by lipopolysaccharide (LPS). CP rat models were established via left common carotid artery ligation. Apoptosis levels in cells and CP rats were assessed using flow cytometry, quantitative reverse transcription polymerase chain reaction (RT–qPCR), Western blotting, and TUNEL analysis. The results demonstrated successful isolation of hAMSC-Exos via ultracentrifugation, as the isolated cells were positive for CD9 (79.7%) and CD63 (80.2%). Treatment with hAMSC-Exos significantly mitigated the reduction in cell viability induced by LPS. Flow cytometry revealed that LPS-induced damage promoted apoptosis, but this effect was attenuated by treatment with hAMSC-Exos. Additionally, the expression of caspase-3 and caspase-9 and the Bcl-2/Bax ratio indicated that excessive apoptosis could be attenuated by treatment with hAMSC-Exos. Furthermore, tail vein injection of hAMSC-Exos improved the neurobehavioral function of CP rats. Histological analysis via HE and TUNEL staining showed that apoptosis-related damage was attenuated following hAMSC-Exo treatment. In conclusion, hAMSC-Exos effectively promote neuronal cell survival by regulating apoptosis, indicating their potential as a promising therapeutic option for CP that merits further investigation. [Display omitted] • hAMSC-Exos enhance neurobehavioral outcomes in cerebral palsy model rats. • hAMSC-Exos counteract LPS-induced damage, preserving neuronal viability in vitro. • Caspase-3 expression, Caspase-9 expression, the Bcl-2/Bax ratio suggest that hAMSC-Exos suppress apoptosis. • hAMSC-Exos have potential clinical value in cerebral palsy treatment. [ABSTRACT FROM AUTHOR]