Chronic obstructive pulmonary disease is a common chronic lung disease with an ever-increasing incidence. Despite years of drug research and approvals, we are still not able to halt progress or restore normal lung function. Our previous studies have demonstrated that liver growth factor—LGF has an effect on the repair of the affected tissue in a mouse model of cigarette smoke exposure, but by what pathways it achieves this is unknown. The present study aimed to identify differentially expressed genes between emphysematous mice treated with LGF to identify potential therapeutic targets for the treatment of pulmonary emphysema. The emphysema mouse model was induced by prolonged exposure to cigarette smoke. To determine the gene expression profile of the lung in smokers treated or not with LGF, lung messenger RNA gene expression was assessed with the Agilent Array platform. We carried out differentially expressed gene analysis, functional enrichment and validated in treated mouse lung samples. The treated group significantly improved lung function (~35%) and emphysema level (~20%), consistent with our previous published studies. Microarray analysis demonstrated 290 differentially expressed genes in total (2.0-fold over or lower expressed). Injury repair-associated genes and pathways were further enhanced in the lung of LGF treated mice. The expression trends of two genes (Zscan2 and Bag6) were different in emphysematous lungs treated with LGF compared to untreated lungs. Therefore, Zscan2 and Bag6 genes could play a role in regulating inflammation and the immune response in the lung that undergoes partial lung regeneration. However, further studies are necessary to demonstrate this causal relationship.

Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder. It is characterized by the accumulation of misfolded α-synuclein (α-syn) and progressive loss of dopaminergic neurons in the substantia nigra. Due to the limitations of current therapies, mesenchymal stromal cell (MSC) transplantation has emerged as a promising neuroprotective strategy. This study evaluated the neuroprotective potential of decidua-derived mesenchymal stromal cells (DMSCs) in vitro using a human neuroblastoma cell line (NB69) exposed to the neurotoxin 1-methyl-4-phenylpyridinium (MPP+) as a PD model. The NB69 cells were differentiated into a mature dopaminergic phenotype using dibutyryl cyclic adenosine monophosphate (dbcAMP) and then exposed to MPP+. In proliferative NB69 cells, the effect of DMSCs was masked by their inherent antitumor activity against the neuroblastoma phenotype. Conversely, in the differentiated NB69 model, DMSCs demonstrated a significant protective role against MPP+-induced cytotoxicity. Interestingly, the mechanism by which DMSCs might exert a neuroprotective effect against MPP+ damage in differentiated NB69 cells appears to involve improving mitochondrial function by reducing free radicals. In summary, these findings suggest that DMSCs exert a neuroprotective effect in a dopaminergic-like context and highlight the importance of using differentiated cell models to accurately evaluate cell-based therapies for PD in the striatum.

Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder, characterized by the accumulation of misfolded α-synuclein (α-syn), with the progressive loss of dopaminergic neurons in the substantia nigra. Given the limitations of current therapies, mesenchymal stromal cell (MSC) transplantation has emerged as a promising neuroprotective strategy. This study evaluated the in vitro neuroprotective potential of decidua-derived mesenchymal stem cells (DMSC) using neurotoxin 1-methyl-4-phenylpyridinium (MPP+) neurotoxin-induced damage in a human neuroblastoma cell line (NB69) as a model for PD. NB69 cells were differentiated into a mature dopaminergic phenotype using dibutyryl cyclic adenosine monophosphate (dbcAMP) and subsequently exposed to the MPP+. In proliferative NB69 cells, the effect of DMSC was masked by their inherent anti-tumor activity against the neuroblastoma phenotype. Conversely, in the differentiated NB69 model, DMSC demonstrated a significant protective role against MPP+-induced cytotoxicity. It is interesting that the mechanism by which DMSCs exert a neuroprotective effect against MPP+ damage in differentiated NB69 cells could be through an improvement in mitochondrial function by reducing free radicals. In summary, these findings suggest that DMSC exert a neuroprotective effect in a dopaminergic-like context and highlight the importance of using differentiated cell models to accurately evaluate cell-based therapies for PD in the striatum.