Menstrual blood-derived stem cells (MenSCs) are a novel source of mesenchymal stem cells (MSCs). MenSCs are attracting more and more attention since their discovery in 2007. MenSCs also have no moral dilemma and show some unique features of known adult-derived stem cells, which provide an alternative source for the research and application in regenerative medicine. Currently, people are increasingly interested in their clinical potential due to their high proliferation, remarkable versatility, and periodic acquisition in a non-invasive manner with no other sources of MSCs that are comparable in adult tissue. In this review, the plasticity of pluripotent biological characteristics, immunophenotype and function, differentiative potential, and immunomodulatory properties are assessed. Furthermore, we also summarize their therapeutic effects and functional characteristics in various diseases, including liver disease, diabetes, stroke, Duchenne muscular dystrophy, ovarian-related disease, myocardial infarction, Asherman syndrome, Alzheimer’s disease, acute lung injury, cutaneous wound, endometriosis, and neurodegenerative diseases. Subsequently, the clinical potential of MenSCs is investigated. There is a need for a deeper understanding of its immunomodulatory and diagnostic properties with safety concern on a variety of environmental conditions (such as epidemiological backgrounds, age, hormonal status, and pre-contraceptive). In summary, MenSC has a great potential for reducing mortality and improving the quality of life of severe patients. As a kind of adult stem cells, MenSCs have multiple properties in treating a variety of diseases in regenerative medicine for future clinical applications.

Oxidation of calmodulin-dependent protein kinase II (ox-CaMKII) by ROS has been associated with asthma. However, the contribution of ox-CaMKII to the development of asthma remains to be fully characterized. Here, we tested the effect of ox-CaMKII on IgE-mediated mast cell activation in an allergen-induced mouse model of asthma using oxidant-resistant CaMKII MMVVδ knockin (MMVVδ) mice. Compared with WT mice, the allergen-challenged MMVVδ mice displayed less airway hyperresponsiveness (AHR) and inflammation. These MMVVδ mice exhibited reduced levels of ROS and diminished recruitment of mast cells to the lungs. OVA-activated bone marrow–derived mast cells (BMMCs) from MMVVδ mice showed a significant inhibition of ROS and ox-CaMKII expression. ROS generation was dependent on intracellular Ca ²⁺ concentration in BMMCs. Importantly, OVA-activated MMVVδ BMMCs had suppressed degranulation, histamine release, leukotriene C4, and IL-13 expression. Adoptive transfer of WT, but not MMVVδ, BMMCs, reversed the alleviated AHR and inflammation in allergen-challenged MMVVδ mice. The CaMKII inhibitor KN-93 significantly suppressed IgE-mediated mast cell activation and asthma. These studies support a critical but previously unrecognized role of ox-CaMKII in mast cells that promotes asthma and suggest that therapies to reduce ox-CaMKII may be a novel approach for asthma.

Transformation to small cell lung cancer (SCLC) is one of the mechanisms of resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). However, it is uncertain how it works and there is no standard treatment after the transformation. In this study, 7 patients with transformation of SCLC from advanced lung adenocarcinoma (ADC) were analyzed retrospectively and the clinical pathology, imaging characteristics and treatment were analyzed. We identified 7 patients with primary lung ADC that showed transformation to SCLC on second biopsy during a 6-year period. Clinicopathologic information was analyzed and EGFR mutation results were performed in initial biopsy samples. Seven patients showed transformation from ADC to SCLC, of which 6 patients were 19 del EGFR mutation, only 1 patient is L858R mutations. The imaging forms did not have the typical imaging features of primary SCLC. All patients underwent etoposide and carboplatin (EC) regimen chemotherapy after pathological transformation. However, the response rate of EC was less than primary small cell lung cancer. One of the patients was receiving EC for 4 cycles. After chemotherapy the patients performed radiation therapy and finally with erlotinib maintains treatment, the progress free survival (PFS) was more than 12 months. NSCLC can acquire a neuroendocrine phenotype with EGFR-TKI treatment. The transmutation is more common in 19del mutation patients. A comprehensive treatment based on EC regimen chemotherapy and the maintenance with EGFR-TKI is likely to be the appropriate treatment for these patients.