The static magnetic fields (SMFs) impact on biological systems, induce a variety of biological responses, and have been applied to the clinical treatment of diseases. However, the underlying mechanisms remain largely unclear. In this report, by using human mesenchymal stem cells (MSCs) as a model, we investigated the biological effect of SMFs at a molecular and cellular level. We showed that SMF exposure promotes MSC proliferation and activates the expression of transcriptional factors such as FOS (Fos Proto-Oncogene, AP-1 Transcription Factor Subunit) and EGR1 (Early Growth Response 1). In addition, the expression of signal-transduction proteins p-ERK1/2 and p-JNK oscillate periodically with SMF exposure time. Furthermore, we found that the inhibition of the T-type calcium ion channels negates the biological effects of SMFs on MSCs. Together, we revealed that the SMFs regulate T-type calcium ion channels and mediate MSC proliferation via the MAPK signaling pathways.

Thymidine analogs have long been recognized for their ability to randomly incorporate into DNA. However, their significance in the chemical induction of pluripotency (CIP) remains unclear. Here, we investigated the impact of BrdU/IdU incorporation on the transition of cell fate through DNA damage repair (DDR). Our findings reveal a substaintial upregulation of reprogramming mediator gene H3K27ac and H3K9ac, as well as global DNA demethylation in response to DDR. This process creates a hypomethylated environment that promotes cell fate transition. We term this mechanism as Epigenetic Reshaping through Damage (ERD). Overall, our study sheds light on the dynamic interplay between thymidine analogs, DDR, and epigenetic modifications, providing valuable insights into the mechanisms underlying cell fate transition.

Somatic cells can be reprogrammed into pluripotent stem cells (iPSCs) by overexpressing de-fined transcription factors. Specifically, OCT4 single factor overexpression has been shown to reprogram mouse fibroblasts into iPSCs. Yet, whether other single factor can induce iPSCs from fibroblasts remains unknown. Here, we demonstrate that, under an optimized reprogram-ming medium iCD4, SALL4 alone is capable to reprogram mouse fibroblast into iPSCs. Mech-anistically, SALL4 inhibits somatic genes and activates pluripotent genes (Rsk1, Esrrb and Tfap2c) to facilitate reprogramming. Furthermore, we show that co-overexpressing SALL4 and OCT4 enhances reprogramming efficiency synergistically. In detail, SALL4-activated Rsk1/Esrrb/Tfap2c, OCT4-activated Sox2, SALL4-suppressed Nkx6.1, and OCT4-suppressed Sbsn cooperate to facilitate SALL4/OCT4-mediated reprogramming. Overall, our study estab-lishes an efficient method for iPSCs induction using SALL4 single factor, and provides in-sights into the synergistic effects of SALL4 and OCT4 during somatic cell reprogramming.