PEMF is a method that utilizes electric current using a coil that is powered by dynamic electric current, it will cause a dynamic magnetic field in the coil. In the last few decades, it is known that PEMF has the potential to be used as a modality in the treatment of obesity. For this reason, PEMFs have been studied in vitro as their effect in inhibiting the adipogenesis of Mesenchymal Stem Cells (MSC). But the use of PEMF therapy in inhibiting adipogenesis still has many challenges. Understanding of the mechanisms that occur in cells that are exposed to PEMF is also still very slight. This article reviews the studies that investigated in vitro effect of PEMF in inhibiting adipogenesis studies and the underlying mechanism. In the future, it is hoped that this review can be used as a basic reference for in vivo research and clinical trials related to inhibiting adipogenesis using PEMF.

Objective: This study aims to investigate the possibility of additive cytotoxic effects of cisplatin and Andrographis paniculate (Burm. f.) Nees(AP) via apoptotic, cell cycle and angiogenesis pathways. Methods: CC50 cisplatin, AP and Andrographolide (AG) were determined by the cell viability of SKOV3 after its exposure to these substances. SKOV3 cells were then divided into 6 experimental groups: one negativecontrol group, one with CC50 cisplatin alone, and three where CC50 was combined with CC50 AP, ½CC50 AP, and 1.5CC50 AP, respectively. The additive cytotoxic effect of cisplatin with AP or AG was evaluated through the modulation of several pathways via qRT-PCR of their markers: apoptotic pathways indicated by Bax, BCL2, Caspase 3 and Caspase 9 expression; cell cycle indicated by Cyclin-D expression; angiogenesis pathways by VEGF expression. Results: Cisplatin reduces cell viability to 54%, 37% when combined with AG, and 30%, 23% and 20% with ½CC50 AP, CC50 AP and 1.5CC50 AP, respectively. AG and AP extract decreases SKOV3 cell viability in a dose-dependent manner. Cisplatin combined with AP showed a statistically significant increase in BAX, Caspase 3, Caspase 9 expression and a decrease in BCL2, which indicated synergy in apoptotic pathways. The best result was seen in cisplatin combined with ½CC50 AP. A decrease in Cyclin D and VEGF was seen in all groups, the best seen in ½CC50 AP and CC50 AP, respectively, showing optimal cell cycle arrest and anti-angiogenesis properties when cisplatin is combined with AP extract. Conclusion: Combining cisplatin with AP extract enhanced cell cycle arrest, apoptosis, and anti-angiogenesis properties.

Bone morphogenetic protein 2 (BMP-2) is a protein or growth factor that plays an important role in osteogenic differentiation. Recently, there is an increasing demand for BMP-2, as it is the only osteoinductive growth factor approved by the Food and Drug Administration (FDA) as a substitute for bone grafts. However, recombinant BMP-2 production suffers from low production yields and changes in the biological function of the protein due to the low efficiency of translocation in production hosts. One of the key regulators that influences the efficiency of protein translocation is the signal peptide (SP). SP regulates the process of post-translational protein modification, which determines the fate of the synthesized protein. This literature review aims to explore the role of SP in the process of recombinant protein production in mammalian cells and the utilization of SP in BMP-2 production in the secretome of mesenchymal stem cells (MSCs). The production of recombinant proteins in the MSC secretome is expected to be an innovative therapy because it combines the positive effects of the secretome and BMP-2 together for bone healing.

Background/Objectives: Mesenchymal stem cells (MSCs) are recognized for their therapeutic potential due to their ability to secrete bioactive molecules. Among these secreted factors, bone morphogenetic protein-2 (BMP-2) is known as a secreted factor that plays a crucial role in bone healing and regeneration. However, MSCs naturally secrete only small amounts of BMP-2. To improve the bone healing capacity of MSCs, it is essential to enhance the secretion of BMP-2 in MSCs. One approach that can be used to achieve this goal is by genetically engineering MSCs. Incorporating signal peptides (SPs) into the inserted gene sequence can significantly improve protein secretion efficiency. In this proof-of-concept study, we explored the role of SPs in optimizing BMP-2 secretion in umbilical cord-derived MSCs; Methods: Three human-derived SPs, namely glial-derived neurotrophic factor (GDNF), chemotactic antibacterial glycoprotein 7 (CAP7), and platelet-derived growth factor subunit B (PDGFB), were selected. Transfection of MSCs was performed using polyethylenimine, Lipofectamine 2000^®, and Lipofectamine 3000^®. Transfection efficiency confirmed based on Green Fluorescence Protein expression. BMP-2 secretion levels were quantified using an ELISA assay; Results: Lipofectamine 3000^® achieved the highest transfection efficiency, reaching approximately 10%. BMP-2 secretion levels varied significantly depending on the SPs used, with PDGFB yielding the highest BMP-2 concentration (279.21 ± 6.91 pg/mL), followed by GDNF (265.65 ± 11.49 pg/mL) and CAP7 (233.72 ± 32.33 pg/mL); Conclusions: These findings demonstrate that SP selection critically influences BMP-2 secretion efficiency in genetically engineered MSCs and underscore its potential to enhance the therapeutic applicability of MSC-based strategies for bone healing.