Bone defects resulting from severe trauma, tumors, inflammation, and other factors are increasingly prevalent. Stem cell-based therapies have emerged as a promising alternative. Dental pulp stem cells (DPSCs), sourced from dental pulp, have garnered significant attention owing to their ready accessibility and minimal collection-associated risks. Ongoing investigations into DPSCs have revealed their potential to undergo osteogenic differentiation and their capacity to secrete a diverse array of ontogenetic components, such as extracellular vesicles and cell lysates. This comprehensive review article aims to provide an in-depth analysis of DPSCs and their secretory components, emphasizing extraction techniques and utilization while elucidating the intricate mechanisms governing bone regeneration. Furthermore, we explore the merits and demerits of cell and cell-free therapeutic modalities, as well as discuss the potential prospects, opportunities, and inherent challenges associated with DPSC therapy and cell-free therapies in the context of bone regeneration.

Application of dental pulp stem cells for bone regeneration

Cells can produce stress granules (SGs) to protect itself from damage under stress. The cGAS-STING pathway is one of the important pattern recognition pathways in the natural immune system. This study was investigated whether human mesenchymal stem cells (hMSCs) could protect the liver by inducing M2 macrophages to produce SGs during acute drug induced liver injury (DILI) induced by acetaminophen (APAP). After intragastric administration of APAP in vivo to induce DILI mice model, hMSCs were injected into the tail vein. The co-culture system of hMSCs and M2 macrophages was established in vitro. It was further use SGs inhibitor anisomicin to intervene M2 macrophages. The liver histopathology, liver function, reactive oxygen species (ROS) level, apoptosis pathway, endoplasmic reticulum stress (ERS) level, SGs markers (G3BP1/TIA-1), cGAS-STING pathway, TNF-α, IL-6, IL-1β mRNA levels in liver tissue and M2 macrophages were observed. In vivo experiments, it showed that hMSCs could alleviate liver injury, inhibite the level of ROS, apoptosis and ERS, protect liver function in DILI mice. The mount of M2 was increased in the liver. hMSCs could also induce the production of SGs, inhibit the cGAS-STING pathway and reduce TNF-α, IL-6, IL-1β mRNA expression. The results in vitro showed that hMSCs could induce the production of SGs in macrophages, inhibit the cGAS-STING pathway, promote the secretion of IL-4 and IL-13, and reduce TNF-α, IL-6, IL-1β mRNA level in cells. In the process of IL-4 inducing M2 macrophage activation, anisomycin could inhibit the production of SGs, activate the cGAS-STING pathway, and promote the inflammatory factor TNF-α, IL-6, IL-1β mRNA expression in cells. HMSCs had a protective effect on acute DILI in mice induced by APAP. Its mechanism might involve in activating M2 type macrophages, promoting the production of SGs, inhibiting the cGAS-STING pathway, and reducing the expression of pro-inflammatory factors in macrophages, to reduce hepatocytes damage. 

Inhibition of cGAS-STING pathway by stress granules after activation of M2 macrophages by human mesenchymal stem cells against drug induced liver injury.

Ectodermal mesenchymal stem cells (EMSCs) are cells harvested from the stem cell niche (nasal mucosa) with high therapeutic potential. To the best of our knowledge, however, the anti‑inflammatory properties of these neural crest‑derived EMSCs have been rarely reported. The present study aimed to explore the effects of aerosolized EMSC‑Secretome (EMSC‑Sec) and clarify underlying mechanisms in treating acute lung injury (ALI). EMSCs were isolated by adherent method and identified by immunofluorescence staining. EMSC‑Sec was collected and evaluated using western blotting, BCA and ELISA tests. Then, mouse lung epithelial cells (MLE‑12) were used to mimic inflammatory stimulation with lipopolysaccharide (LPS). After developing an ALI model through intraperitoneal injection of LPS, mice were treated with an EMSC‑Sec spray. The lung in each group underwent an observation and measurement to preliminarily assess the extent of damage. H&E staining, immunohistochemical staining, immunofluorescence and western‑blotting were utilized to further access the impacts of EMSC‑Sec. The results showed that EMSC‑Sec had great anti‑inflammatory potential and was highly successful in vitro and in vivo. EMSC‑Sec mitigated LPS‑induced ALI with low inflammatory cell inflation and mild damage. EMSC‑Sec could regulate inflammation via the NF‑κB(p50/p65)/NLRP3 pathway. Overall, the present study demonstrated that EMSC‑Sec regulated inflammation, hoping to provide a novel strategy for ALI treatment. 

Secretome of EMSCs neutralizes LPS‑induced acute lung injury via aerosol administration

Abstract Spinal cord injury is a severe central nervous system disease. Neural crest-derived ectoderm mesenchymal stem cells (EMSCs) have become an important tool in treating SCI owing to their excellent neuronal differentiation efficiency and promising paracrine effects. Sonic hedgehog (shh) was proven to promote both the proliferation and chemotaxis of NSCs and induce their differentiation into mature neurons and the formation of synapses. In this study, we examined the neuronal differentiation induced by SHH-engineered EMSCs in a co-culture system. The levels of the neuronal markers, tubulin beta 3 class III and growth-associated protein 43, were higher in NSCs in the SHH-EMSC co-culture group, and those of the astrocytic marker glial fibrillary acidic protein (GFAP) were lower, compared with the mono and EMSCs-NSCs groups The expression of GAP43, GFAP, MBP, and NF200 was also confirmed by western blot analysis. Most importantly, the upregulation of con43, con47, smoothen, and integrin might reveal the construction of the gap junction during the overexpression of SHH in EMSCs. Overall, our findings indicate that SHH-EMSCs might facilitate the neuronal differentiation of NSCs via the gap junction formation. 

/pdf/enhanced-neuronic-differentiation-of-neural-stem-cells-by-1gid705r.pdf

Enhanced neuronic differentiation of neural stem cells by SHH gene-engineered EMSCs co-culture in vitro

Abstract Tripartite Motif Containing 35 (TRIM35) is a well-characterized ubiquitin ligase with established roles in antiviral immunity, cancer metabolism, cardiovascular function, and tumor progression. However, its function as a DNA-binding protein has not been previously explored. In this study, we provide the first evidence that TRIM35 directly binds genomic promoters, thereby identifying it as a novel regulator of gene transcription. This finding opens new avenues for understanding the biological functions of TRIM35, expanding its potential role in cellular regulation. Furthermore, our results show that TRIM35 interacts with histone H3 (H3) and catalyzes its non-proteolytic ubiquitination, which serves as a recruitment signal for p300, leading to subsequent H3K27 acetylation and activation of gene transcription. Notably, among the genes regulated, Heat Shock Protein Family A (Hsp70) Member 6 (HSPA6) is significantly upregulated through TRIM35-mediated transcriptional regulation, which suppresses breast cancer progression and mediates TRIM35’s anti-tumor effect. Collectively, our findings reveal a previously unrecognized mechanism by which TRIM35 regulates gene expression through targeted epigenetic modification, providing new insights into its tumor-suppressive role in breast cancer. 

pdf/trim35-a-novel-dna-binding-protein-epigenetically-modifies-hzqcuwfs3mzb.pdf

TRIM35, a novel DNA-binding protein, epigenetically modifies H3 to promote HSPA6 transcription and suppress breast cancer progression

Acute liver injury (ALI) induced by sepsis seriously endangers the health of human beings every year. Mesenchymal stem cells (MSCs) lysate containing various regulators had a positive effect on anti-inflammation, hoping to provide a promising strategy in ALI.Olfactory mucosa-derived mesenchymal stem cells (OM-MSCs) were extracted and identified. The collected OM-MSCs were prepared after repeated freeze-thaw in phosphate buffer solution (PBS). Then, OM-MSCs lysate was filtered for future experiments. To understand the composes of OM-MSCs clearly, we detected the components of OM-MSCs lysate by western blotting. In vitro, OM-MSCs lysate was applied to evaluate the effects on normal human liver cells (LO-2) under stimulation of LPS. Lipopolysaccharide (LPS) was also injected intraperitoneally to build ALI model in mice. We further assessed the anti-inflammatory capacity of OM-MSCs lysate on ALI in vivo by aminotransferase determination, pathology observation, and immunohistochemical staining. Moreover, the immunoblot technique was performed to recognize the changes in inflammatory factors and related proteins.In this study, we found that OM-MSCs lysate could protect structure effectively, improve the plasma aminotransferases, diminish inflammation by releasing interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β). A significant decrease in tumor necrosis factor-α (TNF-α) also occurred under the treatment of OM-MSCs lysate. In addition, trophic factors originating from OM-MSCs lysate provided a supportive micro-environment for liver recovery. Especially, up-expression of vascular endothelial growth factor (VEGF) in vivo revealed that OM-MSCs might have a great potential for healing.Our results demonstrated that OM-MSCs lysate could alleviate LPS-induced ALI via decreasing inflammatory cytokines and promoting recovery. 

/pdf/olfactory-mucosa-tissue-derived-mesenchymal-stem-cells-2jg35dyw.pdf

Olfactory mucosa tissue-derived mesenchymal stem cells lysate ameliorates LPS-induced acute liver injury in mice

E2F1 Mediates Traumatic Brain Injury and Regulates BDNF-AS to Promote the Progression of Alzheimer's Disease.

There are a lot of studies on the treatment of tumors with hyperbaric oxygen, while most of them are in breast cancer, prostate cancer and so on. However, there are still few studies on hyperbaric oxygen in treating hepatocellular carcinoma (HCC). According to the current data, hyperbaric oxygen is an effective means to intervene in tumors. The Warburg effect is a unique marker of glucose metabolism in tumors related to hypoxia, making it possible for hyperbaric oxygen to interfere with the tumor through the Warburg effect.We used the hypoxia/hyperbaric oxygen(HBO)-exposed HCC cells for in vitro studies. Glucose uptake, lactic acid, and adenosine triphosphate (ATP) assessed the Warburg effect. The expression of miR-103a-3p in HCC was detected by using qRT-PCR. The effect of miR-103a-3p/TRIM35 expression level on the cells was measured using the CCK8 method and flow cytometry. The molecular biological mechanism of miR-103a-3p in HCC was examined using the luciferase reporter, MS2-RIP assays.HBO inhibited the Warburg effect in hypoxic HCC cells. HBO suppressed the expression of miR-103a-3p in hypoxic HCC cells, and miR-103a-3p inhibited the expression of TRIM35 in hypoxic HCC cells. With HBO exposure, miR-103a-3p/TRIM35 regulated the Warburg effect of hypoxic HCC cells.These findings reveal that HBO regulates the Warburg effect of hypoxic HCC cells through miR-103a-3p/TRIM35 and inhibits tumor growth. 

HBO regulates the Warburg effect of hypoxic HCC cells through miR-103a-3p/TRIM35.

Fructus lycii oligosaccharide alleviates acute liver injury via PI3K/Akt/mTOR pathway

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Olfactory mucosa tissue-derived mesenchymal stem cells lysate ameliorates LPS-induced acute liver injury in mice

E2F1 Mediates Traumatic Brain Injury and Regulates BDNF-AS to Promote the Progression of Alzheimer's Disease.

HBO regulates the Warburg effect of hypoxic HCC cells through miR-103a-3p/TRIM35.

Fructus lycii oligosaccharide alleviates acute liver injury via PI3K/Akt/mTOR pathway