The Use of 810 and 1064 nm Lasers on Dental Implants: In Vitro Analysis of Temperature, Surface Alterations, and Biological Behavior in Human Gingival Fibroblasts.

Objective: The primary objective of this study was to evaluate the safety of 810 and 1064 nm laser treatment on dental implants. Background: Peri-implantitis is a challenge for clinicians and researchers. Methods: A pig mandible model was used to evaluate temperature increases during laser irradiation. Surface alterations on processed pure titanium discs were analyzed via scanning electron microscopy and measurement of surface contact angles. Processed titanium discs were cocultured in vitro with human gingival fibroblasts; subsequently, cell proliferation was measured. Results: The maximum temperature and time to reach each threshold were comparable. No surface alterations were detected after 810 nm laser irradiation, whereas surface cracks were observed after 1064 nm laser irradiation under the parameter setting of 31.84 W/cm2. Compared with unaltered processed pure titanium discs, the proliferation of human gingival fibroblasts was significantly greater on altered processed pure titanium discs. Conclusions: The use of either 810 or 1064 nm laser treatments may increase the risk of thermal damage in terms of increased temperature if the parameter setting is not warranted. In addition, the use of 1064 nm laser treatment could lead to changes in pure titanium discs that do not negatively affect cell proliferation. Further investigations of laser-assisted therapy are necessary to improve guidelines concerning the treatment of peri-implantitis. Clinical trial registration number: 2021-P2-098-01.

ApoC1 promotes glioma metastasis by enhancing epithelial-mesenchymal transition and activating the STAT3 pathway.

OBJECTIVE: One of the apolipoprotein's members, apolipoprotein C1 (ApoC1), is critical in the metabolism of both very-low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) cholesterols. Multiple studies have recently revealed that ApoC1 may be a viable therapeutic target in solid malignancies. However, the motor protein ApoC1's specific role and mechanism in glioblastoma remain unknown. METHODS: In this study, the Cancer Genome Atlas (TCGA) database was used to look at the level of ApoC1 in glioma tissues and normal tissues, as well as how it related to the prognosis of glioma. Glioma cell lines (U87 and U251) were subjected to a wide range of experiments to determine the involvement of ApoC1 in cell proliferation, migration, and invasion. RESULTS: Cell proliferation, migration, and invasion decreased in glioma cell lines when ApoC1 was silenced. Furthermore, ApoC1 increased glioma cell metastasis through the epithelial-mesenchymal transition (EMT), while ApoC1 deletion reduced this impact. Additionally, APOC1 influenced the evolution of glioma by affecting the STAT3 pathway. In addition, APOC1 knockdown reduced the activation of the phosphorylated-total signal transducer and activator of transcription (STAT3) in the glioma cells. ApoC1-induced glioma cell metastatic ability was prevented by niclosamide (a STAT3 inhibitor). CONCLUSIONS: These results uncover that ApoC1 may serve as a biomarker or therapeutic target for future fundamental study or clinical treatment of glioma.

Tetramethylpyrazine Inhibits the Proliferation and Invasion of Glioma Cells by Regulating the UBL7-AS1/miR-144-3p Pathway.

This work aims to investigate the effects of tetramethylpyrazine (TMP) on the proliferation, migration, and invasion of glioma cells and to analyze the regulation mechanism of TMP on the long noncoding RNA UBL7-AS1/miR-144-3p pathway. Glioma cell line and normal astrocytes were collected. The expression of UBL7-AS1 was detected by real-time PCR. The glioma cells were overexpressed with UBL7-AS1. CCK-8 and Transwell assays were used to detect cell proliferation and cell invasion ability, respectively. Bioinformatics was adopted to predict the possible regulatory mechanisms of UBL7-AS1. The dual luciferase reporter gene was applied to verify the regulatory effect of RNA UBL7-AS1 with miR-144-3p. TMP inhibited the proliferation and invasion of glioma cells. UBL7-AS1 was highly expressed in glioma tissues and cells. The overexpression of UBL7-AS1 promotes the cell proliferation and invasion of glioma. UBL7-AS1 can act as a sponge for miR-144-3p in glioma cells. The overexpression of UBL7-AS1 can reverse the inhibition of TMP on proliferation, migration, and invasion of glioma cells. TMP inhibits the proliferation, migration, and invasion of glioma cells by regulating the UBL7-AS1/miR-144-3p pathway.

KDELR2 knockdown synergizes with temozolomide to induce glioma cell apoptosis through the CHOP and JNK/p38 pathways.

BACKGROUND: The C-terminal tetrapeptide Lys-Asp-Glu-Leu receptors (KDELRs) are transmembrane proteins that regulate ER stress (ERS) response, growth, differentiation, and immune responses. There is an association between KDELR2and promotion of glioblastoma tumorigenesis. The aim of the present study was to explore the functional mechanism of KDELR2 in glioma and during response to chemotherapy to temozolomide (TMZ). METHODS: The expression of KDELR2 in glioma tissues and cells was evaluated by immunohistochemistry, western blot and RT-qPCR assay. Then role of KDELR2 was demonstrated by CCK8, colony formation, flow cytometry and Hochest 33258 assays. The expression of genes (ATF4, ATF6, PERK, eIF2-α, GRP78 and CHOP) in U373 cells was evaluated by RT-qPCR. The protein expression of genes (cleaved caspase 3, caspase 3, cleaved PARP, PARP, Bax, Bcl-2, JNK, p-JNK, p38, p-p38, ATF4, ATF6, XBP-1s, PERK, p-PERK, GRP78 and CHOP) was measured by western blot assay. RESULTS: The expression of KDELR2 was upregulated in high-grade gliomas tissues. KDELR2 knockdown suppressed cell proliferation but increased cell apoptosis. Further, Knockdown of KDELR2 also activated the ER stress (ERS)-dependent CHOP pathway, and resulted in increased levels of phosphorylated c-Jun N-terminal kinase (JNK) and p38. Moreover, the combination of KDELR2 knockdown and TMZ application showed a synergistic cytotoxic effect in U373 cells through the ERS-dependent CHOP and JNK/p38 pathways. CONCLUSIONS: KDELR2 knockdown induces apoptosis and sensitizes glioma cells to TMZ, which is mediated by the ERS-dependent CHOP and JNK/p38 pathways.

LINC00467 knockdown repressed cell proliferation but stimulated cell apoptosis in glioblastoma via miR-339-3p/IP6K2 axis.

BACKGROUND: Glioma is considered to be one of the most common and lethal malignant brain tumors, accounting for 40% to 50% of brain tumors. Long non-coding RNAs (lncRNAs) have been widely proved to play an irreplaceable role in the tumorigenesis and progression. Nevertheless, the role of LINC00467 in glioblastoma remained unclear. AIM: The current study was aimed to explore the functional mechanism of LINC00467 in glioblastoma. METHODS: The expression of LINC00467/miR-339-3p/IP6K2 glioblastoma tissues and cells was evaluated by RT-qPCR. The protein expression of genes (cleaved PARP, PARP, cleaved caspase 3, caspase 3, Bax, Bcl-2 and IP6K2) was measured by western blot assay. Then role of LINC00467 was demonstrated by EdU, colony formation, flow cytometry and TUNEL assays. The relationship between miR-339-3p and LINC00467/IP6K2 was validated by RNA pull down and luciferase reporter assays. RESULTS: The expression of LINC00467 was upregulated in glioblastoma tissues and cells. LINC00467 knockdown suppressed cell proliferation but activated cell apoptosis. Further, LINC00467 high expression was associated with shorter overall survival rate in glioblastoma patients. Further, LINC00467 could bind with miR-339-3p, and IP6K2 was targeted by miR-339-3p. IP6K2 expression was regulated by LINC00467/miR-339-3p in a ceRNA pattern. Moreover, LINC00467 could regulate the development of glioblastoma via miR-339-3p/IP6K2 axis. CONCLUSIONS: LINC00467 knockdown repressed cell proliferation but stimulated cell apoptosis in glioblastoma via miR-339-3p/IP6K2 axis, which may enlighten to find a novel therapeutic tactic for glioblastoma patients.

New methods for inducing the differentiation of amniotic-derived mesenchymal stem cells into motor neuron precursor cells.

Our study investigates the differentiation of amniotic-derived mesenchymal stem cells (ADMSCs) into motor neuron (MN) precursor cells induced by a combination of extracellular matrix (ECM) and multi-cell factors. Membrane-like ECM was made by an enzymatic and chemical extraction method and exhibited good biological compatibility. Cells in the experimental group (EG) were treated with ECM and multi-cell factors in a multi-step induction process, while the control group (CG) was treated similarly, except without ECM. In the EG, after induction, the cells formed processes that connected with neighboring cells to form a net that had directionality. In these cells, neuron-specific enolase (NSE) and synaptophysin (SYN) expression levels increased and glial fibrillary acidic protein (GFAP) expression decreased. The SYN expression in the EG cells was higher compared with those in the CG. In the CG, NSE expression increased, while the expression of Nestin and SYN did not change. These were several changes in the levels of other genes: ADMSCs at passage 1 expressed Nanog, SOX2, octamer-binding transcription factor 4 (OCT4) and Nestin. In the EG, at the beginning of induction, the expression of Nanog decreased and that of SOX2 and Nestin increased. After 2 days, the cells expressed Nestin, OCT4 and SYNIII, and after 3 days, they expressed Olig2, OCT4, Nestin, SYNII and Islet1 (ISL1). Finally, at day 6, the cells expressed Nestin, SYNI, SYNIII, ISL-1, homeobox 9 (Hb9) and oligodendrocyte lineage transcription factor 2 (Olig2). In the CG, the cells never expressed SYNI, SYNII or Hb9. Our studies therefore demonstrate that the extracted ECM was capable of promoting the maturation of synapses. Human ADMSCs are composed of multiple cell subsets, including neural progenitor cells. The multi-step induction method used in this study causes human ADMSCs to differentiate into MN precursor cells.

[Improvement of spinal cord semi-transected and lump defect model by quantitate semi-transected blade in rats].

OBJECTIVE: To investigate the effect of quantitative semi-transected blade on the improvement of spinal cord semi-transected and lump defect model. METHODS: Forty-eight male Sprague Dawley rats (weighing 220-250 g) were divided into the experimental group (n = 24) and control group (n = 24). The spinal cord semi-transected and lump defect model was made by self-made quantitative semi-transected blade in the experimental group, and by ophthalmic scalpel in the control group. Then, the complications were observed; the electrophysiological results were detected before modeling and at 21 days after modeling; the histological changes at margin of lump defect were observed at 6 hours, 5 days, and 28 days; Basso, Beattie, and Bresnahan (BBB) scores were detected at 1, 3, 5, 7, 14, 21, 28, 35, 42, 56, and 84 days after modeling. RESULTS: There was significant difference in the mortality between the experimental group (0) and the control group (26.67%) (P = 0.028). Electrophysiological examination: there was no significant difference in latency and amplitude of motor evoked potentials (MEP) and sensory evoked potentials (SEP) between 2 groups at preoperation (P > 0.05); at 21 days after operation, latencies of MEP and SEP increased and the amplitude decreased in the control group, showing significant differences when compared with those in the experimental group and the preoperative values (P < 0.05), but no significant difference was seen between preoperation and postoperation in the experimental group (P > 0.05). Histological examination: in the control group, small hematoma could be observed at normal side at 6 hours after modeling, increased spaces of spinal tissue and perineural invasion were observed at 5 days, and small cavity formed without normal motoneurons at 28 days in the margin of lump defect. In the experimental group, no small hematoma could be observed at 6 hours after modeling, no inreversible injury of neuron and small cavity were observed at 5 days, and normal motoneurons were observed without small cavity at 28 days in the margin of lump defect. BBB scores: except the scores between experimental group and control group at affected side (P > 0.05), there were significant differences between groups, and between normal side and affected side for intragroup (P < 0.05). CONCLUSION: Semi-transected and lump defect model could be set up successfully by self-made quantitate semi-transected blade, procedure is repetitive and the model is stable. This model is an ideal model for semi-transected spinal cord injury.