Detection of mitochondrial coupling factor 6 in placental tissues from preeclamptic pregnancies and its influence on biological behavior of trophoblast cells

xlomafota13 shared this article with you from Inoreader Detection of mitochondrial coupling factor 6 in placental tissues from preeclamptic pregnancies and its influence on biological behavior of trophoblast cells Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1185. doi: 10.3892/etm.2021.10619. Epub 2021 Aug 16. ABSTRACT Increased levels of mitochondrial coupling factor 6 (CF6) are present in the peripheral blood of patients with preeclamptic pregnancies, and are particularly evident in cases of early-onset or severe preeclampsia. The present study examined the location and expression levels of CF6 in the placental tissue and its effect on the biological behavior of trophoblast cells. Placental tissue microarrays, including placental villous cytotrophoblast and extravillous cytotrophoblast microarrays, were used to detect the location and relative expression levels of CF6 in the placenta using immunohistochemistry. It was found that CF6 was expressed in both the normal and preeclamptic placenta, but its levels were higher in the preeclamptic tissues. In addition, the effects of the hypoxic environment on the biological behaviors of trophoblast cells were investig ated in the JAR and JEG-3 cell lines. Following induction of hypoxia, the expression levels of CF6 were increased. Moreover, exogenous addition of human recombinant CF6 attenuated cell invasion, but exerted no effect on cell proliferation. At the molecular level, the expression levels of MMP-2 were decreased and were accompanied with a reduction in cell invasion following addition of exogenous CF6. In conclusion, the increased expression levels of CF6 and its effects in reducing the invasive abilities of trophoblast cells may be involved in the pathogenesis of severe preeclampsia. PMID:34475975 | PMC:PMC8406808 | DOI:10.3892/etm.2021.10619 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Rosuvastatin protects PC12 cells from hypoxia/reoxygenation-induced injury by inhibiting endoplasmic reticulum stress-induced apoptosis

xlomafota13 shared this article with you from Inoreader Rosuvastatin protects PC12 cells from hypoxia/reoxygenation-induced injury by inhibiting endoplasmic reticulum stress-induced apoptosis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1189. doi: 10.3892/etm.2021.10623. Epub 2021 Aug 17. ABSTRACT The endoplasmic reticulum stress (ERS) response serves an important role in cerebral ischemia-reperfusion injury (CIRI). However, to the best of the our knowledge, the effect of rosuvastatin on the ERS response in CIRI has not yet been studied. In the present study, the effect of rosuvastatin on cell damage in CIRI was investigated; furthermore, the effect of rosuvastatin on the ERS response was explored. Firstly, a hypoxia/reoxygenation (H/R)-induced cell damage model was established in PC12 cells. Cell viability was subsequently detected by a Cell Counting Kit-8 assay. A lactate dehydrogenase kit was used to detect cytotoxicity. TUNEL assay was then used to measure the extent of cell apoptosis, and western blotting was used to analyze the expression levels of the apoptosis-associated proteins Bax, Bcl-2, cleaved caspase-3 and cleaved caspase-9. In addition, western blotting was used to detect the expression levels of ERS-associated proteins, including phosphorylated (p)-protein kinase R-like endoplasmic reticulum kinase (PERK), p-eukaryotic initiation factor 2α and other proteins. Treatment with rosuvastatin led to an increased activity of H/R-induced PC12 cells and a decrease in their cytotoxicity. Rosuvastatin also led to an inhibition in apoptosis and ERS in H/R-induced PC12 cells. After administration of the ERS response activator thapsigargin (TG), TG was found to reverse the protective effect of rosuvastatin on injury of H/R-induced PC12 cells. Taken together, these findings have shown that rosuvastatin is able to protect PC12 cells from H/R-induced injury via inhibiting ERS-induced apoptosis, providing a strong theoretical basis for the use of rosuvastatin in the clinical treatment of CIRI. PMID:34475979 | PMC:PMC8406900 | DOI:10.3892/etm.2021.10623 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Effect of the acid suppressor omeprazole on the proliferation, migration, invasion and cell cycle of esophageal squamous cell carcinoma cells via the aryl hydrocarbon receptor pathway

xlomafota13 shared this article with you from Inoreader Effect of the acid suppressor omeprazole on the proliferation, migration, invasion and cell cycle of esophageal squamous cell carcinoma cells via the aryl hydrocarbon receptor pathway Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1187. doi: 10.3892/etm.2021.10621. Epub 2021 Aug 17. ABSTRACT Esophageal cancer is a malignant tumor type with one of the highest mortality rates worldwide. The aryl hydrocarbon receptor (AHR), which has been investigated in recent years, has been confirmed to be associated with the occurrence and development of esophageal cancer. AHR has a variety of different ligands, which regulate its activity following binding. The widely known acid inhibitor omeprazole (OME) also affects AHR and its downstream proteins (such as the cytochrome P450 family) by non-ligand binding; however, the mechanisms have remained to be fully elucidated. Therefore, the aim of the present study was to investigate the role of OME in esophageal squamous cell carcinoma (ESCC), whether the mechanism proceeds via the AHR pathway and how OME regulates AHR to affect the occurrence and development of esophageal carcinoma. The AHR-selective re gulator OME was used to treat the ESCC cell lines TE1 and KYSE150. Western blot analysis was used to verify the effect of OME on AHR and proliferating cell nuclear antigen (PCNA) protein expression levels, while Cell Counting Kit (CCK)-8, wound-healing and Transwell assays were used to determine the proliferation, migration and invasion of the ESCCs, respectively, following treatment with OME. In addition, flow cytometry was used to investigate the cell cycle distribution of the ESCCs following incubation with OME. AHR was highly expressed in the ESCCs and following treatment with OME, the protein expression levels of AHR and PCNA were downregulated. The CCK-8 assay indicated that the proliferation of the ESCCs was also reduced following treatment with OME. Furthermore, flow cytometry revealed a notable block of the cells in G1/G0 phase, while the results of the wound-healing and Transwell assays respectively suggested that cell migration and invasion were redu ced. In conclusion, OME inhibited the proliferation, migration and invasion of ESCC cells and blocked the cell cycle via the AHR pathway, which may provide a therapeutic effect on esophageal squamous cell cancer. PMID:34475977 | PMC:PMC8406681 | DOI:10.3892/etm.2021.10621 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Rapamycin suppresses the PI3K/AKT/mTOR signaling pathway by targeting SIRT1 in esophageal cancer

xlomafota13 shared this article with you from Inoreader Rapamycin suppresses the PI3K/AKT/mTOR signaling pathway by targeting <em>SIRT1</em> in esophageal cancer Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1190. doi: 10.3892/etm.2021.10624. Epub 2021 Aug 17. ABSTRACT Rapamycin, a secondary metabolite produced by Streptomyces hygroscopicus, is known for its pharmacological effects, especially antitumor and immunosuppressive activities. However, the antitumoral effects of rapamycin in human esophageal cancer (EC) are still poorly understood. To investigate the potential of rapamycin in EC treatment, sirtuin 1 (SIRT1) mRNA expression was quantified in the tissue of patients with EC or in EC cell lines using reverse transcription-quantitative PCR. The protein levels of SIRT1 and PI3K/AKT/mTOR were measured via western blotting. Furthermore, cell viability, migration and invasion were investigated by Cell Counting Kit-8, wound healing and Transwell assays, respectively. The present results suggested that SIRT1 expression was upregulated in EC. In vitro, the inhibitory effect of r apamycin on cell viability in EC was strengthened or weakened after small interfering (si)-SIRT1 or pcDNA3.1/SIRT1 transfection. Furthermore, SIRT1 rescued the inhibitory effect of rapamycin on the migration and invasion of EC cells. In vivo, si-SIRT1 or SIRT1 overexpression in mice could enhance or rescue the inhibitory effects of rapamycin on tumor growth. In addition, SIRT1 transfection rescued the decreased level of phosphorylated (p)-PI3K, p-AKT and p-mTOR induced by rapamycin treatment. Taken together, the present results suggested that rapamycin suppressed the cell viability, migration, invasion and PI3K/AKT/mTOR signaling pathway in EC by negatively regulating SIRT1. PMID:34475980 | PMC:PMC8406672 | DOI:10.3892/etm.2021.10624 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Endoscopic measurement of nasal septum perforations. German version

xlomafota13 shared this article with you from Inoreader Endoscopic measurement of nasal septum perforations. German version Via hno HNO. 2021 Sep 3. doi: 10.1007/s00106-021-01101-5. Online ahead of print. ABSTRACT BACKGROUND: Nasal septum perforations (NSP) have many uncomfortable symptoms for the patient and a highly negative impact on quality of life. NSPs are closed using patient-specific implants or surgery. Implants are created either under anesthesia using silicone impressions or using 3D models from CT data. Disadvantages for patient safety are the increased risk of morbidity or radiation exposure . MATERIALS AND METHODS: In the context of otorhinolaryngologic surgery, we present a gentle approach to treating NSP with a new image-based, contactless, and radiation-free measurement method using a 3D endoscope. The method relies on image information only and makes use of real-time capable computer vision algorithms to compute 3D information. This endoscopic method can be repeated as often as desired in the clinical course and has already proven its accuracy and robustness for robotic-assisted surgery (RAS) and surgical microscopy. We expand our method for nasal surgery, as there are additional spatial and stereoperspective challenges. RESULTS: After measuring 3 relevant parameters (NSP extension: axial, coronal, and NSP circumference) of 6 patients and comparing the results of 2 stereoendoscopes with CT data, it was shown that the image-based measurements can achieve comparable accuracies to CT data. One patient could be only partially evaluated because the NSP was l arger than the endoscopic field of view. CONCLUSION: Based on the very good measurements, we outline a therapeutic procedure which should enable the production of patient-specific NSP implants based on endoscopic data only. PMID:34477908 | DOI:10.1007/s00106-021-01101-5 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

MicroRNA-206 relieves irradiation-induced neuroinflammation by regulating connexin 43

xlomafota13 shared this article with you from Inoreader MicroRNA-206 relieves irradiation-induced neuroinflammation by regulating connexin 43 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1186. doi: 10.3892/etm.2021.10620. Epub 2021 Aug 16. ABSTRACT Radiation therapy has been widely used for the treatment of various types of cancer; however, it may cause neuroinflammation during the pathological process of the disease. Astrocytes, the most abundant cell type in the central nervous system, have been confirmed to play vital roles in various diseases. Connexin (Cx)43, the main Cx type in astrocytes, which has been identified as a direct target gene of microRNA (miR)-206, was found to be involved in diseases pathologies in regions with astrocytes. The aim of the present study was to investigate the mechanism through which γ-radiation may cause astrocyte neuroinflammation and determine the specific mechanism underlying the effects of miR-206 in irradiation-induced HA-1800 cells. A dual-luciferase reporter system was used to predict and verify the target binding site between Cx43 and miR-206. HA- 1800 cell viability and apoptosis were determined using a MTT assay and flow cytometry, respectively. In addition, the HA-1800 cells were induced by γ-radiation, then the protein and mRNA expression levels of Cx43, miR-206 and cleaved-caspase-3 were determined using western blot and reverse transcription-quantitative PCR analyses, respectively. ELISA was also performed to evaluate the concentrations of different inflammatory cytokines (TNF-α, IL-β, IL-6 and IFN-γ). The dual-luciferase reporter system indicated that Cx43 was a direct target of miR-206. miR-206 mimics increased the expression level of miR-206 in the astrocytes. Irradiation suppressed cell proliferation, increased apoptotic cells and enhanced cleaved-caspase-3 expression and inflammatory cytokines secretion in astrocytes. Furthermore, miR-206 was found to be downregulated and its expression was inversely associated with that of Cx43 in γ-radiation-induced astrocytes. Overexpression of miR-206 enhanced miR-206 an d suppressed Cx43 expression, while Cx43 was upregulated in HA-1800 cells transfected with miR-206 mimic + Cx43-plasmid. However, the expression level of miR-206 was not significantly different in the Cx43-plasmid transfected group. In addition, it was found that miR-206 mimics relieved irradiation-induced neuroinflammation, which was confirmed by increased cell viability, and reduced cell apoptosis and cleaved caspase-3 protein expression, as well as decreased inflammatory cytokine secretion. Furthermore, all the effects of miR-206 mimics on γ-radiation-induced astrocytes were reversed by Cx43-plasmid. In summary, the results of the present study indicated that miR-206 may relieve irradiation-induced neural damage by regulating Cx43, which may provide a novel research direction and a potential therapeutic target for the clinical treatment of inflammation-associated neuronal injury following irradiation. PMID:34475976 | PMC:PMC8406811 | DOI:10.3892/etm.2021.10620 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The differential expression of perilipin-2 in hepatoblastoma and its association with prognosis

xlomafota13 shared this article with you from Inoreader The differential expression of perilipin-2 in hepatoblastoma and its association with prognosis Via Cellular and Molecular Biology Histol Histopathol. 2021 Sep 3:18371. doi: 10.14670/HH-18-371. Online ahead of print. ABSTRACT Perilipin-2, a lipid droplet (LD) coating protein, has been found to be involved in cancer progression. However, its role in hepatoblastoma (HB) is undefined. We collected 87 HB samples and the corresponding clinical data. Immunohistochemistry (IHC) staining was performed to detect perilipin-2 and the association of the perilipin-2 expression with clinical characteristics and prognosis was analyzed. The expression of perilipin-2 was increased in fetal HB components in comparison to embryonal HB components. The predominant staining pattern was vesicular in fetal HB cells, while it was granular in embryonal HB cells. Furthermore, strong expression of perilipin-2 was associated with the histopathological type of fetal predominant HB. Although event-free survival (EFS) did not differ to a statistically significant extent between the strong and we ak expression groups in a univariate survival analysis, a multivariate survival analysis revealed that EFS was significantly improved in the strong perilipin-2 expression group. In conclusion, perilipin-2 is differentially expressed in HB and the strong expression of perilipin-2 predicts a better prognosis. PMID:34477212 | DOI:10.14670/HH-18-371 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.