Lorentzenmcfadden9058

OBJECTIVE Transforming growth factor beta 1 (TGF-β1) can promote myocyte hypertrophy, thus playing an important role in ventricular remodeling after myocardial infarction (MI). MATERIALS AND METHODS In this study, the model of MI was established in rats through ligating the left anterior descending coronary artery. Subsequently, the messenger ribonucleic acid (mRNA) and protein expression levels of TGF-β1 in myocardial cells in both model group and sham operation group were determined. The effects of TGF-β1 treatment on myocardial cell apoptosis in MI rats were explored. Moreover, the changes of mitogen-activated protein kinase (MAPK) signaling pathway in rats with acute MI were verified. In addition, the protein expressions of phosphorylated-MAPK kinases 3/6 (p-MKK3/6) and MKK3/6 in myocardial cells of the two groups were analyzed. RESULTS The mRNA and protein expression levels of TGF-β1 in myocardial cells of acute MI rats were significantly higher than those in the sham operation group (p less then 0.01). After treatment with TGF-β1, the expression level of B-cell lymphoma 2 (Bcl-2) associated X protein (Bax) was obviously down-regulated. The Bax/Bcl-2 ratio was notably lower than that in control group (p less then 0.01). Meanwhile, the proportion of apoptotic cells decreased remarkably (p less then 0.01). In the model group, no evident change was observed in the protein expression level of MKK3/6, whereas the levels of p-MKK3/6 were prominently up-regulated (p less then 0.01). selleck compound CONCLUSIONS TGF-β1 can activate MKK3/6 in the MAPK signaling pathway to resist the apoptosis of myocardial cells in acute MI rats.OBJECTIVE   Diabetic nephropathy (DN) is one of the most serious complications of diabetes mellitus (DM) and has become the major cause of end-stage renal failure. MicroRNAs (miRs) play key roles in many pathologic processes for initiating and progressing, including DN. Epithelial-mesenchymal transition (EMT) and renal fibrogenesis are important features of DN. However, the role of miR-30c-5p in high glucose (HG)-induced EMT and renal fibrogenesis is not clear. This study was aimed at determining the regulatory network of miR-30c-5p and JAK1 in DN. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot assays were performed to detect expressions of miR-30c-5p, JAK1, vimentin, α-SMA, and E-cadherin. The possible binding sites between miR-30c-5p and JAK1 were predicted by TargetScan online database and verified by Luciferase report assay. The secretion of fibronectin (FN) and Collagen IV (Col IV) in the supernatant was detected by Enzyme-linked immunosorbent (ELISA) assay. RESULTS MiR-30c-5p was downregulated and JAK1 was upregulated in renal fibrosis tissue and HG stimulated HK2 cells. Transfection of miR-30c-5p inhibited HG-induced EMT and renal fibrogenesis in HK2 cells, which was reversed by miR-30c-5p inhibitor. Moreover, JAK1 was confirmed as a direct target of miR-30c-5 and knockdown of JAK1 markedly inhibited HG-induced renal fibrogenesis and EMT in HK2 cells. Furthermore, overexpression of JAK1 attenuated the inhibitory effect of miR-30c-5p on HG-induced EMT and renal fibrogenesis in HK2 cells. CONCLUSIONS MiR-30c-5p evidently inhibited HG-induced EMT and renal fibrogenesis by down-regulation JAK1 in DN, providing a promising therapeutic strategy for the treatment of DN.OBJECTIVE This study aimed to investigate the physiological function and molecular mechanism of microRNA-181a (miRNA-181a) in the carcinogenesis of osteosarcoma. MATERIALS AND METHODS The relative expression of miRNA-181a in tissues and cultured cells was detected by quantitative real time-polymerase chain reaction (qRT-PCR). MiR-181a inhibitor and miR-181a mimics were used to manipulate its level in cells. Cell proliferation and invasion were measured using Cell Counting Kit-8 (CCK-8) assay and transwell assay, respectively. The protein levels of the targeted genes were detected by Western blotting and immunohistochemistry. Terminal Deoxynucleotidyl Transferase (TdT)-mediated dUTP Nick-End Labeling (TUNEL) assay was employed to detect cell apoptosis. Moreover, a xenograft tumor bearing mice model was used to evaluate the effect of miR-181a in vivo. RESULTS We found that miRNA-181a was aberrantly elevated in osteosarcoma tissues and cells. Moreover, the overexpression of miRNA-181a could facilitate cell proliferation and migration. By contrast, miRNA-181a knockdown reverses these effects. Additionally, downregulation of miRNA-181a could activate NOD-like receptor protein 3 (NLRP3)-dependent pyroptosis, as evidenced by the increase of pyroptosis-related genes (NLRP3, caspase-1, interleukin-18, and interleukin-1β) in miRNA-181a inhibitor transfected cells compared with the control. Further mechanistic studies identified that miRNA-181a knockdown suppresses cell proliferation and invasion by activating NLRP3-dependent pyroptosis. Silencing NLRP3 could effectively reverse the effects mediated by miRNA-181a inhibitor. Consistently, in vitro results also demonstrated that blockade of miRNA-181a notably suppresses tumor growth via activating pyroptosis. CONCLUSIONS These results provide that miRNA-181a might serve as potential therapeutic target for osteosarcoma patients.OBJECTIVE To study the influence of micro ribonucleic acid (miR)-137 on osteoporosis rats by regulating runt-related transcription factor 2 (RUNX2). MATERIALS AND METHODS A total of 36 Sprague-Dawley rats were randomly assigned to the normal group (n=12), model group (n=12), and inhibitor group (n=12). No treatment was performed in the normal group. The osteoporosis model in rats was prepared in the model group, and miR-137 inhibitor was administered in osteoporosis rats of inhibitor group. Following 12 weeks of intervention, sampling was conducted. The expression of RUNX2 was detected via immunohistochemistry, and its protein expression level was determined via Western blotting. Quantitative Polymerase Chain Reaction (qPCR) was carried out to detect the mRNA level of miR-137. The contents of serum bone Gla protein (BGP) and total alkaline phosphatase (TALP) were measured using enzyme-linked immunosorbent assay (ELISA). Finally, bone mineral density was determined with a dual-energy X-ray absorptiometry instrr group had substantially lower contents of serum BGP and TALP than the normal group (p less then 0.05), and that their contents rose dramatically in the inhibitor group compared with that in the model group (p less then 0.05). Additionally, based on the measurement of bone mineral density, compared with that in the normal group, bone mineral density declined considerably in the model group and inhibitor group (p less then 0.05). It was markedly elevated in inhibitor group in comparison with that in the model group (p less then 0.05). CONCLUSIONS MiR-137 regulates RUNX2 to affect the bone mineral density of osteoporosis model rats.OBJECTIVE Chordoma is a rare malignant tumor difficult to diagnose and treat. Long non-coding RNAs acting as novel biomarkers are frequently reported in numerous cancers. The purpose of this study was to investigate the role of long intergenic non-coding RNA 00662 (LINC00662) and its associated action mechanisms in chordoma. MATERIALS AND METHODS The expression of LINC00662, Ring finger protein 144B (RNF144B), and microRNA-16-5p (miR-16-5p) was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The protein levels of RNF144B, cell proliferation markers (Cyclin D1 and Ki67), epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin and N-cadherin), and glycolysis markers [glucose transporter 1 (GLUT1), hexokinase II (HK2), and lactic dehydrogenase A (LDHA)] were determined by Western blot. Cell proliferation, the number of colonies, migration, and invasion were investigated by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, and transw RNF144B by acting as a sponge of miR-16-5p, suggesting that LINC00662 was a promising therapeutic target for chordoma.OBJECTIVE In the last decades, immediate breast reconstruction (IBR) raised in frequency, and prepectoral positioning of the implant is becoming the trend nowadays. The aim of this paper is to describe our case series in IBR with prepectoral implant placement and complete coverage of it with the TiLoop® Bra titanium-coated polypropylene mesh (TCPM), pre-shaped as a pocket. PATIENTS AND METHODS Eighteen women with breast tumors were selected and underwent mono- or bilateral mastectomies and prepectoral IBR with tissue expanders or prostheses. After the prepectoral lodge was ready, the implants were inserted into TiLoop® Bra Pocket meshes and positioned over the pectoralis major muscle fascia. The mean surgical time of their positioning was four minutes. RESULTS This preliminary study showed meaningful results in prepectoral IBR with TiLoop® Bra Pocket covering the implants, for we observed a reduction of implant's exposure time and risk of bacterial contamination. Of the 18 patients that underwent this procedure, only three presented complications that resolved in a maximum of four weeks. CONCLUSIONS A considering reduction of surgical time in implant positioning was achieved, lowering exposure time and risk of complications as infection.OBJECTIVE The aim of this study was to investigate the expression characteristics of lncRNA CRNDE in Wilms' tumor and to further investigate whether it could promote the development of Wilms' tumor via regulating microRNA-424. PATIENTS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to examine the expression level of CRNDE in tumor tissues and para-cancerous tissues of patients with Wilms' tumor. Meanwhile, the expression of CRNDE in Wilms' tumor cell lines was analyzed as well. CRNDE overexpression and knockdown models were constructed using lentivirus transfection in HFWT and 17-94 cell lines, respectively. Subsequently, cell counting kit-8 (CCK-8), cell colony formation, and transwell assays were performed to explore the influence of CRNDE on the biological functions of Wilms' tumor cells. Furthermore, luciferase reporter gene assay and cell reversal experiment were applied to explore the interplay between CRNDE and microRNA-424. RESULTS RT-qPCR results revealed that the expression of CRNDE was correlated with the incidence rate of lymph node metastasis in patients with Wilms' tumor. In addition, CRNDE might accelerate the progression of Wilms' tumor via modulating microRNA-424.OBJECTIVE Bladder cancer (BLCA) is the most common genitourinary malignancy in the world. Recent studies have revealed that circular RNAs (circRNAs) are dysregulated in malignant tumors and participate in carcinogenesis. The purpose of our work is to uncover how hsa_circ_0017247 functions in BLCA. PATIENTS AND METHODS In this research, Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was conducted to monitor hsa_circ_0017247 expression in BLCA samples. Besides, proliferation assay, colony formation assay, and flow cytometry assay were performed in BLCA cells after hsa_circ_0017247 was knocked down. Meanwhile, the Western blot assay was conducted to explore the target signaling pathway of hsa_circ_0017247. Furthermore, tumor formation and metastasis assays were also conducted in vivo. RESULTS Compared with the adjacent tissues, a significant upregulation in hsa_circ_0017247 expression was observed in BLCA samples. Functional assays showed that the inhibition of cell proliferation was induced via downregulating hsa_circ_0017247 in BLCA in vitro, while the promotion of cell proliferation was induced via downregulating hsa_circ_0017247 in BLCA in vitro.