The synergism between cardiomyogenesis and angiogenesis is essential for cardiac regeneration. Circular RNAs (circRNAs) play pivotal roles in cell growth and angiogenesis, but their functions in cardiac regeneration are not yet known. In this study, we investigated the role and underlying mechanisms of circRNA Hipk3 (circHipk3) in both cardiomyogenesis and angiogenesis during cardiac regeneration. We found that circHipk3 was overexpressed in the fetal or neonatal heart of mice. The transcription factor Gata4 bound to the circHipk3 promoter and increased circHipk3 expression. Cardiomyocyte (CM) proliferation in vitro and in vivo was inhibited by circHipk3 knockdown and increased by circHipk3 overexpression. Moreover, circHipk3 overexpression promoted coronary vessel endothelial cell proliferation, migration, and tube-forming capacity and subsequent angiogenesis. More importantly, circHipk3 overexpression attenuated cardiac dysfunction and decreased fibrotic area after myocardial infarction (MI). Mechanistically, circHipk3 promoted CM proliferation by increasing Notch1 intracellular domain (N1ICD) acetylation, thereby increasing N1ICD stability and preventing its degradation. In addition, circHipk3 acted as a sponge for microRNA (miR)-133a to promote connective tissue growth factor (CTGF) expression, which activated endothelial cells. Our findings suggested that circHipk3 might be a novel therapeutic target for preventing heart failure post-MI.
The width and height of the atlas lateral mass were larger than that of the C2 pedicle, and there was enough space to insert a 3.5-mm diameter screw in the atlas lateral mass over the C2 nerve. The pullout force of the screw on the lateral mass of the atlas was the same as that of the C2 pedicle screw. It is possible toinsert a 3.5-mm screw in the lateral mass of the atlas. The direction of the screw should be about 20 degrees anterosuperior in the vertical plane and 15 degrees inward in the horizontal plane. The suitable length of the screw should be approximately 22 mm inside the lateral mass.
Because of a general lack of knowledge regarding the precise anatomy of the seminal vesicle system, efforts to use transurethral seminal vesiculoscopy (TSV) are currently constrained. We investigated 26 normal adult male specimens. Contrast medium was injected into the seminal vesicle system in 18 specimens and the openings of the ejaculatory ducts were examined with an operating microscope. India ink was injected into the urethra in four specimens to investigate the function of the ejaculatory duct valve. Another four specimens were examined histologically to identify the anatomical relationships of the seminal vesicle system. We found that the openings of the ejaculatory ducts were covered by the ejaculatory duct valve, which could be classified into two types and acted as a one-way valve. The apex of the seminal colliculus together with the right and left openings of the ejaculatory ducts formed a shape resembling an isosceles triangle. This could be used to locate the openings of the ejaculatory ducts during TSV. The ejaculatory ducts can be classified into two types according to their course. During surgery, efforts must be made to protect the ejaculatory duct valve. During inspection or surgery, the second segment and the angles of the ejaculatory ducts, particularly in Type I b and Type II cases, require particular attention.
Bone growth and remodeling is inhibited by denervation in adults and children, resulting in alterations of linear growth and bone mass and increased risk for osteoporosis and pathologic fractures. Transforming growth factor beta (TGF-β) isoforms are a key group of growth factors that enhance bone formation. To explore the relation between denervation-induced reduction of bone formation and TGF-β gene expression, we measured mRNA levels of TGF-β in denervation mouse bone and found decreased mRNA levels of TGF-β1, TGF-β2 and TGF-β3. These changes were accompanied by diminishing weight loss, bone mineral density (BMD), trabecular thickness, trabecular separation and trabecular number of femur and lumbar, serum osteocalcin, total calcium, intact parathyroid hormone, and increased serum C telopeptide. Recombinant human TGF-β1 (rhTGF-β1) prevented denervation-induced reduction of BMD further supporting our hypothesis that denervation-induced reduction of bone formation is a result of inhibition of TGF-β gene expression. In addition, antiprogestins RU 38486 blunted the denervation-induced decrease in mRNA levels of TGF-β group, while dexamethasone (DEX) decreased TGF-β group mRNA levels in normal mice. Furthermore, the denervated-mice exhibited a threefold increase in plasma corticosterone. These results suggest that denervation-induced reduction of bone formation may be regulated by glucocorticoids via inhibition of TGF-β gene expression at least in part.
Background Ubinuclein-2 (UBN2) is a nuclear protein that interacts with many transcription factors. The molecular role and mechanism of UBN2 in the development and progression of cancers, including colorectal cancer (CRC), is not well understood. The current study explored the role of UBN2 in the development and progression CRC. Methods Oncomine network and The Cancer Genome Atlas (TCGA) database were downloaded and Gene Set Enrichment Analysis (GSEA) was performed to compare the UBN2′s expression between normal and tumor tissues, as well as the potential correlation of UBN2 expression with signaling pathways. Immunohistochemistry (IHC), qRT-PCR and Western blotting were performed to determine the expression of UBN2 in CRC tissues or cell lines. In vitro proliferation and invasion assays, and orthotopic mouse metastatic model were used to analyze the effect of UBN2 on the development and progression of CRC. Results The analysis of UBN2 expression using Oncomine network showed that UBN2 was upregulated in CRC tissues compared to matched adjacent normal intestinal epithelial tissues. IHC, qRT-PCR and Western blotting confirmed that UBN2 expression is higher in CRC tissues compared with matched adjacent normal intestinal epithelial tissues. In addition, analyses of TCGA data revealed that high UBN2 expression was associated with advanced stages of lymph node metastasis, distant metastasis, and short survival time in CRC patients. IHC showed that high UBN2 expression is correlated with advanced stages of CRC. Moreover, UBN2 is highly expressed in the liver metastatic lesions. Furthermore, knockdown of UBN2 inhibited the growth, invasiveness and metastasis of CRC cells via regulation of the Ras/MAPK signaling pathway. Conclusion The current study demonstrates that UBN2 promotes tumor progression in CRC. UBN2 may be used as a promising biomarker for predicting the prognosis of CRC patients. Electronic supplementary material The online version of this article (10.1186/s12935-019-0848-4) contains supplementary material, which is available to authorized users.
Flap prefabrication is started with transposition of a vascular pedicle into a donor area that lacks an axial blood supply. Adipose-derived stem cells (ASCs) have been proven beneficial for promoting neovascularization and tissue regeneration in several animal models. Here we investigated the feasibility of applying ASCs as a novel strategy to promote flap prefabrication, which involves the processes of neovascularization and regeneration. Prefabricated flaps were performed by two-stage procedure in a rat model. At stage one, the right femoral vascular pedicle was dissected and embedded underneath the abdominal flap to form a man-made axial flap. At stage two, the prefabricated abdominal flap was elevated as an island flap based on the implanted femoral vessel. Ninety rats were randomly divided into 3 groups and received allogeneic ASCs, chondrocytes and phosphate-buffered saline (PBS), respectively during the first operation. Eighteen flaps of each group were harvested for vascular endothelial growth factor-A (VEGF-A) protein assay after the first surgery. The other flaps were processed for flap viability measurements by flap survival rate and capillary density after the second surgery. Results demonstrated that the ASCs treated group had higher survival percentage and capillary density of flap as compared with either PBS group or chondrocyte group. Furthermore, the ASC group had the highest level of in vivo VEGF-A among three groups, while the chondrocyte group had the lowest. These results indicate that ASCs are capable of promoting flap prefabrication, and its therapeutic potential is correlated with the angiogenic cytokines such as VEGF-A.
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