Objective To investigate the correlation between serum homeodomain interacting protein ki-nase 2(HIPK2),annexin A5(ANXA5)and coronary stenosis and prognosis in patients with acute myocardial infarction(AMI).Methods A total of 277 AMI patients who received interventional treatment in this hospi-tal from January 2021 to July 2023 were selected as the AMI group,and another 140 cases with normal or very mild stenosis in coronary angiography during the same period were selected as the control group.According to the degree of coronary artery stenosis(Gensini score),the AMI patients were divided into mild coronary arter-y stenosis group(86 cases),moderate coronary artery disease group(111 cases)and severe coronary artery disease group(80 cases).According to the prognosis,they were divided into poor prognosis group(80 cases)and good prognosis group(197 cases).Enzyme-linked immunosorbent assay was used to detect the serum HIPK2 and ANXA5 levels.Spearman correlation analysis was used to analyze the correlation between serum HIPK2 and ANXA5 levels and Gensini score in patients with AMI.Multivariate unconditional Logistic regres-sion was used to determine the relationship between serum HIPK2 and ANXA5 levels and prognosis of AMI patients.Receiver operating characteristic(ROC)curve was used to analyze the predictive efficiency of serum HIPK2 and ANXA5 levels on prognosis of AMI patients.Results Compared with the control group,the ser-um HIPK2 level in the AMI group increased and the ANXA5 level decreased,and the differences were statisti-cally significant(P＜0.05).The serum HIPK2 levels in the mild coronary artery stenosis group,moderate coronary artery stenosis group and severe coronary artery stenosis group increased successively,while the ANXA5 levels decreased successively,and the differences were statistically significant(P＜0.05).Gensini score was positively correlated with serum HIPK2 level and negatively correlated with serum ANXA5 level in AMI patients(P＜0.05).The Gensini score of AMI patients was positively correlated with the serum HIPK2 level(r=0.785,P＜0.05),and negatively correlated with the serum ANXA5 level(r=-0.798,P＜0.05).Compared with the good prognosis group,the serum HIPK2 level in the poor prognosis group increased(P＜0.05),and the ANXA5 level decreased(P＜0.05).After adjusting for confounding factors,high HIPK2 was an independent risk factor for poor prognosis in AMI patients(P＜0.05),and high ANXA5 was an independ-ent protective factor(P＜0.05).The area under the curve of the combined prediction of serum HIPK2 and ANXA5 levels for the prognosis of AMI patients was 0.875,which was greater than 0.778 and 0.784 predic-ted by serum HIPK2 and ANXA5 levels alone(P＜0.05).Conclusion The serum HIPK2 level is increased and the ANXA5 level is decreased in patients with AMI,which is related to the aggravation of coronary steno-sis and the poor prognosis.The combination of serum HIPK2 and ANXA5 levels is more effective in predic-ting the prognosis of patients with AMI.

Purpose To investigate the expression of bone sialoprotein(BSP)in the tissues and cells of endome-trial cancer(EC)and its effects on the proliferation and invasion of EC cells.Methods The expression of BSP was assessed by immunohistochemistry in 235 EC tissues and 88 normal endometrial tissues,and its correlation with clinico-pathological features was analyzed.Western blot was used to compare BSP levels between human endometrial carcinoma cell line(HHUA)and normal human endumetial epithelial cells(HEEC).BSP was knocked down in HHUA cells via transient transfection,and the cells were divided into blank control group and BSP-knockdown group.The effects of BSP knockdown on cell cycle,proliferation,migration,invasion,and apoptosis were evaluated using PI staining,CCK-8,scratch,Transwell,and Annexin V-FITC assays,respectively.Protein levels of TGF-β signaling pathway compo-nents were analyzed by Western blot.Results BSP expression was significantly higher in EC tissues than in normal endometrium(P＜0.001)and correlated with lymph node metastasis and advanced FIGO stage(P＜0.05).BSP pro-tein level was also significantly elevated in HHUA cells(2.455 8±0.008 9)compared to HEECs(1.571 2±0.005 4)(P＜0.01).After knockdown,compared with the control group,the proliferation index(74.4±3.33),migration rate(0.48±0.03),and invasion ability(0.36±0.11)of the cells were increased,and the apoptosis rate(25.97％)of the cells was increased(P＜0.05).Furthermore,the expression levels of TGF-β signaling pathway downstream proteins TGF-β1(0.290 4±0.002 3)、TGF-β2(0.292 9±0.001 6)、Smad2(0.469 3±0.001 1)、Smad3(0.247 0±0.001 7)、pAKT(0.382 1±0.001 9)、ATK(0.119 6±0.001 6)and MEK1(0.258 9±0.000 3)in the BSP-knockdown group of EC cells decreased(P＜0.01).Conclusion BSP is highly expressed in endometrial cancer and promotes cancer cell proliferation,invasion,and metastasis by activating the TGF-β signaling pathway.

Purpose To investigate the expression of bone sialoprotein(BSP)in the tissues and cells of endome-trial cancer(EC)and its effects on the proliferation and invasion of EC cells.Methods The expression of BSP was assessed by immunohistochemistry in 235 EC tissues and 88 normal endometrial tissues,and its correlation with clinico-pathological features was analyzed.Western blot was used to compare BSP levels between human endometrial carcinoma cell line(HHUA)and normal human endumetial epithelial cells(HEEC).BSP was knocked down in HHUA cells via transient transfection,and the cells were divided into blank control group and BSP-knockdown group.The effects of BSP knockdown on cell cycle,proliferation,migration,invasion,and apoptosis were evaluated using PI staining,CCK-8,scratch,Transwell,and Annexin V-FITC assays,respectively.Protein levels of TGF-β signaling pathway compo-nents were analyzed by Western blot.Results BSP expression was significantly higher in EC tissues than in normal endometrium(P＜0.001)and correlated with lymph node metastasis and advanced FIGO stage(P＜0.05).BSP pro-tein level was also significantly elevated in HHUA cells(2.455 8±0.008 9)compared to HEECs(1.571 2±0.005 4)(P＜0.01).After knockdown,compared with the control group,the proliferation index(74.4±3.33),migration rate(0.48±0.03),and invasion ability(0.36±0.11)of the cells were increased,and the apoptosis rate(25.97％)of the cells was increased(P＜0.05).Furthermore,the expression levels of TGF-β signaling pathway downstream proteins TGF-β1(0.290 4±0.002 3)、TGF-β2(0.292 9±0.001 6)、Smad2(0.469 3±0.001 1)、Smad3(0.247 0±0.001 7)、pAKT(0.382 1±0.001 9)、ATK(0.119 6±0.001 6)and MEK1(0.258 9±0.000 3)in the BSP-knockdown group of EC cells decreased(P＜0.01).Conclusion BSP is highly expressed in endometrial cancer and promotes cancer cell proliferation,invasion,and metastasis by activating the TGF-β signaling pathway.

Spinal cord injury and regeneration involves transcriptional activity of many genes, of which many remain unknown. Using the rat spinal cord full- transection model, bioinformatics, cloning, expression assays, fusion proteins, and transfection techniques, we identified and characterized one such differentially expressed gene, termed scirr1 (spinal cord injury and/or regeneration related gene 1). Fourteen orthologs were found in 13 species from echinoderm to insect and human by Blast search of NCBI protein reference sequence database. However, no further information is available for these homologues. Using whole-mount in situ hybridization, mouse scirr1 mRNA was expressed temporally and spatially in accordance with the early development sequence of the central nervous system. In adult rat spinal cord, expression of scirr1 mRNA was localized to neurons of gray matter by in situ hybridization. Using immunohistochemistry, SCIRR1 protein was found to be up-regulated and expressed more highly in spinal cord neurons farther from the epicenter of injury. Although the precise function of SCIRR1 is unknown, its unique pattern of expression during CNS early development and up-regulation after spinal cord injury suggest that SCIRR1 should be involved in the succeeding injury and/or repair processes of the injured spinal cord. Also, the typical F-box and leucine-rich repeat (LRR) architecture of rat SCIRR1 indicated that it may play an important substrate recruiting role in the pleiotropic ubiquitin/proteasome pathway. All these make scirr1 a new interesting start to study the spinal cord injury and regeneration mechanism.
Amino Acid Sequence ; Animals ; Base Sequence ; Brain/embryology/metabolism ; Embryo, Mammalian/metabolism ; F-Box Proteins/*biosynthesis ; Gene Expression Regulation, Developmental ; Male ; Mice ; Molecular Sequence Data ; Organ Specificity ; PC12 Cells ; Phylogeny ; Rats ; Rats, Wistar ; Spinal Cord/embryology/metabolism ; Spinal Cord Injuries/*metabolism ; Up-Regulation

Objective To clone injury-regeneration-related genes after primary neurons of spinal cord were injured in rat, and to elucidate the molecular mechanism of injury and regeneration in CNS. Methods An in vitro spinal cord primary neuron injury model was replicated in rat. The differentially expressed genes during injury and regeneration periods of spinal cord primary neurons were cloned by improved subtractive hybridization. Results Twenty-seven differentially expressed sequences were obtained, 23 were known genes and the others were unknown. Among these known sequences, cDNA for synuclein and clusterin, together with several other gene sequences, were closely related with nerve degenerative diseases. Conclusion Primary neuron injury-regeneration-related genes of the spinal cord can be successfully cloned by improved subtractive hybridization.