MiR-214 Regulates the Human Hair Follicle Stem Cell Proliferation and Differentiation by Targeting EZH2 and Wnt/b- Catenin Signaling Way In Vitro

Ke-Tao Du,Jia-Qin Deng,Xu-Guang He,Zhao-ping Liu,Cheng Peng,Mingsheng Zhang 한국조직공학과 재생의학회 2018 조직공학과 재생의학 Vol.15 No.3

miR-214 plays a major role in the self-renewal of skin tissue. However, whether miR-214 regulates the proliferation and differentiation of human hair follicle stem cells (HFSCs) is unknown. Primary HFSCs were isolated from human scalp skin tissue, cultured, and identified using flow cytometry. An miR-214 mimic and inhibitor were constructed for transfection into HFSCs. The MTS and colony formation assays examined cell proliferation. Immunofluorescence detected the localization and expression levels of TCF4, b-catenin, and differentiation markers. Luciferase reporter and TOP/FOP Flash assays investigated whether miR-214 targeted EZH2 and regulated the Wnt/b-catenin signaling pathway. Western blot determined the expression levels of enhancer of zeste homolog 2 (EZH2), Wnt/b-catenin signaling-related proteins, and HFSC differentiation markers in cells subjected to miR-214 transfection. miR-214 expression was remarkably decreased during the proliferation and differentiation of HFSCs into transit-amplifying (TA) cells. Downregulation of miR- 214 promotes the proliferation and differentiation of HFSCs. Overexpression of miR-214 led to decreased expression of EZH2, b-catenin, and TCF-4, whereas downregulation of miR-214 resulted in increased expression of EZH2, b-catenin, and TCF-4 as well as TA differentiation markers. Immunofluorescence assay revealed that inhibiting miR-214 triggered the entry of b-catenin and TCF-4 into the nucleus. The luciferase reporter and TOP/FOP Flash assays demonstrated that miR- 214 directly targets EZH2 and affects Wnt/b-catenin signaling. The miR-214/EZH2/b-catenin axis could be considered a candidate target in tissue engineering and regenerative medicine for HFSCs.

Study on Apparel EDI Standardization Based on XML

( Ke Tao ),( Yi Xiong Yang ),( Rong Chen ) 한국의류산업학회 2004 Clothing Research Journal Vol.2 No.1

Activating transcription factor 4 aggravates angiotensin II-induced cell dysfunction in human vascular aortic smooth muscle cells via transcriptionally activating fibroblast growth factor 21

Ke Tao,Ming Li,Xuefeng Gu,Ming Wang,Tianwei Qian,Lijun Hu,Jiang Li 대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.5

Abdominal aortic aneurysm (AAA) is a life-threatening disorder worldwide. Fibroblast growth factor 21 (FGF21) was shown to display a high level in the plasma of patients with AAA; however, its detailed functions underlying AAA pathogenesis are unclear. An in vitro AAA model was established in human aortic vascular smooth muscle cells (HASMCs) by angiotensin II (Ang-II) stimulation. Cell counting kit-8, wound healing, and Transwell assays were utilized for measuring cell proliferation and migration. RT-qPCR was used for detecting mRNA expression of FGF21 and activating transcription factor 4 (ATF4). Western blotting was utilized for assessing protein levels of FGF21, ATF4, and markers for the contractile phenotype of HASMCs. ChIP and luciferase reporter assays were implemented for identifying the binding relation between AFT4 and FGF21 promoters. FGF21 and ATF4 were both upregulated in Ang-II-treated HASMCs. Knocking down FGF21 attenuated Ang-IIinduced proliferation, migration, and phenotype switch of HASMCs. ATF4 activated FGF21 transcription by binding to its promoter. FGF21 overexpression reversed AFT4 silencing-mediated inhibition of cell proliferation, migration, and phenotype switch. ATF4 transcriptionally upregulates FGF21 to promote the proliferation, migration, and phenotype switch of Ang-II-treated HASMCs.

Inhibition of MicroRNA-15a/16 Expression Alleviates Neuropathic Pain Development through Upregulation of G Protein-Coupled Receptor Kinase 2

( Tao Li ),( Yingchun Wan ),( Lijuan Sun ),( Shoujun Tao ),( Peng Chen ),( Caihua Liu ),( Ke Wang ),( Changyu Zhou ),( Guoqing Zhao ) 한국응용약물학회 2019 Biomolecules & Therapeutics(구 응용약물학회지) Vol.27 No.4

There is accumulating evidence that microRNAs are emerging as pivotal regulators in the development and progression of neuropathic pain. MicroRNA-15a/16 (miR-15a/16) have been reported to play an important role in various diseases and inflammation response processes. However, whether miR-15a/16 participates in the regulation of neuroinflammation and neuropathic pain development remains unknown. In this study, we established a mouse model of neuropathic pain by chronic constriction injury (CCI) of the sciatic nerves. Our results showed that both miR-15a and miR-16 expression was significantly upregulated in the spinal cord of CCI rats. Downregulation of the expression of miR-15a and miR-16 by intrathecal injection of a specific inhibitor significantly attenuated the mechanical allodynia and thermal hyperalgesia of CCI rats. Furthermore, inhibition of miR-15a and miR-16 downregulated the expression of interleukin-1β and tumor-necrosis factor-αin the spinal cord of CCI rats. Bioinformatic analysis predicted that G protein-coupled receptor kinase 2 (GRK2), an important regulator in neuropathic pain and inflammation, was a potential target gene of miR-15a and miR-16. Inhibition of miR-15a and miR-16 markedly increased the expression of GRK2 while downregulating the activation of p38 mitogen-activated protein kinase and NF-κB in CCI rats. Notably, the silencing of GRK2 significantly reversed the inhibitory effects of miR-15a/16 inhibition in neuropathic pain. In conclusion, our results suggest that inhibition of miR-15a/16 expression alleviates neuropathic pain development by targeting GRK2. These findings provide novel insights into the molecular pathogenesis of neuropathic pain and suggest potential therapeutic targets for preventing neuropathic pain development.

A New Directional Relation Model

Ke Zhang,Tao Liu,Zhong Li,Wei Zhao 보안공학연구지원센터(IJSIP) 2014 International Journal of Signal Processing, Image Vol.7 No.2

Simulated Ion Velocity Distribution and Its Incoherent Scattering Spectrum in the High-latitude Ionosphere

Bao-Ke Ma,Li-Xin Guo,Hong-Tao Su,Bei-Chen Zhang 한국물리학회 2013 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.63 No.8

If the relatively larger convection electric field and small the collision frequency between ions andneutrals in the high-latitude ionosphere are considered, the integral solution of the non-Maxwellianion velocity distribution function for the relaxation collision model is simplified, and a torus distributionfunction of the ion velocity is obtained. Also, the feature of the torus velocity distributionfunction is analyzed and simulated with different parameters in high-latitude ionosphere. Furthermore,by using the electromagnetic radiation theory of Sheffield and taking into account the iontemperature anisotropy and its variation with the electric field, we simulate the incoherent scatteringspectrum of ions in different directions. The research shows that the ionospheric convectionelectric field, the ion-neutral collision frequency and the ion anisotropic temperature distributionall have an effect on the incoherent scattering spectrum.

Factors Potentially Associated with Chemotherapy-induced Anemia in Patients with Solid Cancers

Cheng, Ke,Zhao, Feng,Gao, Feng,Dong, Hang,Men, Hai-Tao,Chen, Ye,Li, Long-Hao,Ge, Jun,Tang, Jie,Ding, Jing,Chen, Xin,Du, Yang,Luo, Wu-Xia,Liu, Ji-Yan Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.10

Purpose: Chemotherapy-induced anemia (CIA) is one of the most important causes of anemia in cancer patients. This study was conducted to describe the prevalence and characteristics of CIA in solid cancer patients in the Chinese population, and to explore the relationship of white blood cell (WBC) or platelet decrease with CIA. Methods: Data on age, gender, tumor diagnosis, anti-cancer treatment and blood cell analyses were available from 220 untreated non-anemic cancer patients who received at least 2 cycles of chemotherapy, and the data were analyzed to assess their relationship with CIA or its severity. Results: 139 patients (63.2%) presented anemia, most being Grade 1 or 2. Esophageal and lung cancers were associated with a high prevalence. G3/4 leucopenia and decrease of platelets were identified as independent risk factors for the occurrence of CIA. Moreover, G3/4 leucopenia, decrease of platelet and G3/4 thrombocytopenia were found to be also associated with the severity of CIA. Cisplatin-containing regimens were a main potential factor in causing CIA, although significant association was only found on univariate analysis. Conclusion: Anemia or decrease in hematoglobin are common in Chinese cancer patients receiving chemotherapy. Cisplatin-containing regimens might be an important factor influencing the occurrence of CIA. Our analysis firstly described some risk factors, such as decrease of platelets or WBCs, severity of leucopenia or thrombocytopenia, associated with the occurrence and severity of CIA.

Cloning and characterization of a novel gene with alternative splicing in murine mesenchymal stem cell Line C3H/10T1/2 by gene trap screening

( Ming Ke Wang ),( Hui Qin Sun ),( Fan Jiang ),( Jing Han ),( Feng Ye ),( Tao Wang ),( Yong Ping Su ),( Zhong Min Zou ) 생화학분자생물학회 (구 한국생화학분자생물학회) 2010 BMB Reports Vol.43 No.12

A novel gene, designated mgt-6, containing four splicing variants, was isolated from a gene trap clone library of C3H/10T1/ 2 cells transfected with retroviral promoterless gene-trap vector, ROSAFARY. The transcript variants were differentially expressed in murine tissues and cell lines and differentially responded to diverse stimuli including TGF-β1 and mitogen-activated protein kinase (MAPK) inhibitors. The mgt-6 gene encoded a protein of 37 or 11 amino acid residuals with cytoplasmic distribution. However, when C3H/10T1/2 cells were treated with 5-azacytidine, the protein translocated into cell nucleus as indicated by fused LacZ or C-terminally tagged EGFP. Our preliminary results suggest that further study on the role of mgt-6 gene in cell transformation and differentiation may be of significance. [BMB reports 2010; 43(12): 789-794]

Investigation on Bond Behavior between Self-compacting Rubberized Concrete and Rectangular Steel Tubes

Xiaojun Ke,Zhukai Tang,Jianzeng Shen,Yanying Tao 대한토목학회 2022 KSCE JOURNAL OF CIVIL ENGINEERING Vol.26 No.8

The combination of self-compacting rubberized concrete (SCRC) and rectangular steel tubes to be a composite structure is a new attempt to apply it to a broader range of engineering fields while making up for the shortcomings of SCRC. This study presents experimental and analytical studies on the bonding behavior of rectangular self-compacting rubber concrete-filled steel tubes (SCRCFST). A total of 17 SCRCFST specimens were performed on push-out test with different parameters of 1) interface bonding length, 2) rubber aggregate replacementrate, 3) rubber particle size, and 4) water-cement ratio (W/C). Based on the failure mode, strain analysis, and the evolution of damage on the interface between the SCRC and steel tubes, test results determined the effects of the parameters, and a prediction equation for the bond strength was derived from developing a relationship of bond-slip. The results indicated that the increase of rubber content, rubber particle size, W/C harmed the bond strength of SCRCFST, and bond length had little effect on bonding strength. Furthermore, the strain distribution of the rectangular steel tube was not uniformly distributed. The achievement of this research is the investigation of the bonding properties of the new structure, to provide guidance for future research scholars.

LncRNA KIAA0087 suppresses the progression of osteosarcoma by mediating the SOCS1/JAK2/STAT3 signaling pathway

Gong Haoli,Tao Ye,Xiao Sheng,Li Xin,Fang Ke,Wen Jie,He Pan,Zeng Ming 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

Long noncoding RNAs (lncRNAs), widely expressed in mammalian cells, play pivotal roles in osteosarcoma (OS) progression. Nevertheless, the detailed molecular mechanisms of lncRNA KIAA0087 in OS remain obscure. Here, the roles of KIAA0087 in OS tumorigenesis were investigated. KIAA0087 and miR-411-3p levels were detected by RT-qPCR. Malignant properties were assessed by CCK-8, colony formation, flow cytometry, wound healing, and transwell assays. SOCS1, EMT, and JAK2/STAT3 pathway-related protein levels were measured by western blotting. Direct binding between miR-411-3p and KIAA0087/SOCS1 was validated by a dual-luciferase reporter, RIP, and FISH assays. In vivo growth and lung metastasis were evaluated in nude mice. The expression levels of SOCS1, Ki-67, E-cadherin, and N-cadherin in tumor tissues were measured by immunohistochemical staining. Downregulation of KIAA0087 and SOCS1 and upregulation of miR-411-3p were found in OS tissues and cells. Low expression of KIAA0087 was associated with a poor survival rate. Forced expression of KIAA0087 or miR-411-3p inhibition repressed the growth, migration, invasion, EMT, and activation of the JAK2/STAT3 pathway and triggered apoptosis of OS cells. However, the opposite results were found with KIAA0087 knockdown or miR-411-3p overexpression. Mechanistic experiments indicated that KIAA0087 enhanced SOCS1 expression to inactivate the JAK2/STAT3 pathway by sponging miR-411-3p. Rescue experiments revealed that the antitumor effects of KIAA0087 overexpression or miR-411-3p suppression were counteracted by miR-411-3p mimics or SOCS1 inhibition, respectively. Finally, in vivo tumor growth and lung metastasis were inhibited in KIAA0087-overexpressing or miR-411-3p-inhibited OS cells. In summary, the downregulation of KIAA0087 promotes the growth, metastasis, and EMT of OS by targeting the miR-411-3p-mediated SOCS1/JAK2/STAT3 pathway.