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RISS 인기검색어
- 검색키워드
- 저자 : Zheng Han-Xuan (검색결과 4 건)
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Yu, Liming,Tu, Qisheng,Han, Qianqian,Zhang, Lan,Sui, Lei,Zheng, Leilei,Meng, Shu,Tang, Yin,Xuan, Dongying,Zhang, Jin,Murray, Dana,Shen, Qingping,Cheng, Jessica,Kim, Sung-Hoon,Dong, Lily Q.,Valverde, P Wiley (John WileySons) 2015 Stem Cells Vol.33 No.1
<P>Adiponectin (APN) is an adipocyte-secreted adipokine that exerts well-characterized antidiabetic properties. Patients with type 2 diabetes (T2D) are characterized by reduced APN levels in circulation and impaired stem cell and progenitor cell mobilization from the bone marrow for tissue repair and remodeling. In this study, we found that APN regulates the mobilization and recruitment of bone marrow-derived mesenchymal stem cells (BMSCs) to participate in tissue repair and regeneration. APN facilitated BMSCs migrating from the bone marrow into the circulation to regenerate bone by regulating stromal cell-derived factor (SDF)-1 in a mouse bone defect model. More importantly, we found that systemic APN infusion ameliorated diabetic mobilopathy of BMSCs, lowered glucose concentration, and promoted bone regeneration in diet-induced obesity mice. In vitro studies allowed us to identify Smad1/5/8 as a novel signaling mediator of APN receptor (AdipoR)-1 in BMSCs and osteoblasts. APN stimulation of MC3T3-E1 osteoblastic cells led to Smad1/5/8 phosphorylation and nuclear localization and increased SDF1 mRNA expression. Although APN-mediated phosphorylation of Smad1/5/8 occurred independently from adaptor protein, phosphotyrosine interaction, pleckstrin homology domain, and leucine zipper containing 1, it correlated with the disassembly of protein kinase casein kinase 2 and AdipoR1 in immunoprecipitation experiments. Taken together, this study identified APN as a regulator of BMSCs migration in response to bone injury. Therefore, our findings suggest APN signaling could be a potential therapeutic target to improve bone regeneration and homeostasis, especially in obese and T2D patients.</P>
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Gan Hui,Zhang Li,Chen Hui,Xiao Han,Wang Lu,Zhai Xuan,Jiang Ning,Liang Ping,Zheng Shuyue,Zhao Jing 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
The NLRC4 inflammasome, a member of the nucleotide-binding and oligomerization domain-like receptor (NLR) family, amplifies inflammation by facilitating the processing of caspase-1, interleukin (IL)–1β, and IL-18. We explored whether NLRC4 knockdown alleviated inflammatory injury following intracerebral hemorrhage (ICH). Furthermore, we investigated whether NLRC4 inflammasome activation can be adjusted by the regulator of G protein signaling 2/leucine-rich repeat kinase-2 pathway. Fifty microliters of arterial blood was drawn and injected into the basal ganglion to simulate the ICH model. NLRC4 small interfering RNAs (siRNAs) were utilized to knockdown NLRC4. An LRRK2 inhibitor (GNE7915) was injected into the abdominal cavity. Short hairpin (sh) RNA lentiviruses and lentiviruses containing RGS2 were designed and applied to knockdown and promote RGS2 expression. Neurological functions, brain edema, Western blot, enzyme-linked immunosorbent, hematoxylin and eosin staining, Nissl staining, immunoprecipitation, immunofluorescence assay and Evans blue dye extravasation and autofluorescence assay were evaluated. It was shown that the NLRC4 inflammasome was activated following ICH injury. NLRC4 knockdown extenuated neuronal death, damage to the blood-brain barrier, brain edema and neurological deficiency 3 days after ICH. NLRC4 knockdown reduced myeloperoxidase (MPO) cells as well as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-18 following ICH. GNE7915 reduced pNLRC4 and NLRC4 inflammasome activation. RGS2 suppressed the interaction of LRRK2 and NLRC4 and NLRC4 inflammasome activation by regulating pLRRK2. Our study demonstrated that the NLRC4 inflammasome may aggravate the inflammatory injury induced by ICH and that RGS2/LRRK2 may relieve inflammatory injury by restraining NLRC4 inflammasome activation.
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Hai-bin Wei,Bing-yi Guo,Yao-fen Tu,Xuan-han Hu,Wei Zheng,Da-hong Zhang,Jian Zhuo 대한비뇨의학회 2022 Investigative and Clinical Urology Vol.63 No.3
Purpose: The selection of open prostatectomy (OP) over transurethral laser surgery is controversial for large volume prostates. Thus, we aim to compare the efficacy and safety of transurethral laser versus OP, and provide the latest evidence of clinical practice for large-sized benign prostatic hyperplasia (BPH). Materials and Methods: This meta-analysis used Review Manager V5.3 software and the systematic literature search of Cochrane Library, Embase, PubMed, and Web of Science datasets was performed for citations published from 2000 to 2020 that compared transurethral laser with OP for the treatment of large BPH. Variables of interest assessing the two techniques included clinical characteristics, and the perioperation-, effectiveness-, and complication-related outcomes. Results: The meta-analysis included twelve studies containing 1,514 patients, with 792 laser and 722 OP. The transurethral laser group was associated with shorter hospital stay and catheterization duration, and less hemoglobin decreased in the perioperative variables. There was no significant difference in the international prostate symptom score, post-void residual urine volume, maximum flow rate, and quality of life score. Transurethral laser group had a significantly lower incidence of blood transfusion than OP group (odds ratio, 0.10; 95% confidence interval, 0.05 to 0.19; p<0.001; I2=8%), and no statistical differences were found with respect to the other complications. Conclusions: Both OP and transurethral laser prostatectomy are effective and safe treatments for large prostate adenomas. With these advantages of less blood loss and transfusion, and shorter catheterization time and hospital stay, laser may be a better choice for large BPH.
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Fibulin2: a negative regulator of BMSC osteogenic differentiation in infected bone fracture healing
Li Shi-Dan,Xing Wei,Wang Shao-Chuan,Li You-Bin,Jiang Hao,Zheng Han-Xuan,Li Xiao-Ming,Yang Jing,Guo De-Bin,Xie Xiao-Yu,Jiang Ren-Qing,Fan Chao,Li Lei,Xu Xiang,Fei Jun 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Bone fracture remains a common occurrence, with a population-weighted incidence of approximately 3.21 per 1000. In addition, approximately 2% to 50% of patients with skeletal fractures will develop an infection, one of the causes of disordered bone healing. Dysfunction of bone marrow mesenchymal stem cells (BMSCs) plays a key role in disordered bone repair. However, the specific mechanisms underlying BMSC dysfunction caused by bone infection are largely unknown. In this study, we discovered that Fibulin2 expression was upregulated in infected bone tissues and that BMSCs were the source of infection-induced Fibulin2. Importantly, Fibulin2 knockout accelerated mineralized bone formation during skeletal development and inhibited inflammatory bone resorption. We demonstrated that Fibulin2 suppressed BMSC osteogenic differentiation by binding to Notch2 and inactivating the Notch2 signaling pathway. Moreover, Fibulin2 knockdown restored Notch2 pathway activation and promoted BMSC osteogenesis; these outcomes were abolished by DAPT, a Notch inhibitor. Furthermore, transplanted Fibulin2 knockdown BMSCs displayed better bone repair potential in vivo. Altogether, Fibulin2 is a negative regulator of BMSC osteogenic differentiation that inhibits osteogenesis by inactivating the Notch2 signaling pathway in infected bone.
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