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BACKGROUND:Wnt signaling pathway is overexpressed in degenerative intervertebral discs,and inhibition of its expression can delay the process of intervertebral disc degeneration.Therefore,Wnt signaling pathway is closely related to intervertebral disc degeneration. OBJECTIVE:To summarize the relationship between Wnt signaling pathway and intervertebral disc,especially the specific role and influence of Wnt signaling pathway in intervertebral disc degeneration. METHODS:The first author took"intervertebral disc,Wnt,cell proliferation,cell senescence,cell apoptosis,extracellular matrix"as the English search terms.PubMed,Web of science and OVID LWWSpringerlink were searched for articles published from 2000 to January 2023,and articles related to Wnt signaling pathway and disc degeneration were consulted.Totally 54 articles were reviewed by reading,collating and preserving. RESULTS AND CONCLUSION:(1)During intervertebral disc formation in embryos,Wnt signaling pathway is overexpressed,which is involved in intervertebral disc formation and promotes posterior extension of notochord.(2)During intervertebral disc degeneration,Wnt signaling pathway can inhibit cell proliferation by stagnating cell cycle,increase the expression of age-related proteins and promote cell aging by participating in oxidative stress,and participate in cell apoptosis by regulation of long non-coding RNA.(3)Wnt signaling pathway can also decrease extracellular matrix related protein synthesis,promote extracellular matrix degradation and accelerate intervertebral disc degeneration.(4)Wnt signaling pathway can promote cell regeneration by activating as early intervertebral disc formation signal and participate in inducing stem cells to differentiate into intervertebral disc cells to repair damaged intervertebral disc.For example,Wnt signaling pathway can induce stem cells from cartilage endplate cells to migrate and transform to intervertebral disc.
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Oligodendrocytes (OLs) are myelinating glial cells that form myelin sheaths around axons to ensure rapid and focal conduction of action potentials. Here, we found that an axonal outgrowth regulatory molecule, AATYK (apoptosis-associated tyrosine kinase), was up-regulated with OL differentiation and remyelination. We therefore studied its role in OL differentiation. The results showed that AATYK knockdown inhibited OL differentiation and the expression of myelin genes in vitro. Moreover, AATYK-deficiency maintained the proliferation status of OLs but did not affect their survival. Thus, AATYK is essential for the differentiation of OLs.
Subject(s)
Animals , Mice , Rats , Animals, Newborn , Apoptosis Regulatory Proteins , Genetics , Metabolism , Cell Differentiation , Physiology , Cell Proliferation , Genetics , Cells, Cultured , Cuprizone , Toxicity , Demyelinating Diseases , Metabolism , Pathology , Embryo, Mammalian , Gene Expression Regulation, Developmental , Genetics , Ki-67 Antigen , Metabolism , Mice, Inbred C57BL , Myelin Basic Protein , Metabolism , Myelin Proteolipid Protein , Metabolism , Myelin Sheath , Metabolism , Oligodendroglia , Metabolism , Protein-Tyrosine Kinases , Genetics , Metabolism , RNA, Small Interfering , Genetics , Metabolism , Rats, Sprague-DawleyABSTRACT
ObjectiveToinvestigatetheMunicipalHospital(Ezhoucity)theimplementationofruralbasic public health service mode of linkage of areaeffect.Methods The hospital public health division of functions and du-ties,the integration of technology and equipment strength,mobilize theinformation flow,focused team of experts,stand-ardize the informationnetwork,to carry out drive rural area of basic public health work.Results The three level hos-pitals of Ezhou played a leading role,has been associated with lower hospital ( Taihe, Gedian) to establish a long-term cooperative relations,for the scientific management of basic public health items the purpose of the make and model.Conclusion The comprehensive hospital,reflect the public interest in public health work,to achieve the inte-gration of urban and rural public health pattern.
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BACKGROUND:There have been a large number of reports on establishing induced pluripotent stem celllines, but studies concerning large-scale in vitro induced differentiation of induced pluripotent stem cels into hematopoietic progenitor cels stil have a lack of in-depth discussion. OBJECTIVE:To develop methods to induce differentiation of induced pluripotent stem cels into hematopoietic progenitor cels in vitro. METHODS: Using the method of infection with lentivirus particles containing four transcriptionfactor genes, which are Oct4, Sox2, Nanog and Lin28, human skin fibroblasts are transduced into induced pluripotent stem cels. In the induced differentiation system, Y-27632, a kind of tyrosine kinase inhibitor-ROCK (p160-Rho-associated coiled-coil kinase), was added, which obviously suppressed apoptosis of cels. Based on conditioned medium with OP9 cels, a differentiation system of inducing induced pluripotent stem cels differentiating into hematopoietic progenitor cels was established. RESULTS AND CONCLUSION:(1) Apoptosis of induced pluripotent stem cels at the first three passages was very obvious, and the cels were difficult in a large-scale expansion. After Y-27632 was added, the apoptosis of embryonic stem cels was obviously inhibited. (2) During embryoid body differentiation, induced pluripotent stem cels cultured in OP9 conditional growth medium differentiated into hematopoietic progenitor celsin vitro that were positive for CD34.
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Objective To investigate the effect of botulinum toxin type A injection on the expres-sion of substance P, TGF-β1 and α-SMA in rabbit ear model of hypertrophic scar. Methods The hyper-trophic sear model was established in 24 Japanese rabbits'ears. The wounds in ventral surface of ear were divided in Group I (lateral wounds) and Group S (medial wounds), 3 wounds each side per ear, totally 72 wounds each group. The wound-healing time and the growth of scar were observed and recorded. On post-wounding day 28, the wounds were created in another 6 rabbits in the same way and the normal skin were harvested as Group C. Likewise, the scar samples in Groups I and S were harvested. The mRNA expression of substance P, TGF-β1 and α-SMA were detected quantitatively by using real-time PCR and α-SMA was also detected with Western blot. Results No difference between the ratio of healed or infec-tious wounds on post-wounding day 14. The mRNA expression of SP, TGF-β1 and α-SMA in Group I was significantly lower than Group S, but higher than those in Group C (P<0. 01 and <0. 05, respec-tively). The blot density of α-SMA and the ratio of blot density of a-SMA to β-actin in Group I were be-tween that of the other two groups. Conclusion Without delaying the wound-healing, botulinum toxin type A injection significantly decreases the expression of SP, TGF-β1 and α-SMA in rabbit ear model of hypertrophic scar.
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<p><b>OBJECTIVE</b>To study the injury process of the skin due to expansion.</p><p><b>METHODS</b>New Zealand rabbits were divided into 4 groups: rapid expansion and slow expansion as well as two control groups. The changes of skin TGF-beta 1 were observed immediately after expansion and at 1, 12, 24 weeks after expansion. Immunohistochemistry and in situ hybridization technique were applied.</p><p><b>RESULTS</b>TGF-beta 1 increased in the skin immediately after expansion. In groups of rapid expansion, TGF-beta 1 increased faster and then decreased also faster than slow expansion groups. The results from immunohistochemistry and in situ hybridization were almost same.</p><p><b>CONCLUSION</b>Expansion resulted in skin injury. Rapid expansion injured the skin more seriously than slow expansion. TGF-beta 1 may be the main regulating factor to repairing process.</p>