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Pinzani M 《Journal of hepatology》2011,55(2):459-465
The possibility that epithelial-mesenchymal transition (EMT) could contribute to hepatic fibrogenesis in chronic liver diseases as reported in other organs, particularly the kidney, reinforced the concept that activated hepatic stellate cells were not the only key players in the hepatic fibrogenic process and that other cell types, either hepatic (i.e. portal fibroblast) or extrahepatic (bone marrow-derived cells and circulating fibrocytes) could contribute to this process. The possibility of the rapid mobilization of a large amount of fibrogenic cells by EMT after liver tissue injury made this phenomenon a relevant and suitable target for anti-fibrogenic strategies. Following an initial enthusiasm for the discovery of this novel pathway in fibrogenesis and the publication of a several highly quoted papers, more recent research has started to cast serious doubts upon the real relevance of this phenomenon in human fibrogenetic disorders. The debate on the authenticity of EMT or at least on its real contribution to the fibrogenic process has become very animated, sometimes reaching levels of "religious" integralism. The overall result is a general confusion on the meaning and on the definition of several key aspects. The aim of this article is to analyze and discuss the evidence supporting or confuting this possibility in order to reach reasonable and useful conclusions. 相似文献
85.
角膜瘢痕是继发于多种角膜疾病的病理性改变,是许多角膜疾病造成视力不同程度损害甚至丧失的直接原因,也是影响角膜屈光手术效果的重要因素.对于角膜损伤愈合后的角膜瘢痕,目前临床上主要治疗方法是穿透性或者板层角膜移植术,但因为角膜供体材料缺乏和经济原因,大量的患者无法得到手术治疗而最终丧失视力. 相似文献
86.
Farias VA Linares-Fernández JL Peñalver JL Payá Colmenero JA Ferrón GO Duran EL Fernández RM Olivares EG O'Valle F Puertas A Oliver FJ Ruiz de Almodóvar JM 《Placenta》2011,32(1):86-95
Background
It has been demonstrated that human umbilical cord stromal stem cells (UCSSCs) are bio-equivalent to bone marrow mesenchymal stem cells. However, little is known about their tissue origin or in vivo functions, and data on their expansion properties are limited due to early senescence in the culture methods described to date.Methods
UC sections and cultured UCSSCs were analyzed with a panel of 12 antibodies. UCSSCs were grown in low-FCS containing medium at 5% or 21% oxygen and were assayed for their clonogenic properties, karyotype stability, expression of specific cellular markers, and multi-lineage potential. UCSSC contractile properties were evaluated by using collagen gel contraction assays under cytokine stimulus.Results
Immunohistochemistry studies showed that the UCSSCs were derived from the Wharton’s jelly and not from the vascular smooth muscle sheath of the blood vessels. UCSSC growth properties were increased in a 5% oxygen atmosphere in comparison to normoxic culture conditions. In both culture conditions, UCSSCs were CD14-, CD34-, and CD45-negative while expressing high levels of CD73, CD90 and CD105 and maintaining their differentiation potentialities. UCSSCs expressed alpha smooth muscle actin and behaved as functional myofibroblasts when cellular contraction was challenged with appropriate stimuli.Conclusions
UCSCs are mesenchymal stem cells that reside in the perivascular area of Wharton’s jelly and are phenotypically and functionally related to myofibroblasts. 相似文献87.
The fibroblasts and the myofibroblasts are key players for maintaining skin homeostasis and for orchestrating physiological tissue repair. The (myo)fibroblasts are embedded in a sophisticated extracellular matrix (ECM) that they secrete, and a complex and interactive dialogue exists between (myo)fibroblasts and their microenvironment. The composition of the ECM around (myo)fibroblasts is variable depending on the situation and, in addition to the secretion of the ECM, the (myo)fibroblasts, by secreting matrix metalloproteinases and tissue inhibitors of metalloproteinases can remodel this ECM. The (myo)fibroblasts and their microenvironment form a changing network with reciprocal actions leading to cell differentiation, proliferation, quiescence or apoptosis, and also acting on growth factor biodisponibility. In pathological situations (such as chronic wounds or excessive scarring), or during ageing, especially due to ultraviolet exposition, this dialogue between the (myo)fibroblasts and their microenvironment is disrupted, leading to repair defects or to skin injuries with unaesthetic alterations such as wrinkles. Knowing the intimate exchanges between the (myo)fibroblasts and their microenvironment represents a fascinating domain important not only for characterizing new targets and drugs able to prevent pathological developments but also for interfering with skin alterations observed during ageing. 相似文献
88.
Liu J Wang Y Pan Q Su Y Zhang Z Han J Zhu X Tang C Hu D 《Journal of dermatological science》2012,65(1):38-49
Background
Fibroblast-to-myofibroblast transition is a key event during wound healing and hypertrophic scar formation. Previous studies suggested Wnt/β-catenin signaling might be involved in the wound healing. However, its specific role in skin fibroblast-to-myofibroblast transition remains unclear.Objective
To investigate the specific role of β-catenin during the transforming growth factor-β1 induced normal skin myofibroblasts transition.Methods
By real-time quantitative polymerase chain reaction, Western-blot and immunocytochemistry, the activation of Wnt/β-catenin pathway in cultured human normal skin fibroblasts during TGF-β1 induced fibroblast-to-myofibroblast transition was investigated. The effects of β-catenin on myofibroblasts transition were also investigated when SB-216763, over-expression and siRNA of β-catenin were utilized. In addition, fibroblasts populated collagen lattices contraction assays were conducted to examine the effects of β-catenin on the contractility of the fibroblasts induced by TGF-β1. Furthermore, the effects of β-catenin on the expression of α-smooth muscle actin and collagen types I and III in hypertrophic scar derived fibroblasts were studied.Results
The expression of Wnts mRNA and β-catenin protein was up-regulated by TGF-β1 stimulation during the myofibroblasts transition. Both of SB-216763 and β-catenin over-expression was paralleled with decreased expression of α-smooth muscle actin, collagen types I and III, while siRNA targeting β-catenin leads to up-regulation of α-smooth muscle actin, collagen types I and III. The increased contractility and α-smooth muscle actin expression of the fibroblasts in the collagen lattices induced by TGF-β1 was inhibited by SB-216763. In addition, the expression levels of α-smooth muscle actin, collagen types I and III in hypertrophic scar derived fibroblasts were also down-regulated by SB-216763.Conclusion
Specifically in normal skin fibroblasts, β-catenin might be involved in the myofibroblasts transition and negatively regulate the TGF-β1-induced myofibroblast transition. 相似文献89.
Yang L Hashimoto K Tohyama M Okazaki H Dai X Hanakawa Y Sayama K Shirakata Y 《Journal of dermatological science》2012,65(1):50-57
Background
During skin wounding and healing, skin homeostasis is interrupted. How the altered epithelial-mesenchymal interactions influence scar formation and epidermogenesis should be investigated using three-dimensional models that are similar to in vivo structures.Objective
In this study, we assessed the effects of epithelial-mesenchymal interactions on myofibroblast differentiation and how myofibroblasts influence epidermogenesis using a human living skin equivalent (LSE) model.Methods
We constructed a fibroblast-populated type I collagen gel upon which LSEs were formed by seeding with normal human keratinocytes. Samples of the collagen gel and LSEs were collected at different time points. Myofibroblast differentiation, epidermal differentiation, and proliferation status were investigated immunohistochemically. Several measures were taken to suppress α-smooth muscle actin (α-SMA) expression to determine the effects of myofibroblasts on epidermogenesis, including the addition of basic fibroblast growth factor or a transformation growth factor-β (TGF-β) kinase inhibitor to the culture medium and the inclusion of an amniotic membrane (AM) in the dermal matrix.Results
The myofibroblast/fibroblast ratio in the fibroblast-populated collagen gel kept rising during culture. In the LSEs, most fibroblasts were α-SMA-negative, except for those along the dermal-epidermal junction. The suppression of α-SMA expression enhanced epidermal differentiation and decreased TGF-β1 expression in the epidermis. The inhibition of TGF-β kinase completely suppressed α-SMA expression in the dermal matrix.Conclusions
Epidermogenesis suppressed α-SMA expression in the fibroblast-rich dermal matrix, except near the dermal-epidermal junction. The α-SMA-positive cells at the dermal-epidermal junction contributed to the hyperproliferative phenotype of the epidermis. In contrast, the hyperproliferative epidermis expressed more TGF-β1, which is responsible for myofibroblast differentiation. 相似文献90.