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1.
Journal of Biomedical Engineering ; (6): 609-616, 2023.
Artículo en Chino | WPRIM | ID: wpr-1008879

RESUMEN

Stem cells have been regarded with promising application potential in tissue engineering and regenerative medicine due to their self-renewal and multidirectional differentiation abilities. However, their fate is relied on their local microenvironment, or niche. Recent studied have demonstrated that biophysical factors, defined as physical microenvironment in which stem cells located play a vital role in regulating stem cell committed differentiation. In vitro, synthetic physical microenvironments can be used to precisely control a variety of biophysical properties. On this basis, the effect of biophysical properties such as matrix stiffness, matrix topography and mechanical force on the committed differentiation of stem cells was further investigated. This paper summarizes the approach of mechanical models of artificial physical microenvironment and reviews the effects of different biophysical characteristics on stem cell differentiation, in order to provide reference for future research and development in related fields.


Asunto(s)
Señales (Psicología) , Células Madre , Diferenciación Celular , Medicina Regenerativa , Ingeniería de Tejidos
2.
International Journal of Biomedical Engineering ; (6): 120-124, 2019.
Artículo en Chino | WPRIM | ID: wpr-751598

RESUMEN

Objective To investigate the role of Wnt/β-catenin signaling pathway in the osteogenic differentiation of human dental pulp stem cells (hDPSCs). Methods After 14 days of the calcium hydroxide training, the cytoskeletal changes of hDPSCs, the expression of β-catenin, i.e. the key promoter of in the Wnt signaling pathway, and the cell localization were detected by laser scanning confocal technique. The Wnt signaling pathways were up-regulated and inhibited, and the osteogenic differentiation and mineralization of hDPSCs were detected by Western Blot and alizarin red staining after 14 days of the training. Results The cytoskeleton of hDPSCs was rearranged by the effect of calcium hydroxide, and theβ-catenin migration from nucleus to cytoplasm were observed. The number of calcium nodules in hDPSCs was decreased after blocking Wnt signaling pathway by Dickkopf-related protein 1 (DKK-1). The calcium hydroxide treatment can promoted dentin sialophosphoprotein (DSPP) expression in hDPSCs. Conclusions Calcium hydroxide can down-regulate the expression of canonical Wnt signaling pathway and promote osteogenic differentiation and mineralization and odontogenetic differentiation of hDPSCs.

3.
Chinese Journal of Tissue Engineering Research ; (53): 1946-1952, 2017.
Artículo en Chino | WPRIM | ID: wpr-513451

RESUMEN

BACKGROUND:Numerous diseases like cardiac hypertrophy and intervertebral disc degeneration are known to be implicated in the changes of mechanical stress acting on surrounding tissues or cells, and autophagy contributes to the pathogenesis of these diseases. OBJECTIVE:To review the effects of mechanical factors on autophagy in different tissues and the underlying molecular mechanisms, thereby providing references for the research of autophagy and the prevention and treatment of related diseases. METHODS:A search of Web of Science and PubMed databases was performed for the literatures addressing the effects of mechanical factors on autophagy using the English keywords ofautophagy, mechanicaland the articles were summarized systematically. Finally, 52 literatures were enrolled according to the inclusion and exclusion criteria. RESULTS AND CONCLUSION:Mechanical factors make great effects on autophagy of various cells, such as myocardial cells, endothelial cells, chondrocytes and skeletal muscle cells. Autophagy is a self-protective reaction, and the mechanical stress of physiological conditions induces autophagy to maintain cellhomeostasis, normal function and survival. The mechanism of autophagy induced by mechanical stress may involve PI3K-AKT-mTOR, oxygen free radical, AKT-FoxO and other pathways, and the definite mechanism needs to be further studied.

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