Bls 1 frá 54 niðurstöður
BACKGROUND
We aimed to evaluate the potential enhancing effect of celastrol on the stemness of human tendon-derived stem cells (hTSCs) in vitro and the underlying molecular mechanisms.
METHODS
The capability of hTSC self-renewal was assessed by cell proliferation and colony formation as determined
We aimed to investigate the potential beneficial effect of ferulic acid (FA) on stemness of human tendon-derived stem cells (hTSCs) in vitro and to elucidate the underlying molecular mechanism. The self-renewal ability of hTSCs was evaluated by colony formation and cell proliferation was determined
Introduction. Stem cells are regularly cultured under normoxic conditions. However, the physiological oxygen tension in the stem cell niche is known to be as low as 1-2% oxygen, suggesting that hypoxia has a distinct impact on stem cell maintenance. Periodontal ligament cells (PDLCs) and dental pulp
Background and aim: Inadequate vascularization is a challenge in bone tissue engineering because internal cells are prone to necrosis due to a lack of nutrient supply. Rat bone marrow-derived mesenchymal stem cells (rBMSCs) and human
Retroviral transduction of four transcription factors (Oct4, Sox2, Klf4 and c-Myc) or three factors, excluding c-Myc, has been shown to initiate a reprogramming process that results in the transformation of murine fibroblasts to induced pluripotent stem (iPS) cells, and there has been a rapid
OBJECTIVE
This study aimed to investigate the effects of hypoxia on the characteristics of human dental follicle cells (hDFCs).
METHODS
The tissue explant collagenase method was used to isolate hDFCs from young permanent teeth. The immunofluorescence technique was used to detect cell surface
Objective: To investigate the effects of hypoxia-pretreated rat adipose-derived mesenchymal stem cells (ADSCs) conditioned medium on wound healing of rats with full-thickness defects. Methods: (1) A 6-week-old male Sprague-Dawley rat was sacrificed by cervical dislocation, the
Objective: To investigate the impact of hypoxia-reoxygenation environment on the level of autophagy in osteoblasts. Methods: Osteoblasts were purified from the skulls of newborn SD rats within 24-48 hours by tissue block adherence culture and differential centrifugation. The
OBJECTIVE
To compare the osteogenic effect of bone marrow mesenchymal stem cells (BMSCs) transfected by adenovirus-bone morphogenetic protein 2-internal ribosome entry site-hypoxia inducible factor 1alpha(mu) (Ad-BMP-2-IRES-HIF-1alpha(mu)) and by Ad-cytomegalovirus (CMV)-BMP-2-IRES-human renilla
Objective: To investigate the effects of hypoxia condition and hypoxia-reoxygenation condition on the cell viability, apoptosis rate and gene expression of osteoblasts cultured in vitro. Methods: The cranium osteoblasts from newborn Sprague Dawley rats within 48 hours were cultured and purified
OBJECTIVE
Severe hypoxia always inhibits the cell proliferation, osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs), and hinders bone defect repair. Herein we explored the effects of mechano-growth factor (MGF) E peptide on the proliferation and osteogenic
The effects of hypoxia on the osteogenic potential of mesenchymal stem cells (MSCs) have been previously reported. From these studies, possible factors affecting the association between hypoxia and the osteogenic differentiation of MSCs have been suggested, including hypoxia severity, cell origin
Hypoxia is a crucial microenvironment for inflamed periodontal tissue and periodontal wound healing. Enamel matrix proteins (EMPs) potentially can promote the formation of new periodontium. The effects of EMPs on periodontal ligament cells under hypoxia, however, remain unclear. We investigated the
Studies have proved that miRNAs participate in the regulation of osteoblast differentiation (OD), and abnormal expression of miRNAs is related with various states of OD. In this study, we investigated the role of miRNA-1-3p in OD using MC3T3-E1 cells. BMP2 is used to induce OD of MC3T3-E1 cells.
Craniofacial anomalies can arise from both genetic and environmental factors, including prenatal hypoxia. Recent clinical evidence correlates hypoxia to craniofacial malformations. However, the mechanisms by which hypoxia mediates these defects are not yet understood. We examined the cellular