The extracellular matrix with a continuous gradient of SDF1guides the oriented migration of human umbilical cord mesenchymal stem cells.

The extracellular matrix (ECM) plays a crucial role in maintaining cell morphology and facilitating intercellular signal transmission within the human body. ECM has been extensively utilized for tissue injury repair. However, the consideration of factor gradients during ECM preparation has been limited.

A functionalized collagen-I scaffold delivers microRNA 21-loaded exosomes for spinal cord injury repair.

MicroRNA (miRNA)-based therapies have shown great potential in the repair of spinal cord injury (SCI). MicroRNA 21 (miR21) has been proven to have an essential protective effect on SCI. However, there are some challenges for miRNAs application due to their easy degradation and ineffective cell penetration.

The Extracellular Matrix Enriched With Exosomes for the Treatment on Pulmonary Fibrosis in Mice.

Pulmonary fibrosis (PF) is a severe respiratory disease caused by lung microenvironment changes. TGF-β/Smad3 signaling pathway plays a critical role in the fibrotic process. MicroRNA-29 (miR-29) has proved to alleviate the occurrence of PF by downregulating TGF-β/Smad3 signaling pathway.

A functional extracellular matrix biomaterial enriched with VEGFA and bFGF as vehicle of human umbilical cord mesenchymal stem cells in skin wound healing.

The construction of microvascular network is one of the greatest challenges for tissue engineering and cell therapy. Endothelial cells are essential for the construction of network of blood vessels. However, their application meets challenges in clinic due to the limited resource of autologous endothelium.

PM collecting in a tire manufacturing plant affects epithelial differentiation of human umbilical cord derived mesenchymal stem cells by Wnt/β-catenin pathway.

Mesenchymal stem cells (MSCs) can differentiate into pulmonary epithelial cells by Wnt/β-catenin pathway and promote lung repair. However, whether fine particulate matter (PM) could affect Wnt pathway and finally reduce the ability of MSCs to differentiate into epithelial cells is still unknown. This study aimed to investigate whether PM could inhibit the epithelial differentiation of human umbilical cord-derived MSCs cells (hUCMSCs) and the related underlying mechanism.

Comprehensive analysis of the lncRNA-associated ceRNA network identifies neuroinflammation biomarkers for Alzheimer's disease.

Accumulating evidence has highlighted the important roles of long non-coding RNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) in Alzheimer's disease (AD). In this study, we constructed an AD-derived lncRNA-associated ceRNA network (LncACeNET) based on the ceRNA hypothesis and co-expressed correlation analysis of RNAs (miRNAs, mRNAs and lncRNAs) from AD patients. Based on this network, we preliminarily identified new potential AD biomarkers including hsa-miR-155-5p, CERS6-AS1, and CTB-89H12.

Single cell derived spheres of umbilical cord mesenchymal stem cells enhance cell stemness properties, survival ability and therapeutic potential on liver failure.

Umbilical cord mesenchymal stem cells (UCMSCs) have shown great potentials in regenerative medicine for their extensive sources, multilineage differentiation potential, low immunogenicity and self-renewal ability. However, the clinical application of UCMSCs still confronts many challenges including the requirement of large quantity of cells, low survival ability in vivo and the loss of main original characteristics due to two-dimensional (2D) culture. The traditional three-dimensional (3D)-spheroid culture can mimic in vivo conditions, but still has limitations in clinical application due to large size of spheroid against direct injection and inner cell death.

The extracellular matrix enriched with membrane metalloendopeptidase and insulin-degrading enzyme suppresses the deposition of amyloid-beta peptide in Alzheimer's disease cell models.

Amyloid plaque is a typical feature of Alzheimer's disease (AD) and is one of the targets for AD therapy. Membrane metalloendopeptidase (MME) and insulin-degrading enzyme (IDE) are two types of proteases that could cleave beta-amyloid (Aβ) peptides generated by neuron cells of AD patients. Extracellular matrix (ECM) plays a crucial role in regulating tissue-specific functions and is an ideal biomaterial for tissue repair.

Quantitative assessment of human uterine fibroid xenograft using sequential in vivo bioluminescence imaging.

Uterine fibroid is one of the most common solid tumors occurring in reproductive age women. Lack of accurate methods for quantitative assessment of uterine fibroid progression severely impedes the basic research and drug screen of this disease. To solve this problem, the correlation between bioluminescence imaging (BLI) and initial cell number used to form xenograft was investigated in this study.

TP53I11 suppresses epithelial-mesenchymal transition and metastasis of breast cancer cells.

Epithelial-mesenchymal transition (EMT) is widely-considered to be a modulating factor of anoikis and cancer metastasis. We found that, in MDA-MB-231 cells, TP53I11 (tumor protein P53 inducible protein 11) suppressed EMT and migration in vitro, and inhibited metastasis in vivo. Our findings showed that hypoxic treatment upregulated the expression of HIF1α, but reduced TP53I11 protein levels and TP53I11 overexpression reduced HIF1α expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells.

Loss of TP53I11 Enhances the Extracellular Matrix-independent Survival by Promoting Activation of AMPK.

Extracellular matrix (ECM)-independent survival is an essential prerequisite for tumor metastasis, and a hallmark of epithelial cancer stem cells and epithelial-mesenchymal transition (EMT). Here, we found that loss of TP53I11 enhanced, and overexpression of TP53I11 suppressed the ECM-independent survival, EMT, and migration in MCF10A cells. TP53I11 has long been considered as a transcriptional target of TP53.

Nuclear respiratory factor 1 promotes spheroid survival and mesenchymal transition in mammary epithelial cells.

Epithelial cells aggregate into spheroids when deprived of matrix, and the proclivity for spheroid formation and survival is a hallmark of normal and tumorigenic mammary stem cells. We show here that Nuclear Respiratory Factor 1 (NRF1) is a spheroid promoter by in silico identification of this transcription factor as highly connected to top shRNA-hits deduced from re-iterative selections for shRNAs enriched in MCF10A spheroids. NRF1-promoted spheroid survival is linked to its stimulation of mitochondrial OXPHOS, cell migration, invasion, and mesenchymal transition.

BCL11A expression in acute phase chronic myeloid leukemia.

Chronic myeloid leukemia (CML) has chronic and acute phases. In chronic phase myeloid differentiation is preserved whereas in acute phase myeloid differentiation is blocked. Acute phase CML resembles acute myeloid leukemia (AML).

BCL11A expression in acute myeloid leukemia.

Background: BCL11A encodes a C2H2 type zinc-finger protein. During normal haematopoietic cell differentiation BCL11A expression is down-regulated. Data in mice suggest up-regulation of BCL11A is involved in the pathogenesis of myeloid leukaemias.