Angiotensin (1-7) Inhibits Transforming Growth Factor-Β1-Induced Epithelial-Mesenchymal Transition of Human Keratinocyte Hacat Cells in vitro.

Introduction: Angiotensin (1-7) (Ang-(1-7)) is an emerging component of the renin-angiotensin system (RAS) with effective anti-fibrosis properties and has been shown to interfere with epithelial-mesenchymal transition (EMT) by numerous studies. In recent years, EMT has been proposed as a new therapeutic target for skin fibrotic diseases such as keloids. However, the effect of Ang-(1-7) on EMT in skin is still unclear.

Hypoxia activates the PI3K/AKT/HIF-1α pathway to promote the anti-inflammatory effect of adipose mesenchymal stem cells.

This study aimed to investigate the effect of hypoxia on the anti-inflammatory effect of adipose-derived mesenchymal stem cells (AMSCs) in vitro and its possible mechanism. AMSCs were cultured in vitro in a hypoxic environment with 3% O, and a normoxic (21% O) environment was used as the control. The cells were identified by in vitro adipogenic and osteogenic differentiation and cell surface antigen detection, and the cell viability were detected.

Mechanical signals induces reprogramming of mature adipocytes through the YAP/TAZ-binding motif.

Tissue engineering technology will be the main approach to tissue regeneration in the future and are promising for the treatment of large-area burns and refractory wounds. Dedifferentiated fat cells (DFAT) derived from mature adipocytes (MAs) as a seed cell have great potential in cell therapy and tissue engineering for the treatment of a variety of clinical diseases because of their wider availability, stronger proliferation ability, multidirectional redifferentiation potential, higher cell purity, lower heterogeneity, and greater biosafety profile. However, the triggering mechanism for MAs reprogramming in vitro is unclear.