The expression mechanism of programmed cell death 1 ligand 1 and its role in immunomodulatory ability of mesenchymal stem cells.

Programmed cell death 1 ligand 1 (PD-L1) is an important immunosuppressive molecule, which inhibits the function of T cells and other immune cells by binding to the receptor programmed cell death-1. The PD-L1 expression disorder plays an important role in the occurrence, development, and treatment of sepsis or other inflammatory diseases, and has become an important target for the treatment of these diseases. Mesenchymal stem cells (MSCs) are a kind of pluripotent stem cells with multiple differentiation potential.

Interferon-gamma and tumor necrosis factor-alpha synergistically enhance the immunosuppressive capacity of human umbilical-cord-derived mesenchymal stem cells by increasing PD-L1 expression.

Background: The immunosuppressive capacity of mesenchymal stem cells (MSCs) is dependent on the "license" of several proinflammatory factors to express immunosuppressive factors such as programmed cell death 1 ligand 1 (PD-L1), which determines the clinical therapeutic efficacy of MSCs for inflammatory or immune diseases. In MSCs, interferon-gamma (IFN-γ) is a key inducer of PD-L1 expression, which is synergistically enhanced by tumor necrosis factor-alpha (TNF-α); however, the underlying mechanism is unclear.

Aim: To reveal the mechanism of pretreated MSCs express high PD-L1 and explore the application of pretreated MSCs in ulcerative colitis.

Fibroblast-like cells Promote Wound Healing via PD-L1-mediated Inflammation Resolution.

Chronic non-healing wounds fail to progress beyond the inflammatory phase, characterized by a disorder of inflammation resolution. PD-1/PD-L1, a major co-inhibitory checkpoint signaling, plays critical roles in tumor immune surveillance and the occurrence of inflammatory or autoimmune diseases, but its roles in wound healing remains unclear. Here, we described a novel function of PD-L1 in fibroblast-like cells as a positive regulator of wound healing.

HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer.

Background: Emerging evidence suggests that epithelial mesenchymal transition (EMT) and epigenetic mechanisms promote metastasis. Histone deacetylases (HDACs) and noncoding RNAs (ncRNAs) are important epigenetic regulators. Here, we elucidated a novel role of histone deacetylase 2 (HDAC2) in regulating EMT and CRC metastasis via ncRNA.

Full title: High glucose protects mesenchymal stem cells from metformin-induced apoptosis through the AMPK-mediated mTOR pathway.

Micro- and macro-vascular events are directly associated with hyperglycemia in patients with type 2 diabetes mellitus (TDM), but whether intensive glucose control decreases the risk of diabetic cardiovascular complications remains uncertain. Many studies have confirmed that impaired quality and quantity of mesenchymal stem cells (MSCs) plays a pathogenic role in diabetes. Our previous study found that the abundance of circulating MSCs was significantly decreased in patients with TDM, which was correlated with the progression of diabetic complications.

Metformin induces apoptosis in mesenchymal stromal cells and dampens their therapeutic efficacy in infarcted myocardium.

Background: Cardiovascular complications, especially myocardial infarctions (MIs), are the leading mortality cause in diabetic patients. The transplantation of stem cells into damaged hearts has had considerable success as a treatment for MI, although whether antidiabetic drugs affect the therapeutic efficacy of stem cell transplantation is still unknown. This study aims to understand whether and how metformin, one of the first-line drugs used to treat type 2 diabetes mellitus (TDM), induces mesenchymal stromal cell (MSC) apoptosis and dampens their cardioprotective effect after transplantation into infarcted hearts.

A surgical protocol for bicondylar four-quadrant tibial plateau fractures.

Purpose: Bicondylar tibial plateau fractures involving four articular quadrants are severe and complex injuries, and they remain a challenging problem in orthopaedic trauma. The aim of this study was to introduce a new treatment protocol with dual-incision and multi-plate fixation in the floating supine patient position as well as to report the preliminary clinical results.

Methods: From January 2006 to December 2011, 16 consecutive patients with closed bicondylar four-quadrant tibial plateau fractures (Schatzker type VI, OTA/AO 41C2/3) were treated with posteromedial inverted L-shaped and anterolateral incisions.

Schatzker type IV medial tibial plateau fractures: a computed tomography-based morphological subclassification.

Schatzker type IV medial tibial plateau fractures have an unfavorable prognosis, likely due to the mechanism of injury (fracture-dislocation/subluxation type) and possibly due to the involvement of the posterolateral plateau, which is different from previously thought. The aim of this study was to propose a new subclassification of Schatzker type IV fracture patterns based on 2-dimensional (2-D) computed tomography and three-dimensional (3-D) reconstruction. The authors defined Schatzker type IV medial tibial plateau fractures as AO/OTA 41 type B fractures (partial articular), with partial or total medial plateau involvement, leaving at least the anterolateral quadrant intact.