AT1R-Mediated Apoptosis of Bone Marrow Mesenchymal Stem Cells Is Associated with mtROS Production and mtDNA Reduction.

Angiotensin II (Ang II) is used as an inducer for the differentiation of mesenchymal stem cells (MSCs). Whether the commonly used doses of Ang II for MSC differentiation affect cell apoptosis has not been elucidated. In this study, we investigated the effect of Ang II on the apoptosis of bone marrow MSCs (BMMSCs), and its relations to the activation of Ang II receptor-1- (AT1R-) signaling, mitochondrial ROS (mtROS) generation, and mitochondrial DNA (mtDNA) leakage.

Expression and functional analysis of flotillins in Dugesia japonica.

FLOTILLIN-1 and FLOTILLIN-2 are membrane rafts associated proteins that have been implicated in insulin and growth factor signaling, endocytosis, cell migration, proliferation, differentiation, cytoskeleton remodeling and membrane trafficking. Furthermore, FLOTILLINs also play important roles in the progression of cancer and neurodegenerative diseases. In this study, the roles of flotillins are investigated in planarian Dugesia japonica.

Blocking of autocrine IGF-1 reduces viability of human umbilical cord mesenchymal stem cells via inhibition of the Akt/Gsk-3β signaling pathway.

Human umbilical cord mesenchymal stem cells (hUCMSCs) are able to secrete growth factors, such as hepatocyte growth factor, vascular endothelial growth factor and insulin‑like growth factor‑1 (IGF‑1). The secretion of these growth factors by transplanted hUCMSCs have been identified to stimulate the growth of the host cells in the target organs or tissues. The aim of the present study was to investigate the effect of autocrine IGF‑1 on cell viability of hUCMSCs.

Oxidized low-density lipoprotein (ox-LDL) promotes cardiac differentiation of bone marrow mesenchymal stem cells via activating ERK1/2 signaling.

Background/aims: The differentiation efficiency of bone marrow mesenchymal stem cells (BM-MSCs) is low in vivo after transplantation. Therefore, it is necessary to look for effective reagents for enhancing cardiac differentiation of BM-MSCs. It has been reported that cardiac differentiation of stem cells depends on the activation of extracellular signal-regulated protein 1/2 (ERK1/2) signaling.

Effects of linagliptin and liraglutide on glucose- and angiotensin II-induced collagen formation and cytoskeleton degradation in cardiac fibroblasts in vitro.

Aim: Glucagon-like peptide-1 (GLP-1) agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors can not only lower blood glucose levels, but also alleviate cardiac remodeling after myocardial ischemia and hypertension. In the present study, we investigated the effects of a DPP-4 inhibitor (linagliptin) and a GLP-1 activator (liraglutide) on glucose- and angiotensin II (Ang II)-induced collagen formation and cytoskeleton reorganization in cardiac fibroblasts in vitro, and elucidated the related mechanisms.

Methods: Cardiac fibroblasts were isolated from the hearts of 6-week-old C57BL/6 mice, and then exposed to different concentrations of glucose or Ang II for 24 h.

Sertoli cells promote proliferation of bone marrow-derived mesenchymal stem cells in co-culture.

Bone marrow-derived mesenchymal stem cells (BMSCs) are a major source for cell transplantation. The proliferative ability of BMSCs is an important determinant of the efficiency of transplant therapy. Sertoli cells are "nurse" cells for development of sperm cells.

TGF-β1 induces apoptosis of bone marrow-derived mesenchymal stem cells via regulation of mitochondrial reactive oxygen species production.

Bone marrow-derived mesenchymal stem cells (BMSCs) are the most promising seed cells in regenerative medicine. Our previous study demonstrated that transforming growth factor (TGF)-β1 induced BMSC senescence . Whether TGF-β1 affects the apoptosis of BMSCs has not been examined; therefore the aim of the present study was to investigate this effect.

Small concentrations of TGF-β1 promote proliferation of bone marrow-derived mesenchymal stem cells via activation of Wnt/β-catenin pathway.

Bone marrow-derived mesenchymal stem cells (BMSCs) are the most promising seed cells for cell transplant. The proliferation of BMSCs is one of the most important determinants of the efficiency of MSC-based transplant therapy. It has been reported that transforming growth factor-β1 (TGF-β1) activates Wnt/β-catenin signaling and regulates cell proliferation.

Association between endothelin-1/endothelin receptor A and inflammation in mouse kidneys following acute ischemia/reperfusion.

Renal ischemia/reperfusion (I/R) is a common risk factor for renal failure. Expression of endothelin‑1 (ET‑1) and its receptor ETA were also reported to be involved in the development of acute and chronic renal disease. The present study was designed to investigate the association between inflammation and ET‑1/ETA expression in mouse kidneys following acute I/R.

Overexpression of CyclinA2 ameliorates hypoxia-impaired proliferation of cardiomyocytes.

Hypoxia is a primary mediator for cell survival, and has been reported to inhibit cardiomyocyte proliferation in fetal and neonatal hearts. CyclinA2 is a key regulator of cell proliferation. Whether CyclinA2 affects cardiomyocyte proliferation in hypoxic conditions remains unexamined.

Downregulation of β-catenin and Akt signaling is responsible for poor proliferation of the late passage of bone marrow mesenchymal stem cells.

It is well established that mesenchymal stem cells (MSCs) will partially lose their proliferative ability with continuous expansion. However, the specific mechanisms underlying this effect remain unclear. In the present study, it was identified that β-catenin was downregulated in the late passage (passage 8) of bone marrow mesenchymal stem cells (bmMSCs).

TGF-β1 induces senescence of bone marrow mesenchymal stem cells via increase of mitochondrial ROS production.

Background: Bone marrow derived mesenchymal stem cells (bmMSCs) are multipotent cells that can differentiate into diverse cell types, including cardiomyocytes. BmMSC-based transplantation is capable of repairing acute and chronic myocardial infarction. Prior to the transplantation, MSCs are usually induced in vitro by biological reagents and chemicals for directional differentiation.

Hypoxia induces autophagy of bone marrow-derived mesenchymal stem cells via activation of ERK1/2.

Background: Bone marrow-derived mesenchymal stem cells (bmMSCs) are the most promising seed cells for cell transplant therapy. Hypoxia is a known stimulus of autophagy. Recent studies showed that hypoxia promotes autophagy of human placental chorionic plate-derived mesenchymal stem cells (CP-MSCs).

Aspirin attenuates angiotensin II-induced inflammation in bone marrow mesenchymal stem cells via the inhibition of ERK1/2 and NF-κB activation.

Angiotensin II (Ang II) is a peptide hormone that plays a critical role in numerous physiological and pathophysiological processes. It is also commonly used as an inducer for the directional differentiation of bone marrow mesenchymal stem cells (bmMSCs). Previous studies demonstrated that Ang II induces inflammatory responses in endothelial cells, smooth muscle cells and fibroblasts.

Ox-LDL promotes migration and adhesion of bone marrow-derived mesenchymal stem cells via regulation of MCP-1 expression.

Bone marrow-derived mesenchymal stem cells (bmMSCs) are the most important cell source for stem cell transplant therapy. The migration capacity of MSCs is one of the determinants of the efficiency of MSC-based transplant therapy. Our recent study has shown that low concentrations of oxidized low-density lipoprotein (ox-LDL) can stimulate proliferation of bmMSCs.

MicroRNA-10b promotes the migration of mouse bone marrow-derived mesenchymal stem cells and downregulates the expression of E-cadherin.

The ability of mesenchymal stem cells (MSCs) to migrate is an important determinant of the efficiency of MSC transplant therapy. MicroRNA-10b (miR-10b) has been positively involved in the migration of a number of tumor cells lineages. To date, it remains unknown whether miR-10b affects the migration of MSCs.

Lectin-like oxidized LDL receptor-1 expresses in mouse bone marrow-derived mesenchymal stem cells and stimulates their proliferation.

The bone marrow-derived mesenchymal stem cells (bmMSCs) have been widely used in cell transplant therapy, and the proliferative ability of bmMSCs is one of the determinants of the therapy efficiency. Lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) as a transmembrane protein is responsible for binding, internalizing and degrading oxidized low density lipoprotein (ox-LDL). It has been identified that LOX-1 is expressed in endothelial cells, vascular smooth muscle cells, cardiomyocytes, fibroblasts and monocytes.

Co-culture with Sertoli cells promotes proliferation and migration of umbilical cord mesenchymal stem cells.

Human umbilical cord mesenchymal stem cells (hUCMSCs) have been recently used in transplant therapy. The proliferation and migration of MSCs are the determinants of the efficiency of MSC transplant therapy. Sertoli cells are a kind of "nurse" cells that support the development of sperm cells.