Immunoregulatory paracrine effect of mesenchymal stem cells and mechanism in the treatment of osteoarthritis.

Osteoarthritis (OA) is a degenerative joint disease caused by chronic inflammation that damages articular cartilage. At present, the treatment of OA includes drug therapy to relieve symptoms and joint replacement therapy for advanced OA. However, these palliatives cannot truly block the progression of the disease from the immunological pathogenesis of OA.

Improvement of diabetes-induced spinal cord axon injury with taurine via nerve growth factor-dependent Akt/mTOR pathway.

Diabetic neuropathy (DN) is a common neurological complication caused by diabetes mellitus (DM). Axonal degeneration is generally accepted to be the major pathological change in peripheral DN. Taurine has been evidenced to be neuroprotective in various aspects, but its effect on spinal cord axon injury (SCAI) in DN remains barely reported.

Bone marrow mesenchymal stem cells paracrine TGF-β1 to mediate the biological activity of osteoblasts in bone repair.

Background: Bone marrow mesenchymal stem cells (BMSCs) are an important source of seed cells for regenerative medicine and tissue engineering therapy. BMSCs have multiple differentiation potentials and can release paracrine factors to facilitate tissue repair. Although the role of the osteogenic differentiation of BMSCs has been fully confirmed, the function and mechanism of BMSC paracrine factors in bone repair are still largely unclear.

Long-term potentiation and depression regulatory microRNAs were highlighted in Bisphenol A induced learning and memory impairment by microRNA sequencing and bioinformatics analysis.

The mechanisms of Bisphenol A (BPA) induced learning and memory impairment have still not been fully elucidated. MicroRNAs (miRNAs) are endogenous non-coding small RNA molecules involved in the process of toxicant-induced neurotoxicity. To investigate the role of miRNAs in BPA-induced learning and memory impairment, we analyzed the impacts of BPA on miRNA expression profile by high-throughput sequencing in mice hippocampus.

Taurine Ameliorates Oxidative Stress in Spinal Cords of Diabetic Rats via Keap1-Nrf2 Signaling.

Hyperglycemia associated with diabetes mellitus (DM) causes oxidative stress, which is involved in the onset and development of diabetic neuropathy. Taurine, a powerful antioxidant, is an effective inhibitor of oxidative stress. The present experiment was conducted to explore the effect of taurine treatment on alterations in body weight, blood glucose, oxidative stress, and Keap1-Nrf2 signaling in the spinal cords of DM rats.

Taurine Ameliorates Apoptosis via AKT Pathway in the Kidney of Diabetic Rats.

Diabetic nephropathy is one of the major diabetic complications which has become the major cause of end-stage renal disease. It has been demonstrated that apoptosis induced by hyperglycemia is a critical factor in the pathophysiology of diabetic nephropathy. Taurine is a semi-essential amino acid in mammals and has been shown to be a potent endogenous antioxidant.

Bone marrow mesenchymal stem cells promote remyelination in spinal cord by driving oligodendrocyte progenitor cell differentiation via TNFα/RelB-Hes1 pathway: a rat model study of 2,5-hexanedione-induced neurotoxicity.

Background: N-hexane, with its metabolite 2,5-hexanedine (HD), is an industrial hazardous material. Chronic hexane exposure causes segmental demyelination in the peripheral nerves, and high-dose intoxication may also affect central nervous system. Demyelinating conditions are difficult to treat and stem cell therapy using bone marrow mesenchymal stem cells (BMSCs) is a promising novel strategy.

2,5-Hexanedione induced apoptosis in rat spinal cord neurons and VSC4.1 cells via the proNGF/p75NTR and JNK pathways.

Increasing evidence suggests that n-hexane induces nerve injury via neuronal apoptosis induced by its active metabolite 2,5-hexanedione (HD). However, the underlying mechanism remains unknown. Studies have confirmed that pro-nerve growth factor (proNGF), a precursor of mature nerve growth factor (mNGF), might activate apoptotic signaling by binding to p75 neurotrophin receptor (p75NTR) in neurons.

Taurine ameliorates axonal damage in sciatic nerve of diabetic rats and high glucose exposed DRG neuron by PI3K/Akt/mTOR-dependent pathway.

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes and axonopathy is its main pathological feature. Previous studies suggested an advantage of taurine against diabetes. However, there are few reports which study the effect of taurine against axonopathy.

NGF mediates protection of mesenchymal stem cells-conditioned medium against 2,5-hexanedione-induced apoptosis of VSC4.1 cells via Akt/Bad pathway.

It has been shown that the conditioned medium of bone mesenchymal stem cells (BMSC-CM) can inhibit apoptosis of neural cells exposed to 2,5-hexanedione (HD), but its protective mechanism remains unclear. To investigate the underlying mechanism, VSC4.1 cells were given HD and 5, 10 and 15% BMSC-CM (v/v) in the current experiment.

Taurine inhibits neuron apoptosis in hippocampus of diabetic rats and high glucose exposed HT-22 cells via the NGF-Akt/Bad pathway.

Type 2 Diabetes causes learning and memory deficits that might be mediated by hippocampus neuron apoptosis. Studies found that taurine might improve cognitive deficits under diabetic condition because of its ability to prevent hippocampus neuron apoptosis. However, the effect and mechanism is not clear.

2,5-hexanedione-induced deregulation of axon-related microRNA expression in rat nerve tissues.

Exposure to organic solvent in industry, including n-hexane is correlated with central-peripheral axonopathy, which is mediated by its active metabolite, 2,5-hexanedione (HD). However, the underlying mechanism is still largely unknown. Recently identified microRNAs (miRNAs) may play important roles in toxicant exposure and in the process of toxicant-induced neuropathys.

Correction to: Taurine Ameliorates High Glucose Induced Apoptosis in HT-22 Cells.

Affiliations of authors Muhammad Shahbaz and Shahid Alam were incorrect in the published book. This has now been corrected as below.

The microRNAs Expression Profile in Sciatic Nerves of Diabetic Neuropathy Rats After Taurine Treatment by Sequencing.

Taurine protect against diabetic neuropathy. However, the protective mechanism of taurine has been poorly understood. It has been demonstrated that microRNAs (miRNAs) are involved in regulating gene expression.

Taurine Promotes Neuritic Growth of Dorsal Root Ganglion Cells Exposed to High Glucose in Vitro.

Diabetic neuropathy (DN) is the most common chronic complication of DM and its major pathological changes show axonal dysfunction, atrophy and loss. However, there are few reports that taurine promotes neurite growth of dorsal root ganglion (DRG) cells. In current study, DRG neurons were exposed to high glucose (HG) with or without taurine.

Taurine Ameliorates High Glucose Induced Apoptosis in HT-22 Cells.

Diabetes causes memory loss. Hippocampus is responsible for memory and increased apoptosis was found in diabetes patients. Taurine improved memory in diabetes condition.

Protective Effect of Taurine on Apoptosis of Spinal Cord Cells in Diabetic Neuropathy Rats.

Diabetes mellitus (DM) is a condition characterized by chronic hyperglycemia, which leads to diabetic neuropathy and apoptosis in the spinal cord. Taurine has been found to ameliorate the diabetic neuropathy and control apoptosis in various tissues. However, there are few reports that discuss the direct relationship between spinal cord and anti-apoptotic effect of taurine.

Protection of Taurine Against Neurotoxicity Induced by Arsenic in Primary Cortical Neurons.

Our group previously reported that taurine has a protective capacity on the hippocampus and cerebellum of arsenic (As)-exposed mouse. In the present study, we explore whether taurine demonstrates protection against As toxicity in primary cortical neurons. Primary cortical neurons were exposed to various concentrations of arsenite and cell viability was assessed to confirm the toxicity of As on cortical neurons.

Anti-apoptotic Effect of Taurine on Schwann Cells Exposed to High Glucose In Vitro.

It was reported that apoptosis of Schwann cells could increase in the diabetic rats. The studies showed that taurine inhibited apoptosis in a variety of cells. However, there were few reports on studying the protection of taurine against apoptosis of Schwann cells induced by high glucose (HG) and the underlying mechanism.

Taurine Protects Against Arsenic-Induced Apoptosis Via PI3K/Akt Pathway in Primary Cortical Neurons.

Arsenate, a well known toxicant, can induce injury in nerve system via oxidative stress and apoptosis. This study was designed to explore the protective effect of taurine against arsenite-induced neurotoxicity and its related mechanism in primary cortical neurons. The cells were treated with arsenite with or without taurine.

Effect of Taurine on Thymus Differentiation of Dex-Induced Immunosuppressive Mice.

Taurine (2-aminoethanesulfonic acid) has positive effects on the formation of immune systems. In this study, we evaluated the effects of taurine on the development of T lymphocyte subpopulations in thymus of immunosuppresive mice. The immunosuppressed mice model was established by intraperitoneal injection of dexamethasone (Dex) for 7 days.

Effect of Taurine on Intestinal Microbiota and Immune Cells in Peyer's Patches of Immunosuppressive Mice.

Taurine is a sulfur-containing amino acid which has strong activities in enhancing immunity. Gut microbiota is closely interrelated with intestinal mucosal immunity, but the effects and mechanisms of taurine on intestinal microbiota and mucosal immune cells under an immunosuppressive condition remain unclear. This study was conducted to investigate the effect of taurine on gut microbiota and immune cells in Peyer's patches (PPs) of dexamethasone (Dex)-induced immunosuppressive mice.

Taurine protects against myelin damage of sciatic nerve in diabetic peripheral neuropathy rats by controlling apoptosis of schwann cells via NGF/Akt/GSK3β pathway.

Diabetic peripheral neuropathy is a common complications of Type 2 Diabetes and its main pathological feature is myelin sheath damage of peripheral nerve that was induced by Schwann cells (SCs) apoptosis. Increasing evidence suggested that taurine might play a role in improving DPN because of its ability to prevent SCs apoptosis. In this study, we explore the effect of taurine on preventing SCs apoptosis and its underlying mechanism.

NGF protects bone marrow mesenchymal stem cells against 2,5-hexanedione-induced apoptosis in vitro via Akt/Bad signal pathway.

Mesenchymal stem cell transplantation has been proposed as a promising therapy for regeneration of damaged tissues-especially, bone marrow mesenchymal stem cell (BMSC) transplantation therapy is considered to be an effective strategy for treating various injures in recent years. However, poor viability of transplanted BMSCs in injured tissues has limited their therapeutic efficiency. Nerve growth factor (NGF) has been reported to be a pro-survival factor in series of cells.

Altered Expression Levels of MicroRNA-132 and Nurr1 in Peripheral Blood of Parkinson's Disease: Potential Disease Biomarkers.

MicroRNAs (miRNAs) are small and evolutionary conserved noncoding RNAs that are involved in post-transcriptional gene regulation. Differential expression levels of miRNAs can be used as potential biomarkers of disease. Previous animal studies have indicated that the expression level of miR-132 is negatively correlated with its downstream molecule nuclear receptor related 1 protein (Nurr1), which is one of the key factors for the maintenance of dopaminergic function and is particularly vulnerable in Parkinson's disease (PD).