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#28929261   2017/09/20 Save this To Up

Transplantation of mesenchymal stem cells modulated Cx43 and Cx45 expression in rats with myocardial infarction.

At present, little is known about the influence of mesenchymal stem cell (MSC) transplantation on connexin43 (Cx43) and connexin45 (Cx45) remodeling in the ischemic heart. In this study, we investigated the effect of MSC transplantation on Cx43 and Cx45 remodeling in the ischemic heart. Wistar rats were subjected to left anterior descending artery ligation to induce myocardial infarction (MI) and then randomly allocated to receive an intramyocardial injection of PBS (MI group) or 5-azacytidine-induced MSCs (MSCs group). Histological examination and western blotting were performed 4 weeks after cell transplantation. We found that the MSCs exhibited plasticity by differentiating into cardiomyocyte-like cells. Gap junction remodeling after MI was characterized by a decrease in Cx43 expression and an increase in Cx45 expression. MSC transplantation modulated the MI-induced abnormalities by up-regulating Cx43 and down-regulating Cx45 expression. MSCs exhibited plasticity by differentiating into cardiomyocyte-like cells and modulated abnormal Cx43 and Cx45 remodeling following MI.

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#28919746   2017/09/18 Save this To Up

In vitro and in vivo studies of a novel bacterial cellulose-based acellular bilayer nanocomposite scaffold for the repair of osteochondral defects.

Bacterial cellulose (BC) is a naturally occurring nanofibrous biomaterial which exhibits unique physical properties and is amenable to chemical modifications. To explore whether this versatile material can be used in the treatment of osteochondral defects (OCD), we developed and characterized novel BC-based nanocomposite scaffolds, for example, BC-hydroxyapatite (BC-HA) and BC-glycosaminoglycans (BC-GAG) that mimic bone and cartilage, respectively. In vitro biocompatibility of BC-HA and BC-GAG scaffolds was established using osteosarcoma cells, human articular chondrocytes, and human adipose-derived mesenchymal stem cells. On subcutaneous implantation, the scaffolds allowed tissue ingrowth and induced no adverse immunological reactions suggesting excellent in vivo biocompatibility. Implantation of acellular bilayered scaffolds in OCD created in rat knees induced progressive regeneration of cartilage tissue, deposition of extracellular matrix, and regeneration of subchondral bone by the host cells. The results of micro-CT revealed that bone mineral density and ratio of bone volume to tissue volume were significantly higher in animals receiving bilayered scaffold as compared to the control animals. To the best of our knowledge, this study proves for the first time, the functional performance of acellular BC-based bilayered scaffolds. Thus, this strategy has great potential for clinical translation and can be used in repair of OCD.

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#28916665   2017/09/16 Save this To Up

Integrin α4 Overexpression on Rat Mesenchymal Stem Cells Enhances Transmigration and Reduces Cerebral Embolism After Intracarotid Injection.

Very late antigen-4 (integrin α4β1)/vascular cell adhesion molecule-1 mediates leukocyte trafficking and transendothelial migration after stroke. Mesenchymal stem cells (MSCs) typically express integrin β1 but insufficient ITGA4 (integrin α4), which limits their homing after intravascular transplantation. We tested whether ITGA4 overexpression on MSCs increases cerebral homing after intracarotid transplantation and reduces MSC-borne cerebral embolism.

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#28914133   2017/09/15 Save this To Up

Age of donor of human mesenchymal stem cells affects structural and functional recovery after cell therapy following ischaemic stroke.

Cell transplantation therapy offers great potential to improve impairments after stroke. However, the importance of donor age on therapeutic efficacy is unclear. We investigated the regenerative capacity of transplanted cells focusing on donor age (young vs. old) for ischaemic stroke. The quantities of human mesenchymal stem cell (hMSC) secreted brain-derived neurotrophic factor in vitro and of monocyte chemotactic protein-1 at day 7 in vivo were both significantly higher for young hMSC compared with old hMSC. Male Sprague-Dawley rats subjected to transient middle cerebral artery occlusion that received young hMSC (trans-arterially at 24 h after stroke) showed better behavioural recovery with prevention of brain atrophy compared with rats that received old hMSC. Histological analysis of the peri-infarct cortex showed that rats treated with young hMSC had significantly fewer microglia and more vessels covered with pericytes. Interestingly, migration of neural stem/progenitor cells expressing Musashi-1 positively correlated with astrocyte process alignment, which was more pronounced for young hMSC. Aging of hMSC may be a critical factor that affects cell therapy outcomes, and transplantation of young hMSC appears to provide better functional recovery through anti-inflammatory effects, vessel maturation, and neurogenesis potentially by the dominance of trophic factor secretion.

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#28912509   2017/09/15 Save this To Up

Aspirin inhibits LPS-induced macrophage activation via the NF-κB pathway.

Aspirin (acetylsalicylic acid, ASA) has been shown to improve bone marrow mesenchymal stem cell-based calvarial bone regeneration by promoting osteogenesis and inhibiting osteoclastogenesis. However, it remains unknown whether aspirin influences other immune cells during bone formation. In the present study, we investigated whether ASA treatment influenced macrophage activation during the LPS inducement. We found that ASA could downregulate the expressions of iNOS and TNF-α both in mouse peritoneum macrophages and RAW264.7 cells induced by LPS via the IκK/IκB/NF-κB pathway and a COX2/PGE2/EP2/NF-κB feedback loop, without affecting the expressions of FIZZ/YM-1/ARG1 induced by IL-4. Furthermore, we created a rat mandibular bone defect model and showed that ASA treatment improved bone regeneration by inhibiting LPS-induced macrophage activation in the early stages of inflammation. Taken together, our results indicated that ASA treatment was a feasible strategy for improving bone regeneration, particularly in inflammatory conditions.

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#28903624   2017/09/14 Save this To Up

Repair of calvarial bone defect using Jarid1a-knockdown bone mesenchymal stem cells in rats.

Histone methylation is regarded as an important epigenetic event during stem cell differentiation. Jumonji AT-rich interactive domain 1A (Jarid1a) is a histone demethylase that specifically catalyzes demethylation of dimethyl or trimethyl histone H3K4me3, which is normally associated with transcriptionally active genes. Runt-related transcription factor 2 (Runx2) has been identified as a key transcription factor in the early stage of osteogenesis. A better understanding of this epigenetic mechanism that governs osteogenic differentiation of bone mesenchymal stem cells (BMSCs) can provide new insights into BMSCs based bone tissue engineering. To define the function and regulatory mechanisms of Jarid1a in the osteogenic differentiation of BMSCs, we compared the expression of Jarid1a between undifferentiated and osteo-inductive BMSCs. The expression of osteogenic transcriptional factors in BMSCs after Jarid1a knockdown was explored using western blot. To determine whether Jarid1a was associated with Runx2 during osteogenic differentiation, endogenous co-IP experiments were performed with osteo-inductive BMSCs extracts. Then, we systematically evaluated the function of si-Jarid1a in enhancing BMSCs osteogenesis and the therapeutic potential of si-Jarid1a-modified BMSCs in a rat calvarial bone defect model with β-tricalcium phosphate (β-TCP) scaffolds. Knockdown of Jarid1a by small interfering RNA enhanced osteogenic differentiation of BMSCs in vitro. Knockdown of Jarid1a significantly improved the mRNA and protein expression of bone specific factors. Furthermore, co-immunoprecipitation in BMSCs lysate suggested that Jarid1a was physically and functionally associated with Runx2. The repair potential of bone defect was dramatically improved by Jarid1a-knockdown BMSCs, including increased bone volume, increased bone mineral density (BMD) and decreased scaffold residue in vivo. Altogether, this study explores the functional and regulatory role of Jarid1a in osteogenic differentiation and bone regeneration of BMSCs, and provides a new approach for bone defect repairing using epigenetic modification in vitro and in vivo.

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#28901391   2017/09/13 Save this To Up

Protective effects of heme oxygenase-1-transduced bone marrow-derived mesenchymal stem cells on reduced‑size liver transplantation: Role of autophagy regulated by the ERK/mTOR signaling pathway.

Autophagy is a critical lysosomal pathway that degrades cytoplasmic components to maintain cell homeostasis and provide substrates for energy metabolism. A study revealed that heme oxygenase-1 (HO-1)-transduced bone marrow-derived mesenchymal stem cells (BM-MSCs) could protect 50% reduced-size liver transplantation (RSLT) in a rat model. However, the mechanisms remain mostly unknown. The aim of the present study was to explore the effects and related mechanism of autophagy on the protection conferred by HO-1-transduced BM-MSCs (HO-1/BM-MSCs) on 50% RSLT in a rat model. The authors established an acute rejection model following 50% RSLT in rats, with recipients divided into three groups receiving treatment with BM-MSCs, HO-1/BM-MSCs or normal saline (NS) injected through the dorsal penile vein. Transplanted liver tissues at 0, 1, 3, 5, 7, 10 and 14 days following transplantation were acquired for further analysis. The results indicated that the expression of autophagy-related proteins LC3 and Beclin-1 increased, the levels of ERK and p-ERK increased, and the levels of mammalian target of rapamycin (mTOR) and p-mTOR decreased in the HO-1/BM-MSCs. These observations indicated that autophagy is involved in the protective effects of HO-1/BM-MSCs on liver grafts following RSLT, possibly via upregulation of autophagy-related proteins through the ERK/mTOR signaling pathway.

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#28901185   2017/09/13 Save this To Up

Evaluation of Parametric Response Mapping to Assess Therapeutic Response to Human Mesenchymal Stem Cells after Experimental Stroke.

Stroke is the leading cause of disability in adults. After the very narrow time frame during which treatment by thrombolysis and mechanical thrombectomy is possible, cell therapy has huge potential for enhancing stroke recovery. Accurate analysis of the response to new therapy using imaging biomarkers is needed to assess therapeutic efficacy. The aim of this study was to compare 2 analysis techniques: the parametric response map (PRM), a voxel-based technique, and the standard whole-lesion approach. These 2 analyses were performed on data collected at 4 time points in a transient middle cerebral artery occlusion (MCAo) model, which was treated with human mesenchymal stem cells (hMSCs). The apparent diffusion coefficient (ADC), cerebral blood volume (CBV), and vessel size index (VSI) were mapped using magnetic resonance imaging (MRI). Two groups of rats received an intravenous injection of either 1 mL phosphate-buffered saline (PBS)-glutamine (MCAo-PBS, n = 10) or 3 million hMSCs (MCAo-hMSC, n = 10). One sham group was given PBS-glutamine (sham, n = 12). Each MRI parameter was analyzed by both the PRM and the whole-lesion approach. At day 9, 1 d after grafting, PRM revealed that hMSCs had reduced the fraction of decreased ADC (PRMADC-: MCAo-PBS 6.7% ± 1.7% vs. MCAo-hMSC 3.3% ± 2.4%), abolished the fraction of increased CBV (PRMCBV+: MCAo-PBS 16.1% ± 3.7% vs. MCAo-hMSC 6.4% ± 2.6%), and delayed the fraction of increased VSI (PRMVSI+: MCAo-PBS 17.5% ± 6.3% vs. MCAo-hMSC 5.4% ± 2.6%). The whole-lesion approach was, however, insensitive to these early modifications. PRM thus appears to be a promising technique for the detection of early brain changes following treatments such as cell therapy.

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#28901182   2017/09/13 Save this To Up

Effects of Bone-Marrow-Derived MSC Transplantation on Functional Recovery in a Rat Model of Spinal Cord Injury: Comparisons of Transplant Locations and Cell Concentrations.

Spinal cord injury (SCI) is a widely disabling condition, constraining those affected by it to wheelchairs and requiring intense daily care and assistance. Cell replacement therapies, targeting regeneration of cells in the injured cord, are currently gaining momentum in the field of SCI research. Previous studies indicate that mesenchymal stem cells (MSCs) can reduce functional deficits through immunomodulation and production of trophic factors in a variety of neurological disorders. The present study assessed the efficacy of transplanted bone marrow-derived MSCs at different concentrations and locations for promoting functional recovery following SCI. Although effects were modest, MSCs facilitated an increase in the base of support, as measured by increased distance between the plantar surface of the hind paws, following incomplete contusive SCI, and reduced the density of astroglial scarring. Varying the concentrations or locations of transplanted cells did not provide additional benefits on these measures. These findings indicate that MSC transplants are safe at relatively high concentrations and confer therapeutic benefits that, when used as an adjunctive treatment, could significantly enhance functional recovery following SCI.

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#28894654   2017/09/12 Save this To Up

Evaluation of a Novel Hybrid Viable Bioprosthetic Mesh in a Model of Mesh Infection.

The reported incidence of mesh infection in contaminated operative fields is as high as 30% regardless of material used. Our laboratory previously showed that augmenting acellular bioprosthetic mesh with allogeneic mesenchymal stem cells (MSC) enhances resistance to bacterial colonization in vivo and preserves mesh integrity. This study's aim was to determine whether augmentation of non-crosslinked porcine dermis (Strattice) with commercially available, cryopreserved, viable MSC-containing human placental tissue (Stravix) similarly improves infection resistance after inoculation with Escherichia coli (E. coli) using an established mesh infection model.

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