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Angiotensin II Silencing Alleviates Erectile Dysfunction Through Down-Regulating the Rhoa/Rho Kinase Signaling Pathway in Rats with Diabetes Mellitus

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: We aim to explore the role of angiotensin (Ang) II and the RhoA/Rho kinase signaling pathway in the pathogenesis of erectile dysfunction in diabetes mellitus (DM). Methods: Male Sprague-Dawley (SD) rats were used for experiments and short hairpin RNA (shRNA) was used to silence the AngII gene. The erectile function of rats was observed and intracavernous pressure and mean arterial pressure (ICP/MAP) were measured after electrical stimulation. Relaxation and contraction of smooth muscle in the corpus cavernosum were tested. Western blotting and quantitative RT-PCR were applied to measure the expressions of RhoA, Rho-associated kinase (ROCK) 1 and ROCK2. Radioimmunoassay was applied to detect the levels of AngII. Results: Rats in the control group had the most erectile times, followed by AngII-silenced rats with DMED and rats with DMED. Rats with DMED had worse ICP and MAP than AngII-silenced rats. The contraction ability was markedly improved and relaxation ability was decreased in AngII-silenced rats with DMED as compared with rats with DMED. The levels of AngII were significantly increased in DMED rats while significantly decreased after AngII silencing. The mRNA and proteins of RhoA and ROCK2 were expressed in a similar way. Conclusion: AngII silencing improves erectile dysfunction via down-regulating the RhoA/Rho kinase signaling pathway. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Regulation of Endothelial Permeability by Glutathione S-Transferase Pi Against Actin Polymerization

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Inflammation-induced injury of the endothelial barrier occurs in several pathological conditions, including atherosclerosis, ischemia, and sepsis. Endothelial cytoskeleton rearrangement is an important pathological mechanism by which inflammatory stimulation triggers an increase of vascular endothelial permeability. However, the mechanism maintaining endothelial cell barrier function against inflammatory stress is not fully understood. Glutathione S-transferase pi (GSTpi) exists in various types of cells and protects them against different stresses. In our previous study, GSTpi was found to act as a negative regulator of inflammatory responses. Methods: We used a Transwell permeability assay to test the influence of GSTpi and its transferase activity on the increase of endothelial permeability induced by tumor necrosis factor alpha (TNF-alpha). TNF-alpha-induced actin remodeling and the influence of GSTpi were observed by using laser confocal microscopy. Western blotting was used to test the influence of GSTpi on TNF-alpha-activated p38 mitogen-activated protein kinase (MAPK)/MK2/heat shock protein 27 (HSP27). Results: GSTpi reduced TNF-alpha-induced stress fiber formation and endothelial permeability increase by restraining actin cytoskeleton rearrangement, and this reduction was unrelated to its transferase activity. We found that GSTpi inhibited p38MAPK phosphorylation by directly binding p38 and influenced downstream substrate HSP27-induced actin remodeling. Conclusion: GSTpi inhibited TNF-alpha-induced actin remodeling, stress fiber formation and endothelial permeability increase by inhibiting the p38MAPK/HSP27 signaling pathway. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Upregulated Serum MiR-146b Serves as a Biomarker for Acute Ischemic Stroke

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Stroke is a major cerebrovascular disease threatening human health and life with high morbidity, disability and mortality. It is aimed to find effective biomarkers for the early diagnosis on stroke. Methods: The expressions of 17 previously reported stroke-associated miRNAs were measured using quantitative RT-PCR and the expressions of plasma high-sensitivity C reactive protein (hs-CRP) and serum interleukin 6 (IL-6), the pro-inflammation markers in brain injury, were examined using enzyme-linked immunosorbent assay in 128 acute ischemic stroke (AIS) patients and control group. Results: Serum miR-146b expression was significantly increased within 24 hours after stroke onset in patients compared with control group. In addition, the upregulation of serum miR-146b was strong positively correlated with plasma hs-CRP, infarct volume and National Institutes of Health Stroke Scale (NIHSS) score, and moderate positively correlated with serum IL-6 of patients. Importantly, the combination of plasma hs-CRP and serum miR-146b gained a better sensitivity/specificity for prediction of AIS (AUC from 0.782 to 0.863). Conclusion: Our preliminary findings suggested that upregulated serum miR-146b in acute ischemic stroke might be a potential biomarker for AIS evaluation. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Gastric Neuroendocrine Tumors (G-Nets): Incidence, Prognosis and Recent Trend Toward Improved Survival

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Gastric neuroendocrine tumors (G-NETs) are uncommon neoplasms that can present with or without clinical symptoms. In this study, we evaluated the incidence, prognosis, and temporal trends of G-NETs. Methods: We analyzed all cases of G-NETs registered in the Surveillance, Epidemiology, and End Results (SEER) database from 1973 to 2014. Incidence was estimated by age and joinpoint analyses. Survival rates were calculated and survival trends over time were evaluated. Results: A total of 3740 eligible patients were enrolled in the study. G-NETs incidence increased from 0.31 per 1 000 000 patients in 1975 to 4.85 in 2014, with an annual percentage changes (APCs) of 8.9% (95% confidence interval [CI] = 7.7% to 10.21%, P < 0.001, t test (29) from 1975 to 2001 and 3.6% from 2002 to 2014 (95% CI = 2.3% to 4.9%, P < 0.001). For cases diagnosed between 1973 and 1982, five-year survival was 62.8% +/- 7.0% (Standard error, SE) and increased to 86.7% +/- 0.7% for cases diagnosed between 2003 and 2012 (P < 0.001). Years of diagnosis, gender, age at diagnosis, marital status, grade, tumor size, tumor stage, and surgery performed or not were the strongest predictors of worse survival in both univariate and multivariate analysis (P<0.05). Conclusion: G-NETs are uncommon neoplasms but the incidence is growing. Survival has improved in the past decades. Years of diagnosis, gender, age at diagnosis, marital status, grade, tumor size, tumor stage, and surgery status predict survival in patients with G-NETs. (C) 2018 The Author(s) Published by S. Karger AG, Basel

TRPC3 Overexpression Promotes the Progression of Inflammation-Induced Preterm Labor and Inhibits T Cell Activation

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: To detect the expression of the TRPC3 channel protein in the tissues of women experiencing preterm labor and investigate its interaction with T lymphocytes, providing a theoretical basis for the clinical prevention of threatened preterm labor and the development of drug-targeted therapy. Methods: Forty-seven women experiencing preterm labor and 47 women experiencing normal full-term labor were included in this study. All included women underwent delivery via cesarean section; uterine samples were obtained at delivery. The expression of TRPC3 in uterine tissue was detected by immunohistochemistry, real-time quantitative reverse transcription-PCR, and western blot assay. Activation of T lymphocytes in peripheral blood and uterine tissue were detected by flow cytometry. A TRPC3(-/-) mouse model of inflammation-induced preterm labor was established; expression of TRPC3, Cav3.1, and Cav3.2 were analyzed in mouse uterine tissue. Activation of T lymphocytes in female mouse and human peripheral blood samples was determined using flow cytometry. Results: In women experiencing preterm labor, expression of TRPC3 and the Cav3.1 and Cav3.2 proteins was significantly increased; in addition, the percentage of CD3(+), CD4(+), and CD8(+) T cells in peripheral blood was significantly decreased. TRPC3 knockout significantly delayed the occurrence of preterm labor in mice. The muscle tension of ex vivo uterine strips was lower, Cav3.1 and Cav3.2 protein expression was lower, and the percentage of CD8(+) T lymphocytes was significantly increased in wild-type mice subjected to an inflammation-induced preterm labor than in wild-type mice experiencing normal full-term labor. Conclusion: TRPC3 is closely related to the initiation of labor. TRPC3 relies on Cav3.1 and Cav3.2 proteins to inhibit inflammation-induced preterm labor by inhibiting the activation of T cells, in particular CD8(+) T lymphocytes. (C) 2018 The Author(s) Published by S. Karger AG, Basel

BDNF VAL66MET Polymorphism Elevates the Risk of Bladder Cancer via MiRNA-146b in Micro-Vehicles

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Emerging studies on brain-derived neurotrophic factor (BDNF) have shown that might be novel biomarkers and therapeutic targets for cancer. We explore the role of BDNF in the tumorigenesis of bladder cancer and the underlying molecular mechanism. Methods: 368 patients with diagnosed bladder cancer and 352 healthy controls were enrolled to evaluate the association of BDNF and the miR-146b. Bioinformatics algorithm analysis and luciferase assay were performed to identify the target genes of miR-146b. Real-time PCR and western-blot were carried out to validate the relationship between miR-146b and CRK. MTT assay and FACS were used to evaluated the proliferation and apoptosis of cancer cells. MVs were isolated and transfect into the culture cells to confirm the above observation. Results: The clinical study shows that BDNF Met/Met was significantly associated with the risk of bladder cancer. In addition, comparing with Val/Val and Val/Met, Met/Met has lower miR-146b level. Luciferase assay shows that BDNF Val/Val is apparently enhanced miR-146b promoterluciferase, but not BDNF Met/Met. Based on luciferase assay, CRK is a direct target gene of miR-146b. MiR-146b mimics significantly inhibited the expression of CRK and activation of AKT level. The expression of CRK and the activation of AKT (p-AKT) were significantly inhibited by MV-BDNF Val/Val-miR-146b or MV-BDNF Val/Met-miR-146b, but not MV-BDNF Met/Met-miR-146b. MV-BDNF Val/Val-miR-146b or Val/Met-miR-146b obviously inhibited cell proliferation, which eliminated by CRK. Meanwhile, with MV-BDNF Met/Met-miR-146b or Met/Met-miR-146b+CRK did not affect the proliferation. MV-BDNF Val/Val-miR-146b or Val/Met-miR-146b enhanced cell apoptosis, which could be eliminated by CRK. Meanwhile, MV-BDNF Met/Met-miR-146b or Met/Met-miR-146b+CRK did not promote apoptosis. Conclusion: BDNF VAL66MET polymorphism is associated with miR-146b and its target gene CRK. MiR-146b and CRK mediated BDNF VAL66MET polymorphism associated proliferation and apoptosis via activation of AKT. Thus, BDNF Val66Met is associated with the risk of bladder cancer, and the BDNF variant could be used a biomarker for the diagnosis of bladder cancer. (C) 2018 The Author(s) Published by S. Karger AG, Basel

The Role of Tumor-Associated Macrophages in Colorectal Carcinoma Progression

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Tumor-associated macrophages (TAMs) are one of the most abundant immune cells in the tumor microenvironment, and they play a pivotal role in prompting the various tumor growth. However, the role of TAMs in colorectal carcinoma (CRC) is controversial, because a few papers report that TAMs is beneficial to CRC patients. In this review, we discuss the good or bad roles of TAMs in CRC progression. Interestingly, recent studies provide strong evidence that TAMs facilitate CRC growth, but do not exert tumor suppressive activities. TAMs can stimulate CRC growth by altering extracellular matrix remodeling, tumor metabolism, angiogenesis, as well as the tumor microenvironment. Therefore, TAMs could serve as a target for CRC therapeutic treatment. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Protective Effects of Let-7b on the Expression of Occludin by Targeting P38 MAPK in Preventing Intestinal Barrier Dysfunction

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Let-7b was dramatically reduced after a dicer knockout of mice with intestinal barrier function injuries. This paper aims to investigate the molecular mechanism of let-7b by targeting p38 MAPK in preventing intestinal barrier dysfunction. Methods: A total of 186 patients were enrolled, with 93 in the control group and 93 in the PRO group. Only 158 patients completed the entire study, whereas the others either did not meet the inclusion criteria or refused to participate. To further verify the role of let-7b, intestinal epithelial conditional knockout (IKO) mice of mmu-let-7b model were established. Serum let-7b, zonulin, IL-6, and TNF-alpha concentrations were measured by ELISA or quantitative RT-PCR. Permeability assay was done by ussing chamber. The apoptotic cells were identified using an In Situ Cell Death Detection Kit. Protein was detected by western blot. Results: Probiotics can lower infection-related complications, as well as increase the serum and tissue let-7b levels. P38 MAPK was identified as the target of let-7b, as verified by NCM460 cells. P38 MAPK expression was increased, whereas tight-junction (TJ) proteins were significantly decreased in let-7b IKO mice (both P<0.05). Negative regulation of p38 MAPK molecular signaling pathways was involved in the protective effects of let-7b on intestinal barrier function. Conclusion: Let-7b was identified as a novel diagnosis biomarker or a potential treatment target for preventing intestinal barrier dysfunction. (C) 2018 The Author(s) Published by S. Karger AG, Basel

NF-kappa B-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: The present study addressed the potential involvement of microRNAs in acute respiratory distress syndrome (ARDS)-related inflammation and elucidates the underlying molecular mechanism. Methods: ARDS rat model was established by lipopolysaccharide, with compromised gas exchange capacity and lung edema. The inflammatory cells from bronchoalveolar lavage fluid (BALF) were profiled with automatic blood cell analyzer. The relative fluorescence intensity of BALF-derived macrophages was analyzed by flow cytometry. The relative microRNA expression was determined using microarray and Taqman assay. The secretory interleukin (IL)-10 was measured by enzyme-linked immunosorbent assay. Luciferase reporter assay was performed to determine the regulatory effects of miR-211 and NF-kappa B on IL-10 and miR-211 expressions, respectively. Chromatin immunoprecipitation (ChIP) was conducted to detect the direct binding of NK-kappa B on miR-211 promoter. The protein level was determined by Western blot. Results: The provoked acute inflammation was characterized with increased total cells, macrophages, neutrophils and lymphocytes. The relative expression of miR-211 was aberrantly up-regulated in BALF-derived macrophages from ARDS rats, which was accompanied with reduction of secretory IL-10. We further demonstrated that miR-211 inhibited IL-10 expression by binding to its 3'-UTR. The expression of miR-211 was modulated by NF-kappa B. Conclusion: Here we elucidated a crucial role of NF-kappa B/miR-211/IL-10 signaling axis in ARDS-related inflammation. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Skeletal Extracellular Matrix Supports Cardiac Differentiation of Embryonic Stem Cells: a Potential Scaffold for Engineered Cardiac Tissue

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Decellularized cardiac extracellular matrix (cECM) has been widely considered as an attractive scaffold for engineered cardiac tissue (ECT), however, its application is limited by immunogenicity and shortage of organ donation. Skeletal ECM (sECM) is readily available and shows similarities with cECM. Here we hypothesized that sECM might be an alternative scaffold for ECT strategies. Methods: Murine ventricular tissue and anterior tibial muscles were sectioned into 300 mm-thick, and then cECM and sECM were acquired by pretreatment/SDS/TritonX-100 three-step-method. Acellularity and morphological properties of ECM was assessed. SECM was recellularized with murine embryonic stem cells (mESCs) or mESC-derived cardiomyocytes (mESC-CMs), and was further studied by biocompatibility assessment, immunofluorescent staining, quantitative real-time PCR and electrophysiological experiment. Results: The relative residual contents of DNA, protein and RNA of sECM were comparable with cECM. The morphological properties and microstructure of sECM were similar to cECM. SECM supported mESCs to adhere, survive, proliferate and differentiate into functional cardiac microtissue with both electrical stimulated response and normal adrenergic response. Purified mESC-CMs also could adhere, survive, proliferate and form a sECM-based ECT with synchronized contraction within 6 days of recellularization. Conclusion: ECMs from murine skeletal muscle support survival and cardiac differentiation of mESCs, and are suitable to produce functional ECT patch. This study highlights the potential of patient specific of sECM to replace cECM for bioengineering ECT. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Differential Expression of MiR-106b-5p and MiR-200c-3p in Newly Diagnosed Versus Chronic Primary Immune Thrombocytopenia Patients Based on Systematic Analysis

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: MicroRNAs (miRNAs) have been described to have important roles in primary immune thrombocytopenia (ITP). To gain additional understanding, we have now further evaluated the involvement of miRNAs in ITP. Methods: Microarray experiments were performed to examine the expression profiles of miRNAs and mRNAs in samples from subjects with newly diagnosed ITP (G1), chronic ITP (G2), and normal controls. The systematic Pipeline of Outlier MicroRNA Analysis framework was applied to identify key miRNAs expressed in the G1 and G2 samples. Quantitative PCR and receiver operator characteristic curves were used to confirm the performance of key miRNAs. Results: Compared with normal controls, 14 miRNAs (12 over-expressed and 2 under-expressed) and 7 over-expressed miRNAs were identified as key in G1 and G2 samples, respectively. miR-106b-5p, miR-200c-3p, and miR-92a-3p exhibited significantly different expression profiles among the groups. In particular, miR-106b-5p and miR-200c-3p were expressed at higher levels in patients with ITP compared to the normal controls. Furthermore, these two miRNAs expressions were even higher in patients with chronic ITP. Conclusion: MiR-106b-5p and miR-200c-3p may represent valuable biomarkers of ITP, although further studies are needed to confirm and assess the value of these potential biomarkers at various stages of ITP. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Maternal Vitamin D Status and Risk of Gestational Diabetes: a Meta-Analysis

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Whether maternal vitamin D deficiency is associated with gestational diabetes remains controversial. This meta-analysis aimed to systematically evaluate published evidence on the association between maternal vitamin D status and the risk of gestational diabetes. Methods: We retrieved relevant articles from the PubMed, Medline and Embase databases up to May 2017 for observational studies investigating the association between vitamin D status and the risk of gestational diabetes. Odds ratios (OR) or risk ratios (RR) from individual studies were pooled using the fixed and random effect models. Results: The meta-analysis of 29 observational studies included 28,982 participants, of which 4,634 were diagnosed with gestational diabetes, and showed that maternal vitamin D insufficiency was associated with a significantly increased risk of gestational diabetes by 39% (pooled OR = 1.39, 95% CI = 1.20-1.60) with moderate heterogeneity (I (2) = 50.2%; P = 0.001). Moreover, the 25(OH) D level was significantly lower in gestational diabetes cases than in controls with a pooled effect of -4.79 nmol/L (95% CI = -6.43, -3.15). Significant heterogeneity was also detected (I (2) = 65.0%, P < 0.001). Further subgroup analysis indicated that this association was also evident in most subpopulations. Conclusion: This meta-analysis indicated a significant association between vitamin D insufficiency and increased risk of gestational diabetes. Further well-designed large-scale clinical trials are essential to verify this association. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Change of Peripheral Blood Treg/Thl7 in Cognitive Impairment with Chronic Renal Failure Patients

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: To investigate the changes in peripheral blood Treg/Th17 cell balance and its significance in patients with chronic renal failure (CRF) and cognitive impairment. Methods: A total of 71 patients with CRF were enrolled as a study group. The patients were divided into a cognitive impairment group and a normal cognitive function group according to the Mini-Mental State Examination (MMSE). Peripheral blood Treg and Th17 cells were analyzed by flow cytometry and their relevant cytokines (IL-17, IL-10 and TGF-beta) and other biochemical indicators, including C-reactive protein (CRP) and IL-6, were determined by ELISA. Results: Thepatients with both CRF and cognitive impairment were older than the cognitive normal groups. Peripheral blood Treg cells by Flow cytometry (the CRF cognitive impairment group 5.57 +/- 1.3%, CRF group with normal cognitive function 7.5 +/- 0.9% and normal control group 9.7 +/- 1.7%, P<0.05) and its related cytokines (IL-10 and TGF-beta) by ELISA detection were lower in the group with cognitive impairment than in the group without cognitive impairment (IL-10, 7.4 +/- 4.2 pg/mL, 13.8 +/- 3.9 pg/mL, 18.3 +/- 3.2 pg/mL; TGF-beta 335.6 +/- 175.3 pg/mL, 512.7 +/- 114.6 pg/mL, 953.8 +/- 373.4 pg/mL P < 0.05, respectively). However, Th17 cell numbers (the CRF cognitive impairment group 3.3 +/- 0.7%, CRF group with normal cognitive function2.2 +/- 0.5% and normal control group 1.5 +/- 0.3%), and cytokine levels (IL-17, IL-6 and CRP) were higher in the group with cognitive impairment IL-6 (21.3 +/- 5.1 pg/mL), IL-17 (18.5 +/- 4.2 pg/mL) and CRP (20.3 +/- 5.9 mg/L) in the CRF group with cognitive impairment when compared with the CRF group and normal cognitive function (12.2 +/- 4.5 pg/mL, 12.1 +/- 3.7 pg/mL and 13.5 +/- 4.6 mg/L, respectively) or the normal control group (9.2 +/- 5.8 pg/mL, 7.4 +/- 2.6 pg/mL and 3.2 +/- 1.3 mg/L, respectively, P<0.05). The frequencies of Treg in patients with CRF were positively correlated with the MMSE scores ((r = 0.518, P < 0.05), but the Th17 numbers were negatively correlated (r = -0.435, P < 0.05). Conclusion: An imbalance of peripheral blood Treg/Th17 cells is associated with cognitive impairment in patients with CRF. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Plumbagin Triggers ER Stress-Mediated Apoptosis in Prostate Cancer Cells via Induction of ROS

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Prostate cancer (PCa) is the second most frequently diagnosed cancer in men worldwide. Currently available therapies for hormone-refractory PCa are only marginally effective. Plumbagin (PLB), a natural naphthoquinone isolated from the traditional folk medicine Plumbago zeylanica, is known to selectively kill tumor cells. Nevertheless, antitumor mechanisms initiated by PLB in cancer cells have not been fully defined. Methods: MTT assay was used to evaluate the effect of PLB on the viability of cancer cells. Cell apoptosis and reactive oxygen species (ROS) production were determined by flow cytometry. Protein expression was detected by western blotting. In vivo anti-tumor effect was measured by using tumor xenograft model in nude mice. Results: In the present study, we found that PLB decreases cancer cell growth and induces apoptosis in DU145 and PC-3 cells. In addition, by increasing intracellular ROS levels, PLB induced a lethal endoplasmic reticulum stress response in PCa cells. Importantly, blockage of ROS production significantly reversed PLB-induced ER stress activation and cell apoptosis. In vivo, we found that PLB inhibits the growth of PCa xenografts without exhibiting toxicity. Treatment of mice bearing human PCa xenografts with PLB was also associated with induction of ER stress activation. Conclusion: Inducing ER stress by PLB thus discloses a previously unrecognized mechanism underlying the biological activity of PLB and provides an in-depth insight into the action of PLB in the treatment of hormone refractory PCa. (C) 2018 The Author(s) Published by S. Karger AG, Basel

Transplanted Dental Pulp Stem Cells Migrate to Injured Area and Express Neural Markers in a Rat Model of Cerebral Ischemia

期刊: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2018; 45 (1)

Background/Aims: Ischemic stroke is a major cause of disability and mortality worldwide, while effective restorative treatments are limited at present. Stem cell transplantation holds therapeutic potential for ischemic vascular diseases and may provide an opportunity for neural regeneration. Dental pulp stem cells (DPSCs) origin from neural crest and have neuro-ectodermal features including proliferation and multilineage differentiation potentials. Methods: The rat model of middle cerebral artery occlusion (MCAO) was used to evaluate whether intravenous administration of DPSCs can reduce infarct size and to estimate the migration and trans-differentiation into neuron-like cells in focal cerebral ischemia models. Brain tissues were collected at 4 weeks following cell transplantation and analyzed with immunofluorescence, immunohistochemistry and real-time polymerase chain reaction (RTPCR) methods. Results: Intravenously administration of rat-derived DPSCs were found to migrate into the boundary of ischemic areas and expressed neural specific markers, reducing infarct volume and cerebral edema. Conclusions: These results suggest that DPSCs treatment may serve as a potential therapy for clinical stroke patients in the future. (C) 2018 The Author(s) Published by S. Karger AG, Basel

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