Serum Cystatin, Chemokine, and Gastrin-Releasing Peptide Precursors and Their Clinical Value in Patients with Chronic Renal Failure.

OBJECTIVE: To investigate the serum cystatin (CysC), Chemerin, and gastrin-releasing peptide precursor (ProGRP) levels in patients with chronic renal failure (CRF). METHODS: CRF patients admitted to our hospital from February 2019 to July 2019 were selected as the observation group, and 50 healthy patients were selected as the control group. The serum levels of CysC, Chemerin, ProGRP, and Scr of all subjects were detected. Patients with CRF were admitted for peritoneal dialysis (PD) treatment for 1 week, and continued treatment was performed. The survival rate of patients with CRF in nearly 1 year after continuous treatment was observed. Multivariate analysis of factors affecting survival time of CRF patients undergoing peritoneal dialysis was performed. The results were compared with those in the health group. The expression levels of CysC, Chemerin, ProGRP, and Scr in the observation group were all decreased, and the differences were statistically significant (P < 0.05). Pearson correlation analysis showed that Scr expression in CRF patients is positively correlated with CysC, Chemerin, and ProGRP (P < 0.001). The survival rate of 98 patients with CRF was 80.61% (79/98), and the mortality rate was 19.39% (19/98). Serum levels of CysC, Chemerin, ProGRP, and Scr in the death group are all higher than those in the survival group, and the differences are statistically significant (P < 0.05). CysC, Chemerin, ProGRP, and Scr are independent risk factors affecting survival time (P < 0.05). The AUC aspects of serum CysC, Chemerin, ProGRP, and Scr in predicting the survival rate of CRF patients in the treatment phase are 0.840, 0.775, 0.782, and 0.725, respectively. CONCLUSION: The serum levels of CysC, Chemerin, and ProGRP of CRF patients are abnormally elevated and are positively correlated with serum Scr of patients, which can be used as a reliable indicator of pathogenesis and prognosis assessment of CRF patients.

Exploration of the mechanism of luteolin against ischemic stroke based on network pharmacology, molecular docking and experimental verification.

Stroke is a leading cause of morbidity and mortality worldwide. As the most common type of stroke cases, treatment effectiveness is still limited despite intensive research. Recently, traditional Chinese medicine has attracted attention because of potential benefits for stroke treatment. Among these, luteolin, a natural plant flavonoid compound, offers neuroprotection following against ischemic stroke, although the specific mechanisms are unknown. Here we used network pharmacology, molecular docking, and experimental verification to explore the mechanisms whereby luteolin can benefit stroke recovery. The pharmacological and molecular properties of luteolin were obtained from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. The potential targets of luteolin and ischemic stroke were collected from interrogating public databases. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed by Funrich and Database for Annotation, Visualization and Integrated Discovery respectively, a luteolin-target-pathway network constructed using Cytoscape, Autodock vina was used for molecular docking simulation with Discovery Studio was used to visualize and analyze the docked conformations. Lastly, we employed an in vitro model of stroke injury to evaluate the effects of luteolin on cell survival and expression of the putative targets. From 95 candidate luteolin target genes, our analysis identified six core targets . KEGG analysis of the candidate targets identified that luteolin provides therapeutic effects on stroke through TNF signaling and other pathways. Our experimental analyses confirmed the conclusions analyzed above. In summary, the molecular and pharmacological mechanisms of luteolin against stroke are indicated in our study from a systematic perspective.

The diagnostic and prognostic performance of Lp-PLA2 in acute ischemic stroke.

OBJECTIVE: We aimed to investigate the correlation between serum lipoprotein-associated phospholipase A2 (Lp-PLA2) level and acute ischemic stroke (AIS) severity and recurrence, which could indicate the diagnostic and prognostic values of Lp-PLA2. METHODS: Two hundred and fifty-one AIS patients who were diagnosed in the department of neurology, China-Japan Union Hospital, from April 2018 to June 2019 and 100 non-cerebrovascular disease patients were included in this study. Demographic data and clinical materials including age, sex, BMI, medical history, bad habits, imaging data, blood tests, etc., were collected. Stroke severity and risk were evaluated, respectively. AIS patients were followed up for 6 months for stroke recurrence monitoring. RESULTS: The AIS group had significantly higher Lp-PLA2 level than the control group. High Lp-PLA2 level was the independent risk factor of AIS (OR 1.010; 95% CI 1.007-1.013, P<0.001). Admission NIHSS was compared between Lp-PLA2 categories dichotomized by median. Serum Lp-PLA2 level was positively correlated with NIHSS (r=0.268, P<0.001). Mild stroke group and severe stroke group were defined based on NIHSS. Compared with the mild stroke group, the severe stroke group had higher smoking ratio, posterior circulation stenosis incidence, LDL level, Lp-PLA2 level and admission Essen score. Logistic regression showed Lp-PLA2 levels per 50ng/mL (OR 1.381, 95% CI 1.212-1.573, P<0.001) and Lp-PLA2 category (OR 2.420, 95% CI 1.363-4.297, P=0.003) were both independently associated with severe stroke. During the 6-month follow-up of all 251 AIS patients, 31 stroke recurrence cases were observed. Both Lp-PLA2 levels per 50ng/mL (OR 1.420, 95% CI 1.212-1.664, P<0.001) and Lp-PLA2 category (OR 2.726, 95% CI 1.201-6.178, P=0.016) were significantly associated with the stroke recurrence. Under the receiver Operating Characteristic curve, Lp-PLA2 showed significant predicting ability for stroke recurrence (AUC 0.723; 95% CI 0.620-0.826, P<0.001). CONCLUSION: High serum Lp-PLA2 level is correlated with AIS incidence, disease severity and recurrence, which could be utilized to guide clinical practice.

Proteomic analyses identify a potential mechanism by which extracellular vesicles aggravate ischemic stroke.

AIMS: Extracellular vesicles (EVs) are vital for information exchange between donor and recipient cells. When cells are stressed (e.g., by oxygen glucose deprivation, OGD), the complex information carried by the EVs is altered by the donor cells. Here, we aimed to analyze the proteomic differences between EVs derived from OGD-damaged cells and EVs derived from undamaged cells to explore the potential mechanisms by which EVs aggravate ischemic stroke (IS). MAIN METHODS: EVs released by rat adrenal gland PC12 cells subjected to 0, 3, 6, or 12 h of OGD were isolated. The proteins from the EVs secreted by each of the OGD groups were profiled using liquid chromatography-tandem mass spectroscopy (LC-MS/MS). We predicted the functions, pathways, and interactions of the differentially expressed proteins using Gene Ontology (GO), KEGG pathways, and STRING. We used parallel reaction monitoring (PRM) to validate our results. KEY FINDINGS: We identified several differentially expressed proteins in the OGD groups as compared to the controls: 170 proteins in the 3 h OGD EVs, 44 proteins in the 6 h OGD EVs, and 77 proteins in the 12 h OGD EVs (fold-change ≥1.5; p ≤ 0.05). These proteins were associated with oxidative stress, carbohydrate metabolism, protein synthesis and degradation, and thrombosis. SIGNIFICANCE: We identified changes in protein expression in the EVs secreted by OGD-damaged cells, highlighting potential mechanisms by which EVs aggravate IS. Our results also suggested potential protein targets, which may be useful for the prevention and treatment of IS.

Knockdown of microRNA-17-5p Enhances the Neuroprotective Effect of Act A/Smads Signal Loop After Ischemic Injury.

Cerebral ischemic injury is a leading cause of human mortality and disability, seriously threatening human health in the world. Activin A (Act A), as a well-known neuroprotective factor, could alleviate ischemic brain injury mainly through Act A/Smads signaling. In our previous study, a noncanonical Act A/Smads signal loop with self-amplifying property was found, which strengthened the neuroprotective effect of Act A. However, this neuroprotective effect was limited due to the self-limiting behavior mediated by Smad anchor for receptor activation (SARA) protein. It was reported that microRNA-17-5p (miR-17-5p) could suppress the expression of SARA in esophageal squamous cell carcinoma. Thus we proposed that knockdown of miR-17-5p could strengthen the neuroprotective effect of Act A/Smads signal loop through SARA. To testify this hypothesis, oxygen-glucose deficiency (OGD) was introduced to highly differentiated rattus pheochromocytoma (PC12) cells. After the transfection of miR-17-5p mimic or inhibitor, the activity of Act A signal loop was quantified by the expression of phosphorylated Smad3. The results showed that suppression of miR-17-5p up-regulated the expression of SARA protein, which prolonged and strengthened the activity of Act A signaling through increased phosphorylation of downstream Smad3 and accumulation of Act A ligand. Further luciferase assay confirmed that SARA was a direct target gene of miR-17-5p. These practical discoveries will bring new insight on the endogenous neuroprotective effects of Act A signal loop by interfering a novel target: miR-17-5p.

Synthesis and Discovery Novel Anti-Cancer Stem Cells Compounds Derived from the Natural Triterpenoic Acids.

Cancer stem cells (CSCs) have been reported to be involved in tumorigenesis, tumor recurrence, cancer invasion, metastasis, and drug-resistance. Therefore, the development of drug molecules targeting CSCs has become an attractive therapeutic approach. However, the molecules which can selectively ablate CSCs are extremely rare. To explore the leading compounds targeting CSCs, 52 analogues of triterpenoic acids were synthesized in this study, whose biological activities were evaluated. On the basis of the results of tumorsphere assay, two compounds 48 and 51, derived from oleanolic acid, exhibited suppressive effect on elimination of different type of CSCs. Meanwhile, compounds 48 and 51 could significantly inhibit the growth of several tumors both in vitro and in vivo. Furthermore, treatment of cancer cells with both of two compounds would dramatically increase the level of ROS, which might eliminate the CSCs. Collectively, the leading compounds 48 and 51 were promising anti-CSCs agents that merited further validation as a novel class of chemotherapeutics.

Expression changes of the notch signaling pathway of PC12 cells after oxygen glucose deprivation.

Ischemic stroke is caused by obstructed blood supply to the brain. It is a common as well as a serious health problem worldwide, which is often linked to disability and mortality. Here we studied, under the conditions of oxygen glucose deprivation (OGD), the expression of Notch signaling pathway proteins in PC12 cells. PC12 cells were stimulated and converted into neuron-like cells by nerve growth factor. Exposure to OGD was used as an in vitro model of cerebral hypoxia-ischemia. Our findings demonstrate that, after 3 h of OGD exposure, the expression of Notch1, Hes1 and Hes5 significantly increased, on both mRNA and protein levels. This effect gradually reduced with continuous OGD treatment, but the expression levels of these three genes remained higher, compared to untreated controls, even after 24 h of OGD exposure. Our results suggest that OGD exposure up-regulates the expression of Notch1, Hes1 and Hes5, which are important participants in Notch signaling pathway. Since their regulatory roles appear to change dynamically with the extension of OGD, the activation of the Notch pathway may play an important role in cerebral ischemic injury.

Cortical blindness as a rare presentation of hemorrhagic cerebral hyperperfusion syndrome following vertebral angioplasty.

Cerebral hyperperfusion syndrome (CHS) is a well-documented complication after carotid endarterectomy or stenting. In contrast, CHS following vertebral revascularization is extremely rare. Here we present a case of a 77-year-old man with high-grade vertebral stenosis who subsequently underwent balloon angioplasty, complicated by hemorrhagic CHS manifesting as cortical blindness, although strict postoperative blood pressure control was administered. To our knowledge, cortical blindness as a presentation of hemorrhagic CHS has not previously been reported. This study highlights the fact that identifying high-risk patients, as well as making an individual therapeutic plan, is important prior to revascularization. Further studies are needed to elucidate the exact mechanism of this condition and thereby prevent it.

Neuroprotective effects of Activin A on endoplasmic reticulum stress-mediated apoptotic and autophagic PC12 cell death.

Activin A, a member of the transforming growth factor-beta superfamily, plays a neuroprotective role in multiple neurological diseases. Endoplasmic reticulum (ER) stress-mediated apoptotic and autophagic cell death is implicated in a wide range of diseases, including cerebral ischemia and neurodegenerative diseases. Thapsigargin was used to induce PC12 cell death, and Activin A was used for intervention. Our results showed that Activin A significantly inhibited morphological changes in thapsigargin-induced apoptotic cells, and the expression of apoptosis-associated proteins [cleaved-caspase-12, C/EBP homologous protein (CHOP) and cleaved-caspase-3] and biomarkers of autophagy (Beclin-1 and light chain 3), and downregulated the expression of thapsigargin-induced ER stress-associated proteins [inositol requiring enzyme-1 (IRE1), tumor necrosis factor receptor-associated factor 2 (TRAF2), apoptosis signal-regulating kinase 1 (ASK1), c-Jun N-terminal kinase (JNK) and p38]. The inhibition of thapsigargin-induced cell death was concentration-dependent. These findings suggest that administration of Activin A protects PC12 cells against ER stress-mediated apoptotic and autophagic cell death by inhibiting the activation of the IRE1-TRAF2-ASK1-JNK/p38 cascade.

Efficacy and Prognostic Value of Partial Sensory Rhizotomy and Microvascular Decompression for Primary Trigeminal Neuralgia: A Comparative Study.

BACKGROUND This study aimed to compare the efficacy and prognostic value of partial sensory rhizotomy (PSR) and microvascular decompression (MVD) for primary trigeminal neuralgia (PTN). MATERIAL AND METHODS From June 2010 to June 2012, 117 patients with PTN were recruited for the study, of which 52 cases were treated with MVD (the MVD group) and 65 cases were treated with PSR (the PSR group). Visual Analog Scoring (VAS) was performed at 1 and 2 weeks, and at 1, 3, and 6 month after surgery. The overall response rate (ORR) was determined 1 month after surgery. Barrow Neurological Institute score was adopted to value the reoccurrence at 6, 12, 24, and 36 months after surgery. A 3-year follow-up was conducted and the complications were recorded. RESULTS The ORR 2 weeks after surgery in the MVD and PSR groups was 98.08% and 84.62%, respectively. One and 2 weeks after surgery, the VAS was lower in the MVD group than in the PSR group, but there was no significant difference in VAS between the 2 groups at 1, 3, and 6 months after surgery. Three years after surgery, the recurrence rate was significantly lower in the MVD group than in the PSR group. The recurrence-free survival time was longer in the MVD group than in the PSR group. The occurrence rates of herpes and total postoperative complications were significantly higher in the PSR group than in the MVD group. CONCLUSIONS Compared with PSR, MVD is more suitable for PTN treatment, with less disturbance, lower recurrence rate, and better efficacy.

Activin A/Smads signaling pathway negatively regulates Oxygen Glucose Deprivation-induced autophagy via suppression of JNK and p38 MAPK pathways in neuronal PC12 cells.

Activin A (Act A), a member of the transforming growth factor-beta (TGF-ß), reduces neuronal apoptosis during cerebral ischemia through Act A/Smads signaling pathway. However, little is known about the effect of Act A/Smads pathway on autophagy in neurons. Here, we found that oxygen-glucose deprivation (OGD)-induced autophagy was suppressed by exogenous Act A in a concentration-dependent manner and enhanced by Act A/Smads pathway inhibitor (ActRIIA-Ab) in neuronal PC12 cells. These results indicate that Act A/Smads pathway negatively regulates autophagy in OGD-treated PC12 cells. In addition, we found that c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase pathways are involved in the OGD-induced autophagy. The activation of JNK and p38 MAPK pathways in OGD-treated PC12 cells was suppressed by exogenous Act A and enhanced by ActRIIA-Ab. Together, our results suggest that Act A/Smads signaling pathway negatively regulates OGD-induced autophagy via suppression of JNK and p38 MAPK pathways in neuronal PC12 cells.

Noncanonical Activin A Signaling in PC12 Cells: A Self-Limiting Feedback Loop.

Activin A (Act A), a member of transforming growth factor-ß superfamily, plays a neuroprotective role in multiple neurological diseases through Act A/Smads signal activation. Traditionally, the up-regulation of Act A gene and extracellular Act A accumulation show the signal activation as a linear pathway. However, one of our discoveries indicated that Act A could lead a loop signaling in ischemic injury. To clarify the characteristic of this loop signaling in a non-pathological state, we up-regulated the expression of Act A, monitored extracellular Act A accumulation and examined the activity of Act A signaling, which was quantified by the expression of phosphorylated Smad3 and the fluorescence intensity of Smad4 in nuclei. The results demonstrated a noncanonical Act A signal loop with self-amplifying property in PC12 cells. Further, it showed self-limiting behavior due to temporary activation and spontaneous attenuation. This periodic behavior of Act A signal loop was found to be regulated by the level of Smad anchor for receptor activation (SARA). Moreover, increased activity of Act A signal loop could promote PC12 cell proliferation and enhance the survival rate of cells to Oxygen-Glucose Deprivation. These practical discoveries will bring new insight on the functional outcome of Act A signaling in neurological diseases by the further understanding: loop signaling.

Finasteride reduces microvessel density and expression of vascular endothelial growth factor in renal tissue of diabetic rats.

BACKGROUND: Vascular endothelial growth factor (VEGF) plays a critical role in the pathogenesis of diabetic microvascular complications. Finasteride has been confirmed to decrease VEGF expression in prostate and prostatic suburethral tissue resulting in limiting hematuria from human benign prostatic hyperplasia. The purpose of this study was to evaluate the effects of finasteride on microvessel density (MVD), VEGF protein and mRNA expressions in the renal tissue of diabetic rats. METHODS: Diabetic rats induced by streptozotocin were intragastrically given finasteride at 30 mg/kg body weight once a day for 4 weeks. Histomorphologic changes in kidney were observed under light microscope. Immunohistochemistry for CD34 and VEGF on kidney sections was performed to assess MVD and VEGF protein expression in glomeruli of rats, respectively. The VEGF mRNA expression in the renal tissue was examined using reverse transcription polymerase chain reaction analysis. RESULTS: The glomerular tuft area, glomerular volume, MVD, VEGF protein expression in glomeruli and VEGF mRNA expression in the renal cortex tissue were significantly increased in diabetic rats and finasteride-treated rats when compared with controls (P < 0.01, P < 0.05). When compared with diabetic rats, the glomerular tuft area, glomerular volume, MVD, VEGF protein expression in glomeruli and VEGF mRNA expression in the renal cortex tissue of finasteride-treated rats were significantly decreased (P < 0.05, P < 0.01). CONCLUSIONS: Finasteride reduces the VEGF expression and decreases the MVD in the renal tissue of diabetic rats, suggesting the therapeutic potential of finasteride on diabetic microvascular complications.

Endogenous protection derived from activin A/Smads transduction loop stimulated via ischemic injury in PC12 cells.

Activin A (ActA), a member of transforming growth factor-beta (TGF-b) super- family, affects many cellular processes, including ischemic stroke. Though the neuroprotective effects of exogenous ActA on oxygen-glucose deprivation (OGD) injury have already been reported by us, the endogenous role of ActA remains poorly understood. To further define the role and mechanism of endogenous ActA and its signaling in response to acute ischemic damage, we used an OGD model in PC12 cells to simulate ischemic injury on neurons in vitro. Cells were pre-treated by monoclonal antibody against activin receptor type IIA (ActRII-Ab). We found that ActRII-Ab augments ischemic injury in PC12 cells. Further, the extracellular secretion of ActA as well as phosphorylation of smad3 in PC12 cells was also up-regulated by OGD, but suppressed by ActRII-Ab. Taken together, our results show that ActRII-Ab may augment ischemic injury via blocking of transmembrane signal transduction of ActA, which confirmed the existence of endogenous neuroprotective effects derived from the ActA/Smads pathway. ActRIIA plays an important role in transferring neuronal protective signals inside. It is highly possible that ActA transmembrance signaling is a part of the positive feed-back loop for extracellular ActA secretion.

Effects of SARA on oxygen-glucose deprivation in PC12 cell line.

Ischemic stroke is a major composition of cerebrovascular disease, seriously threatening to human health in the world. Activin A (ActA), belonging to transforming growth factor-beta (TGF-ß) super family, plays an important role in the hypoxic-ischemic brain injury through ActA/Smads pathway. While as an essential phosphorylation assistor in TGF-ß signaling, the functions and mechanisms of smad anchor for receptor activation (SARA) in ischemic brain injury remain poorly understood. To solve this problem and explore the pathological processes of ischemic stroke, we used an Oxygen-Glucose deprivation (OGD) model in nerve growth factor-induced differentiated rattus PC12 pheochromocytoma cells and down regulated the expressions of SARA by RNA interference technology. Our results showed that the repression of SARA before OGD exposure reduced the expressions of Smad2, 3, 4 mRNA and the phosphorylation rate of Smad2 protein, but it did not affect the mRNA expressions of Smad7. After OGD treatment, ActA/Smads pathway was activated and the expression of SARA in the SARA pre-repression group was significantly up-regulated. The pre-repression of SARA increased the sensitivities of nerve-like cells to OGD damage. Moreover, the mRNA expression of Smad7 which was supposed to participate in the negative feedback of ActA/Smads pathway was also elevated due to OGD injury. Taken together, these results suggest a positive role of SARA in assisting the phosphorylation of Smad2 and maintaining the neuron protective effect of ActA/Smads pathway.

Activities of autonomic neurotransmitters in Meibomian gland tissues are associated with menopausal dry eye.

The secretory activities of meibomian glands are regulated by the autonomic nervous system. The change in density and activity of autonomic nerves in meibomian glands during menopause play an important role in the pathogenesis of dry eye. In view of this, we established a dry eye rat model by removing the bilateral ovaries. We used neuropeptide Y and vasoactive intestinal polypeptide as markers of autonomic neurotransmitters. Our results showed that the concentration of estradiol in serum significantly decreased, the density of neuropeptide Y immunoreactivity in nerve fibers significantly increased, the density of vasoactive intestinal polypeptide immunoreactivity in nerve fibers significantly decreased, and the ratio of vasoactive intestinal polypeptide/neuropeptide Y positive staining significantly decreased. These results suggest that a decrease in ovary activity may lead to autonomic nervous system dysfunction, thereby affecting the secretory activity of the meibomian gland, which participates in sexual hormone imbalance-induced dry eye.

Neuroprotective effects of exogenous activin A on oxygen-glucose deprivation in PC12 cells.

Ischemic cerebrovascular disease is one of the most common causes of death in the World. Exogenous activin A (ActA) protects neurons against toxicity and plays a central role in regulating the brain's response to injury. In the present study, we investigated the mechanisms involved in the neuroprotective effects of ActA in a model of hypoxic-ischemic brain disease. We found that ActA could effectively increase the survival rate of PC12 cells and relieve oxygen-glucose deprivation (OGD) damage. To clarify the neuroprotective mechanisms of ActA, the effects of ActA on the ActA/Smad pathway and on the up-regulation of inducible nitric oxide synthase (NOS) and superoxide dismutase (SOD) were investigated using OGD in PC12 cells. The results showed that ActA could increase the expression of activin receptor IIA (ActRIIA), Smad3 and Smad4 and that 50 ng/mL and 100 ng/mL of ActA could reduce NO levels and increase SOD activity by 78.9% and 79.9%, respectively. These results suggested that the neuroprotective effects of ActA in ischemia could be related to the activation of the ActA/Smad signaling pathway and to its anti-oxidant activities.

[Vascular endothelial growth factor expression in focal cerebral ischemia/reperfusion in injury in rats].

OBJECTIVE: To study the vascular endothelial growth factor (VEGF) expression and its role in focal cerebral ischemia/reperfusion injury. METHODS: VEGF protein and mRNA expressions at the site of focal ischemia/reperfusion of rat cerebrum were assessed with immunohistochemistry and hybridization techniques. RESULTS: In normal cerebral tissue there was lower expression of VEGF. It was found to be expressed in the penumbra area after ischemia. With the prolongation of ischemia and ischemia/reperfusion, enhanced expression of VEGF tended to decline to normal level, while it enhanced in the penumbra area. CONCLUSION: Enhanced VEGF expression might play a protective role in focal ischemia/reperfusion injury to the cerebrum.

[Study on multipotential differentiation of human bone marrow mesenchymal stem cells in vitro].

OBJECTIVE: To study the capability of human bone marrow mesenchymal stem cells (MSCs) to differentiate into adipocyte, osteoblasts, and neurocytes under different experimental conditions in vitro. METHODS: The induced human bone marrow MSCs were examined by cytochemistry staining and immunohistochemistry staining. RESULTS: Induced human bone marrow MSCs formed alkaline phosphatase-positive aggregates and Von Kossa stain-positive nodules under the condition of osteogenic differentiation. Under the condition of adipogenic differentiation, the isolated human bone marrow MSCs formed oil red-O-positive cells. Immunohistochemistry results showed that differentiated human bone marrow MSCs expressed neuron-specific enolase (NSE) and neurofilament (NF-M). CONCLUSION: Human bone marrow MSCs have the capability of multipotential differentiation in vitro.