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To investigate the regulation of N6- methyladenosine ( m6A ) modification on L-type calcium channels in atrial myocytes under high hydrostatic pressure, mediated by methyltransferase-like protein 3 ( METTL3 ). Methods C57BL/6J mice were randomly assigned to the control group and the hypertension group ( treated with continuous administration of angiotensin for four weeks ). Masson staining was used to observe the fibrosis of mouse atrial tissue, while dot blot assay and Western blot were used to detect the levels of m6A, METTL3, and Cavi1 2 in the atrial tissue. A high hydrostatic pressure model was constructed using the HL-1 cell line cultured in vitro, and METTL3 was intervened to observe changes in m6A expression levels, METTL3 and Cavi1 2 levels in cells,and action potential duration ( APD ) and L-type calcium current ( I
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Aim To observe whether the mechanosensitive ion channel Piezo1 was involved in the senescence of atrial fibroblasts by activating β-catenin based on our previous study which found marked increase of Piezo1 mRNA in senescent atrial fibroblasts. Methods Primary mouse atrial fibroblasts (MAFs) were isolated from male C57BL/6 mice (3-4 weeks) by enzyme digestion, and tert-butyl hydroperoxide (TBHP) was used to induce the senescence of cells. The ratio of senescent cells was detected by senescence-associated β-galactosidase (SA-β-Gal) staining. The protein levels of Piezo1, β-catenin/p-β-catenin, senescence-associated proteins p53 and p21 in the cells treated with TBHP (100 μmol · L
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Aim To investigate the mechanism of RhoA/ROCK signaling pathway in abnormal aortic contractility in type 2 diabetes (T2DM) mice. Methods The experiment was divided into two groups, the control group (db/m mice) and the model group (db/db mice). Changes of the response to different methods were measured in aorta rings using a Multi Myograph System. At the same time, the protein expression changes of aortic smooth muscle contraction signaling pathway in mice were determined by Western method. Results Compared with the control group, the blood glucose and body weight levels of the mice in the T2DM group significantly increased, and the cardiac function was abnormal (P <0. 01). The contractile response of the aorta of the diabetic mice induced by the contractile agents Phe, 5-HT and CaCl
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Aim To investigate the role of calcium-independent phospholipase A2(iPLA2)in calcium regu-lation of intrarenal artery smooth muscle contraction.Methods The method of measuring the tension of isolated arterioles was used to explore the effect of bromoenol lactone(BEL), a specific inhibitor of iPLA2, on the tension of the intrarenal arteries in mice induced by different calcium channels, and the laser confocal calcium measurement technology was used to investigate the effect of BEL on the intracellular calcium influx mediated by arachidonic acid-mediated calcium channels.Results The intrarenal artery concentration dependent contractile response induced by the vasoconstrictors phenylephrine and 5-hydroxy tryptamine was inhibited by BEL(P<0.01).The contraction curve induced by CaCl2 was also inhibited by BEL(P<0.05).In the calcium-free K-H solution incubated with nifedipine, the intrarenal artery vasoconstriction caused by the release of sarcoplasmic reticulum calcium and the calcium influx of the SOC channel induced by CaCl2 was inhibited by BEL(P<0.05).BEL significantly inhibited the external calcium influx mediated by the ARC channel of human aortic smooth muscle cell lines incubated with nifedipine(P<0.01).Conclusions iPLA2 mediates the contractile response of intrarenal arteries by regulating the functions of L-type calcium channels, sarcoplasmic reticulum calcium release, SOC channels and ARC channels.
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Aim To investigate the mechanism of Pi- ezol in the phenotypic changes of rat coronary arterial smooth muscle cells ( CASMCs) induced by high hydrostatic pressure.Methods CASMCs were isolated from Wistar rats and stimulated for 24 h at 0, 120 and 180 mmHg, respectively.The expressions of Piezol , contractile phenotvpe-related proteins including Cavl.2 ,SM-MHC ,cx-SMA and synthetic phenotvpe-re- lated proteins including OPN , MMP-2, Coll al were detected by Western blot.The effect of calcium influx mediated by Piezol was detected by Laser confocal mi- j j croscopy.CASMCs were treated with Piezol agonist Yodal , inhibitor GsMTx4 and Piezol-siHNA , respectively and the expressions of contractile phenotvpe and synthetic phenotvpe-related proteins were detected by Western blot.Results Compared with control ( 0 mmHg) , the expressions of Piezol , OPN, MMP-2 and Collal increased, but the expressions of Cavl.2,SM- MHC and cx-SMA decreased in 120 mmHg as well as 180 mmHg group.After stimulated by 180 mmHg high pressure, Piezol-mediated calcium influx was stronger than that in 0 mmHg group, hut decreased after Piezol knockdown.Treated with Yodal at 0 mmHg, the expression of contractile phenotvpe-related protein decreased while the expression of synthetic phenotvpe-re- lated protein increased compared with DMSO group..\Jfter using GsMTx4 to inhibit or siRNA to knockdown Piezol at 180 mmHg,the expression of contractile phe- notvpe-related protein increased and the expression of synthetic phenotype-related protein decreased compared with the control group.Conclusion Piezol promotes the transition from contractile phenotvpe to syn-thetic phenotvpe of CASMCs induced by high hydrostatic pressure.
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Aim To investigate the mechanism of TET1 in cardiac fibrosis induced by high pressure. Methods Wistar rats and spontaneous hypertension rats(SHR) were selected to detected the expression of TET1, TGF-β, COL-1 and COL-3 in myocardium by Western blot; HE and Masson staining were used to detect myocardial pathological changes. Neonatal rat cardiac fibroblasts (NRCFs) were isolated from the ventricles of neonatal Sprague-Dawley rats and stimulated by 0 mm-Hg, 120 mmHg and 180 mmHg high pressure. Immunofluorescence was used to detect the changes of 5-hmC in the NRCFs. The changes of 5-hmC and 5-mC in TGF-β promoter region were detected by qRT-PCR. The expressions of TET1, TGF-β, COL-1 and COL-3 were detected by Western blot. Results Compared with Wistar rats, SHR showed increased blood pressure, increased fibrous collagen in ventricular tissues, and significantly increased expressions of TET1, TGF-P, COL-1 and COL-3. Compared with the 0 mmHg group, 120 mmHg and 180 mmHg group significantly induced the increase of TET1, 5-hmC, TGF-p, COL-1 and COL-3. TET1 knockdown significantly reduced the increase of 5-hmC, TGF-β, COL-1 and COL-3 under 180 mmHg pressure. Besides, knockdown TET1 significantly reduced the level of 5-hmC and increased the level of 5-mC and 5-hmC in the TGF-β promoter region. Conclusions High pressure induced cardiac fibrosis is associated with the promotion of TGF-β promoter demethylation and the increased of TGF-β expression by TET1.
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Aim To observe the effects of sacubitril/valsartan (Sac/Val, LCZ696) on atrial remodeling and atrial fibrillation (AF) susceptibility in spontaneously hypertensive rats (SHR). Methods Twenty-four 7-week-old male SHR were randomly divided into SHR group, SHR + Val group (30 mg · kg
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Aim To investigate the role of Ca
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Aim To explore type 1 diabetes mice and the advance glycation end products (AGE) involved in electrical remodeling of atrial myocytes. Methods The diabetic mouse model was induced by intraperitoneal injection of STZ; action potential duration, and the current density of I
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Objective: To investigate whether inflammatory factor tumor necrosis factor-α (TNF-α) is involved in the electrical remodeling of cardiomyocytes by regulating ultra-rapid delayed rectifier K(+) current (I(kur)) and the role of Src kinase. Methods: H9c2 cells, embryonic cardiomyocytes of rat, were cultured in Dulbecco's modified Eagle's medium (DMEM) and atrium-derived HL-1 cells were cultured in Claycomb medium. Both H9c2 and HL-1 cells were cultured at 37 ℃ with 5% CO(2). Cells cultured in normal conditions without additional treatment served as control group. Experimental groups were treated with different concentration of TNF-α (25 or 50 or 100 ng/ml) for 24 hours. To study whether Src specific inhibitor PP1 could abrogate the effect of TNF-α, cells were pre-treated with 10 μmol/L PP1 for 1 hour, followed by TNF-α (100 ng/ml) for 24 hours. Western blot and the whole cell patch clamp technique were used to detect the protein expression of Kv1.5 and Src and I(kur) in each group. Results: (1) In H9c2 cells, high concentration of TNF-α treatment (100 ng/ml) significantly reduced the Kv1.5 protein expression compared with control group and TNF-α 25 ng/ml group (both P<0.05). Compared with control group, the expression of p-Src protein was higher in 25 ng/ml, 50 ng/ml, 100 ng/ml TNF-α group (all P<0.05), but there was no statistical difference in the expression of Src protein among groups (P>0.05). In addition, the current density of I(kur) was decreased in 50 ng/ml, 100 ng/ml TNF-α group (both P<0.05). Furthermore, the expression of Kv1.5 protein and the current density of I(kur) were increased in PP1+TNF-α group compared with TNF-α 100 ng/ml group (both P<0.05). There was no statistical difference in the expression of Kv1.5 protein and the current density of I(kur) between the control group and PP1+TNF-α group (both P>0.05). (2) In atrium-derived HL-1 cells, the expression of Kv1.5 protein was reduced in 100 ng/ml TNF-α group compared with control group and TNF-α 25 ng/ml group (both P<0.01). In addition, the expression of p-Src protein was increased in TNF-α 100 ng/ml group compared with control group (P<0.05), but there was no statistical difference in the protein expression of Src among groups (P>0.05). The expression of Kv1.5 protein was increased in PP1+TNF-α group compared with TNF-α 100 ng/ml group (P<0.05). Conclusion: TNF-α is involved in the pathogenesis of atrial fibrillation, probably via decreasing I(kur) current density in atrium-derived myocytes through the activation of Src kinase.
Subject(s)
Animals , Rats , Down-Regulation , Heart Atria , Myocytes, Cardiac , Tumor Necrosis Factor-alpha , src-Family KinasesABSTRACT
Aim To study whether there was arterial heterogeneity and association with L-type calcium channel (LCC) in different parts of arteries in re-sponse to certain vasoconstrictor. Methods The aor-ta, renal arteries and coronary arteries were dissected from rats. Arterial ring contractions induced by pheny-lephrine (Phe), 5-hydroxyl tryptamine (5-HT) or U46619 in concentration-dependent manner were meas-ured using the Multi Myograph system and the response to nifedipne was observed. Results (1) Phe had no obvious effect on the tension of coronary artery,but in-duced concentration-dependent vasoconstriction in aor-ta and renal artery,and pEC50of aorta was significantly higher than that of renal artery (P<0.05). The inhi-bition rate of nifedipine on the aortic contractile re-sponses was significantly higher than that of renal arter-y (P<0.05). (2) The contraction induced by 5-HT on aorta was not obvious, but was significant on renal artery and coronary artery. The inhibitory rate of nife-dipine on coronary artery vasoconstriction was signifi-cantly higher than that of renal artery (P <0.05). (3) U46619 could induce aorta,renal artery and coro-nary artery concentration- dependent contraction, but the Emaxof them were both higher than that of renal ar-tery (P<0.05). And the pEC50of aorta was the lar-gest (P<0.05). Nifedipine significantly inhibited the contraction of aorta, renal artery and coronary artery induced by U46619 with the greatest inhibitory rate on the coronary artery vasoconstriction and minimal inhibi-tion on aortic vasoconstriction. Conclusions The re-sponse to certain vasoconstrictor is different among aor-ta, renal artery and coronary artery in rats, and the contraction mediated by L-type calcium channel is also different.
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AIM:To investigate the possible mechanism of coronary artery contraction induced by 5-hydroxytryptamine(5-HT).METHODS:Isolated coronary artery rings were obtained from male Wistar rats,and the vas-cular tension meter was used to determine the tension of the coronary artery rings.The effects of inhibitors of different sig-naling pathway on vascular contraction tension induced by 5-HT were observed.RESULTS:Firstly,we found that 5-HT2A receptor antagonist sarpogrelate(1 μmol/L)completely eliminated the coronary artery contraction induced by 5-HT.Phos-pholipase Cβ(PLCβ)inhibitor U73122(10 μmol/L and 50 μmol/L), Rho-related protein kinase inhibitor Y-27632(3 μmol/L and 10 μmol/L)and protein kinase C δ subunit(PKCδ)inhibitor rottlerin(3 μmol/L and 10 μmol/L)signifi-cantly inhibited the contraction of coronary artery ring caused by 5-HT(P<0.05).In addition, compared with the un-treated group,vascular contraction tension induced by 5-HT was also decreased significantly by L-type calcium channel (Cav1.2)blocker nifedipine(1 μmol/L), store-operated Ca2+entry(SOCE)inhibitor SKF96365(10 μmol/L and 30 μmol/L)and 2-aminoethoxydiphenyl borate(2-APB,50 μmol/L and 100 μmol/L)(P<0.05).At the same time,5-HT also induced vasoconstriction after treated with nifedipine(1 μmol/L)Kerbs-Henseleit(K-H)liquid without calcium (P<0.05).CONCLUSION:5-HT activates 5-HT2Areceptor induced coronary artery contraction,possibly related to the PKC/Rho kinase signaling pathway and calcium regulation.
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AIM:To investigate the changes of cardiac structure and function in rats with type 2 diabetic melli-tus(T2DM),and to explore the mechanisms underlying diabetic cardiomyopathy.METHODS:The cardiac structure and function were measured by echocardiography in Zucker diabetic fatty(ZDF)rats and their control Zucker lean(ZL)rats. The size of the cardiomyocytes was determined by wheat germ agglutinin staining.The protein expression of atrial natriuretic peptide(ANP),β-myosin heavy chain(β-MHC), receptor for advanced glycation end products(RAGE), L-type cal-cium channel α1C subunit(CaV1.2)and Orai1 was assessed by Western blot.RESULTS:Compared with the ZL control rats,the thickness of left ventricular wall,ejection fraction(EF),fractional shortening(FS)and the sizes of cardiomyo-cytes were significantly increased,and diastolic function was decreased in the ZDF rats(P<0.05).The protein expression of β-MHC, ANP, RAGE and Orai1 was increased, while the expression of Ca V1.2 was decreased in ZDF rats(P <0.05).CONCLUSION:T2DM rats show the prominent features including cardiomyocyte hypertrophy,ventricular hyper-trophy and compensatory enhancement of cardiac function, and the Ca2+handling and increase in RAGE expression may play important roles in the processes.
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<p><b>OBJECTIVE</b>To investigate the effects of propofol combined with indomethacin on the contractile function of isolated human pulmonary arteries.</p><p><b>METHODS</b>Human pulmonary artery preparations were obtained from patients undergoing surgery for lung carcinoma. The intrapulmonary arteries were dissected and cut into rings under microscope for treatment with propofol or propofol combined with indomethacin. In each group, the rings were divided into endothelium-intact and endothelium-denuded groups and mounted in a Multi Myograph system. In propofol group, the rings were preconstricted by U46619 to induce a sustained contraction, and propofol (10-300 mmol/L) was then applied cumulatively. In the combined treatment group, the rings were pretreated with indomethacin (100 µmol/L) for 30 min before application of U46619 to induce sustained contraction, and propofol (10-300 µmol/L) was added cumulatively after the tension became stable.</p><p><b>RESULTS</b>Propofol (10-100 µmol/L) induced constrictions at low concentrations and caused relaxations at higher concentrations (100-300 µmol/L) in the pulmonary artery rings with prior U46619-induced contraction. Propofol caused stronger constrictions in endothelium-intact rings [EC=4.525∓0.37, Emax=(30.44∓2.92)%] than in endothelium-denuded rings [EC=4.699∓0.12, Emax=(31.19∓5.10)%, P<0.05]. Pretreatment of the rings with indomethacin abolished constrictions, and the relaxation was more obvious in endothelium-intact group [pD=3.713∓0.11, Emax=(98.72∓0.34)%] than in endothelium- denuded group [pD=3.54∓0.03, Emax=(94.56∓0.53)%, P<0.05].</p><p><b>CONCLUSION</b>Propofol induces constriction at low concentrations and relaxation at high concentrations in human intrapulmonary arteries with U46619-induced contraction. Indomethacin abolishes the constriction induced by propofol in isolated intrapulmonary arteries, suggesting that propofol potentiates U46619-mediated pulmonary vasoconstriction by promoting the concomitant production of prostaglandin by cyclooxygenase in pulmonary artery smooth muscle cells, and the mechanism for its relaxation effect may partly depend on the endothelium.</p>
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<p><b>OBJECTIVE</b>To determine the effect of resveratrol on constrictions of isolated human intrapulmonary arteries and its mechanisms.</p><p><b>METHODS</b>Intrapulmonary arteries (1-1.5 mm in diameter) were dissected and cut into rings (1.8-2.0 mm in length) under microscope, and were then mounted in a Multi Myograph system. The rings were stimulated with 100 nmol/L U46619, 30 nmol/L endothelin-1, or 60 mmol/L KCl to produce sustained contraction of the intrapulmonary arteries, after which resveratrol was applied cumulatively. Endothelium denudation, L-NAME and indomethecin were used to investigate the effect of resveratrol on constrictions of the isolated arteries, suing DMSO as the control.</p><p><b>RESULTS</b>Resveratrol induced concentration-dependent relaxations in endothelium-intact rings that contracted in response to stimulations with U46619, ET-1 and KCl, with pD2 of 3.82±0.20, 3.84±0.57, and 3.68±0.27, Emax of (99.58±0.83)%, 100%, and (99.65±0.98)%, respectively. Treatment of the arterial rings with the eNOS inhibitor L-NAME, but not with indomethecin or endothelium denudation, obviously affected the relaxant effects of resveratrol.</p><p><b>CONCLUSION</b>Resveratrol can concentration-dependently produce relaxant effect on human intrapulmonary arteries independent of the endothelium possibly by promoting synthesis and release of NO.</p>
Subject(s)
Humans , 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid , Pharmacology , In Vitro Techniques , Pulmonary Artery , Stilbenes , Pharmacology , VasoconstrictionABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression and functional role of the small conductance Ca(2+)-activated K(+) channels in human atrial myocytes.</p><p><b>METHODS</b>We collected the right atrial appendage tissues from 8 patients with congenital heart defect with sinus rhythm undergoing open-heart surgery. Immunohistochemistry was performed to identify the expression of 3 isoforms of SK channel (SK1, SK2 and SK3). Using the classical two-step enzymatic isolation method, perforated patch clamp and conventional voltage-clamp techniques were performed to record the action potentials (APs) and the whole-cell Ca(2+)-activated K(+) current (I(K, Ca)) in the single atrial myocyte. We compared the changes in action potential duration (APD) before and after the application of a specific SK channels blocker apamin (100 nmol/L).</p><p><b>RESULTS</b>Human atrial myocytes showed positivity for all the SK1, SK2 and SK3 isoform channels. Patch-clamp recording confirmed the presence of I(K,Ca), and apamin significantly prolonged APD at 90% repolarization (APD(90)), but produced no obvious effect on APD(50).</p><p><b>CONCLUSION</b>The three isoforms of SK channels are all expressed in human atrial myocytes. SK channels play a prominent role in the late phase of repolarization in human atrial myocytes, which is distinct from their functional roles in neurons where they mediate the process of afterhyperpolarization following APs.</p>
Subject(s)
Adolescent , Female , Humans , Male , Action Potentials , Physiology , Atrial Appendage , Cell Biology , Cells, Cultured , Myocytes, Cardiac , Metabolism , Patch-Clamp Techniques , Protein Isoforms , Metabolism , Physiology , Small-Conductance Calcium-Activated Potassium Channels , Metabolism , PhysiologyABSTRACT
The effects of ketamine on transient outward potassium current (I(to)) of isolated human atrial myocytes were investigated to understand the mechanism of part of its effects by whole-cell patch-clamp. Atrial myocytes were enzymatically isolated from specimens of human atrial appendage obtained from patients under going cardiac valve displacing. Ito is recorded in voltage-clamp modes using the patch-clamp technique at room temperature. Currents signals were recorded by an Axopatch 200B amplifier with the Digidata 1322A-pClamp 9.0 data acquisition system. Ketamine decreased I(to) of human atrial myocytes in a dose-dependent manner. The current-voltage curve was significantly lowered, 30, 100, 300, and 1000 micromol x L(-1) ketamine decreased respectively I(to) current density about (13.62 +/- 0.04)%, (38.92 +/- 0.05)%, (72.24 +/- 0.10)% and (83.84 +/- 0.05)% at the potential of 50 mV, with an IC50 of 121 micromol x L(-1). The I(to) activation curve, inactivation curve and the recovery curve were not altered by ketamine. So, ketamine concentration-dependently decreased I(to) of human atrial myocytes.
Subject(s)
Adolescent , Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Anesthetics, Dissociative , Pharmacology , Dose-Response Relationship, Drug , Heart Atria , Cell Biology , Ketamine , Pharmacology , Myocytes, Cardiac , Cell Biology , Physiology , Patch-Clamp Techniques , Potassium ChannelsABSTRACT
<p><b>OBJECTIVE</b>To investigate the interaction domains between macrophage migration inhibitory factors (MIF) and the extracellular segment of type-II trans-membrane protein CD74 using a yeast two-hybrid system.</p><p><b>METHODS</b>By using molecular cloning techniques, the DNA fragments encoding MIF, MIF(50-65) and MIF(1-50/65-115) were introduced into the pGBKT7 vector to construct the corresponding recombinant bait plasmids, and the DNA fragments encoding CD74(73-232), CD74(73-109), CD74(1109-149) and CD74(149-232) into the pGADT7 vector to construct the recombinant activation domain (AD) plasmids. PEG/LiAC method was employed to transform the above 3 recombinant bait plasmids paired with each of the 4 recombinant AD plasmids into the chemical competent yeast AH109 cells. The transformed yeast AH109 cells were screened consecutively on SD/-Trp-Leu and SD/-Trp-Leu-Ade-His/X-alpha-gal nutritional media.</p><p><b>RESULTS</b>The results of restriction endonuclease digestion and DNA sequencing verified the correct construction of all the recombinant plasmids. The yeast AH109 cells transformed with each of the 3 recombinant bait plasmids could grow on SD/-trp nutritional media without autonomous activation effect on the reporter gene MEL1. The cells transformed with each of the 4 recombinant AD plasmids could also grow on SD/-leu nutritional media without activation of the reporter gene MEL1. Only the yeast AH109 cells co-transformed with MIF, MIF(50-65), or MIF(1-50/65-115) plasmid and CD74(73-232) plasmid could grow on SD/-Trp-Leu-Ade-His nutritional media with transcription activation of the reporter gene MEL1.</p><p><b>CONCLUSION</b>MIF interacts with the intact extracellular segment of CD74 (CD74(73-232)) independent of the functional domain of MIF(50-65).</p>
Subject(s)
Antigens, Differentiation, B-Lymphocyte , Genetics , Metabolism , Cloning, Molecular , Escherichia coli , Genetics , Metabolism , Extracellular Matrix , Metabolism , Histocompatibility Antigens Class II , Genetics , Metabolism , Macrophage Migration-Inhibitory Factors , Genetics , Metabolism , Peptide Fragments , Genetics , Protein Interaction Domains and Motifs , Genetics , Recombinant Proteins , Genetics , Two-Hybrid System TechniquesABSTRACT
<p><b>OBJECTIVE</b>To investigate the ability of human bone marrow mesenchymal stem cells (hBMSCs), cocultured with semi-permeable membrane separated neonatal rat ventricular myocytes, to differentiate into cardiomyocytes.</p><p><b>METHODS</b>hBMSCs were isolated and purified by density gradient centrifugation and adherence screening method. Cells were expanded as undifferentiated cells in culture for more than 3 passages and their phenotypes were identified with flow cytometer. hBMSCs were cocultured with neonatal rat ventricular myocytes in a rate of 1:10 separated by semi-permeable membrane. GATA4 mRNA was detected by RT-PCR; Immunocytochemistry, and Immunostaining were used to detect sarcomeric alpha-actinin, desmin, cTnT, and cTnI protein level.</p><p><b>RESULTS</b>CD29 (98.64% +/- 0.80%) and CD44 (96.70% +/- 1.50%) were the major surface markers of hBMSCs. After coculturing with semi-permeable membrane separated neonatal rat ventricular myocytes, the first contraction of single cells was noted at day 7 and GATA4 expression was detected on these cells by RT-PCR after 1 to 3 weeks coculture. Desmin, sarcomeric alpha-actinin, cTnI and cTnT could be detected by immunocytochemistry and immunostaining on some of these cells.</p><p><b>CONCLUSION</b>hBMSCs possess the potential to differentiate into myocardial cell phenotype in the cardiac microenvironment. Direct contact with cardiomyocytes was not necessary required for hBMSCs differentiation.</p>