OBJECTIVETo investigate the influence of zoledronic acid on vascular endothelial cells.

METHODSThe influence of zoledronic acid on proliferation, migration and adhesion of vascular endothelial cells were tested with 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), cell migration assay and cell adhesion assay. The results of each experimental group were compared with the control group and the data statistically analyzed.

RESULTSIn a concentration of 0-0.5 mmol/L, the absorbance value decreased from 0.09 to 0.34 as the drug concentration increased. Scratch test showed that the change of width of scratch before and after 24 hours in control, low, medium and high concentration groups were (38.7 ± 0.42), (35.8 ± 4.17), (19.9 ± 0.57) mm (P < 0.001), (12.5 ± 3.89) mm (P < 0.05). Adhesion test showed that the absorbance value in control, low, medium and high concentration groups were 1.14 ± 0.18, 0.95 ± 0.13, 0.81 ± 0.11 (P < 0.01), 0.67 ± 0.19 (P < 0.001). Comparisons between control and experimental groups were analyzed by t-test and P values < 0.05 were considered statistically significant.

CONCLUSIONSZoledronic acid inhibits the proliferation, migration and adhesion of vascular endothelial cells.

Cell Adhesion ; drug effects ; physiology ; Cell Movement ; drug effects ; physiology ; Cell Proliferation ; drug effects ; Diphosphonates ; pharmacokinetics ; pharmacology ; Endothelial Cells ; cytology ; drug effects ; Imidazoles ; pharmacokinetics ; pharmacology

OBJECTIVETo determine whether homocysteine induced endothelial damage through monocyte-endothelial interaction and to characterize both cell types in vitro.

METHODSRadiomethods were performed on monocyte adhesion to/through endothelium and endothelial damage experiments.

RESULTSHomocysteine-treated endothelial cells increased monocyte adhesion and transmigration. Homocysteine-treated monocytes induced endothelial detachment, but this effect was blocked by catalase. These effects were increased with higher concentrations of homocysteine. Monocyte surface glycoprotein antibodies CD11b/CD18 and CD14 inhibited these processes.

CONCLUSIONSHomocysteine alters monocyte-endothelial interaction in vitro, eventually bringing about endothelial damage through release of H(2)O(2). These phenomena are mediated through monocyte surface glycoproteins CD11b/CD18 and CD14. Upregulation of these processes in vivo may contribute to acceleration of atherosclerosis in patients with elevated plasma homocysteine levels.

Arteriosclerosis ; etiology ; Cell Adhesion ; drug effects ; Cell Communication ; drug effects ; Cell Movement ; drug effects ; Dose-Response Relationship, Drug ; Endothelium, Vascular ; cytology ; drug effects ; Homocysteine ; pharmacology ; Humans ; Monocytes ; drug effects ; physiology

BackgroundRecent research indicates that nerve growth factor (NGF) promotes cardiac repair following myocardial infarction by promoting angiogenesis and cardiomyocyte survival. The purpose of this study was to investigate the effects of NGF on cardiac fibroblasts (CFs) proliferation, cell cycle, migration, and myofibroblast transformation in vitro.

MethodsCFs were obtained from ventricles of neonatal Sprague-Dawley rats and incubated with various concentrations of NGF (0, 0.01, 0.1, 1, 10, and 100 ng/ml; 0 ng/ml was designated as the control group). Cell proliferation and cell cycle of the CFs were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry (FCM), respectively. A cell scratch wound model and transwell were carried out to observe effects of NGF on migration of CFs after 24 h of culture. Real-time polymerase chain reaction (RT-PCR) and Western blotting were used to measure α-smooth muscle actin (α-SMA) at mRNA and protein levels after CFs were incubated with various concentrations of NGF.

ResultsExpression of α-SMA measured by RT-PCR and Western blotting significantly increased in the 1 and 10 ng/ml NGF groups (P < 0.05). Absorbance values of CFs showed that NGF did not influence the proliferation of CFs (The Avalues were 0.178 ± 0.038, 0.182 ± 0.011, 0.189 ± 0.005, 0.178 ± 0.010, 0.185 ± 0.025, and 0.177 ± 0.033, respectively, in the 0, 0.01, 0.1, 1, 10, and 100 ng/ml NGF groups [P = 0.800, 0.428, 0.981, 0.596, and 0.913, respectively, compared with control group]), and FCM analysis showed that the percentage of CFs in G0/G1, S, and G2/M phases was not changed (P > 0.05). The cell scratch wound model and transwell showed that CFs migration was not significantly different (P > 0.05).

ConclusionNGF induces myofibroblast transformation but does not influence proliferation, cell cycle, or migration of CFs in vitro.

Actins ; metabolism ; Animals ; Cell Cycle ; drug effects ; physiology ; Cell Movement ; drug effects ; physiology ; Cell Proliferation ; physiology ; Cells, Cultured ; Myofibroblasts ; cytology ; drug effects ; Nerve Growth Factor ; metabolism ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the effects of hypoxia of different duration on movement and proliferation of human epidermal cell line HaCaT.

METHODS(1) HaCaT cells in logarithmic phase were cultured in RPMI 1640 medium containing 10% FBS (the same culture method below). Cells were divided into control group (routine culture) and hypoxia for 1, 3, 6 h groups according to the random number table (the same grouping method below), with 6 wells in each group. Cells in the 3 hypoxia groups were cultured in incubator containing 5% CO2, 2% O2, and 93% N2 (the same hypoxic condition below) for corresponding duration. Range of movement of cells in 3 hours was observed under live cell imaging workstation, and their curvilinear and rectilinear movement speeds were calculated at post observation hour (POH) 1, 2, 3. (2) HaCaT cells in logarithmic phase were divided into control group (routine culture) and hypoxia for 1, 3, 6, 9, 12, 24 h groups, with 20 wells in each group. Cells in the 6 hypoxia groups were cultured under hypoxic condition for corresponding duration. Proliferation of cells was examined with cell counting kit and microplate reader (denoted as absorbance value). (3) HaCaT cells in logarithmic phase were divided into control group (routine culture) and hypoxia for 1, 3, 6, 24 h groups, with 5 wells in each group. Cells in the 4 hypoxia groups were cultured under hypoxic condition for corresponding duration. Protein expression of proliferating cell nuclear antigen (PCNA) was determined with Western blotting. Data were processed with one-way analysis of variance and Dunnett- t test.

RESULTS(1) Compared with that of control group, the movement area of cells was obviously expanded in hypoxia for 1, 3, 6 h groups. The longer the hypoxic treatment, the greater the increase was. At POH 1, 2, 3, the curvilinear movement speeds of cells in hypoxia for 1, 3, 6 h groups were respectively (43 ± 18), (44 ± 17), (43 ± 16) µm/h; (44 ± 16), (44 ± 14), (45 ± 14) µm/h; (55 ± 19), (54 ± 17), (56 ± 18) µm/h. They were significantly higher than those of control group [(33 ± 13), (33 ± 12), (33 ± 10) µm/h, with t values from 2.840 to 9.330, P < 0.05 or P < 0.01]. The curvilinear movement speed of cells was significantly higher in hypoxia for 6 h group than in hypoxia for 1 or 3 h group (with t values from 3.474 to 4.545, P < 0.05 or P < 0.01). There was no significant difference in the curvilinear movement speed among the observation time points within each group (with F values from 0.012 to 0.195, P values above 0.05). At POH 1, the rectilinear movement speed of cells in hypoxia for 1 h group was (22 ± 11) µm/h, which was obviously higher than that of control group [(15 ± 10) µm/h, t = 2.697, P < 0.01]. At POH 1, 2, 3, rectilinear movement speeds of cells in hypoxia for 3 and 6 h groups were respectively (19 ± 14), (12 ± 8), (10 ± 6) µm/h; (32 ± 19), (21 ± 13), (17 ± 12) µm/h. They were significantly higher than those of control group [(9 ± 7) and (6 ± 5) µm/h at POH 2 and 3, with t values from 1.990 to 8.231, P < 0.05 or P < 0.01]. The rectilinear movement speed of cells in hypoxia for 6 h group was obviously higher than that of hypoxia for 1 or 3 h group (with t values from 3.394 to 6.008, P < 0.05 or P < 0.01). The rectilinear movement speed of cells in each group decreased at POH 2 or 3 in comparison with POH 1 (with t values from -8.208 to -4.232, P values below 0.01). The rectilinear movement speed of cells in control group at POH 3 was significantly different from that at POH 2 (t = -1.967, P < 0.05). (2) The proliferation levels of cells in control group and hypoxia for 1, 3, 6, 9, 12, 24 h groups were respectively 1.11 ± 0.08, 1.36 ± 0.10, 1.39 ± 0.05, 1.38 ± 0.05, 1.10 ± 0.14, 1.06 ± 0.09, 0.99 ± 0.06 (F = 39.19, P < 0.01). Compared with that of control group, the rate of proliferation of cells was obviously increased in hypoxia for 1, 3, 6 h groups (with t values respectively 6.639, 7.403, 7.195, P values below 0.01), but obviously decreased in hypoxia for 24 h group (t = -3.136, P < 0.05). The proliferation of cells decreased in hypoxia for 9, 12, 24 h groups in comparison with hypoxia for 1, 3, 6 h groups (with t values from -10.538 to -6.775, P values below 0.01). (3) The protein expressions of PCNA of cells in control group and hypoxia for 1, 3, 6, 24 h groups were respectively 0.93 ± 0.12, 0.97 ± 0.14, 1.62 ± 0.18, 0.95 ± 0.09, 0.66 ± 0.21 (F = 20.11, P < 0.01). Compared with that of control group, the expression of PCNA was obviously increased in hypoxia for 1, 3, 6 h groups (with t values respectively 2.339, 5.783, 2.235, P < 0.05 or P < 0.01), but obviously decreased in hypoxia for 24 h group (t = -1.998, P < 0.05). The protein expression of PCNA was higher in hypoxia for 3 h group than in hypoxia for 1 or 6 h group (with t values respectively 4.312 and 3.947, P values below 0.01), and it was increased in the 3 groups in comparison with that of hypoxia for 24 h group (with t values respectively 2.011, 6.193, 3.287, P < 0.05 or P < 0.01).

CONCLUSIONSShort-time hypoxia (1, 3, 6 h) treatment can promote the movement and proliferation of HaCaT cells. Hypoxia for 6 h is the best condition to promote their movement, while hypoxia for 3 or 6 h is better for their proliferation.

Carbon Dioxide ; pharmacology ; Cell Cycle ; drug effects ; Cell Line ; Cell Movement ; physiology ; Cell Proliferation ; drug effects ; physiology ; Cells, Cultured ; Epithelial Cells ; cytology ; drug effects ; Humans ; Hypoxia ; physiopathology ; Nitric Oxide ; pharmacology ; Oxygen ; pharmacology ; Phosphorylation ; Proliferating Cell Nuclear Antigen ; Signal Transduction

Although heparin is better known as an anticoagulant, it also has several anti-inflammatory effects. Heparin is known to inhibit neutrophil adhesion, chemotaxis and oxygen free radical production. In addition, heparin is also known to act as an oxygen radical scavenger. Our hypothesis was that heparin would attenuate renal ischemia reperfusion injury. In this study, we investigated whether heparin had a protective effect on renal ischemia reperfusion injury. Sheep (n = 12) were prepared for the chronic study with venous, arterial and urinary catheters inserted. In addition, pneumatic occluders and ultrasonic flow probes were placed on renal arteries. After a 5-day recovery period, the sheep were randomized to either a heparin treatment group (400 IU/kg i.v. bolus 10 minutes before renal artery occlusion, followed by a continuous effusion 25,000 IU in 250 ml of 0.9% NaCl at 10 ml/hr, n = 6) or a control group (n = 6), which received an equivalent volume of 0.9% NaCl. All the sheep then underwent 90 minutes of bilateral renal ischemia followed by 24 hours of reperfusion. Blood urea nitrogen (BUN), serum creatinine (Scr), and creatinine clearance (CrCl) were determined at various intervals during both the ischemic and reperfusion periods. Kidney tissue samples were obtained at autopsy for histologic examination. As a result, there were significant differences in the degree of inflammation (1.50 +/- 1.24 Vs 0.50 +/- 0.79, P < 0.05) between the control and heparin treatment groups, but not in the degree of injury (2.83 +/- 0.44 Vs 2.33 +/- 0.28). In this study, heparin significantly attenuated polymorphonuclear leukocytes (PMNs) infiltration within the interstitium, but it did not affect the degree of renal damage as measured by urinary chemistries or renal tubular damage as assessed by histopathologic evaluation.
Animal ; Anticoagulants/pharmacology* ; Cell Movement/drug effects ; Female ; Heparin/pharmacology* ; Ischemia/pathology* ; Kidney/pathology ; Kidney/drug effects* ; Neutrophils/physiology ; Neutrophils/drug effects* ; Renal Circulation* ; Reperfusion Injury/pathology* ; Sheep

OBJECTIVETo investigate whether oxidized low-density lipoprotein (oxLDL) affects the survival and activity of endothelial progenitor cell (EPC) and whether the effects are mediated by lectin-like oxidized low-density lipoprotein receptor (LOX-1).

METHODSCD34+ cells isolated from human umbilical blood were cultured in endothelial cell growth medium-2 (EGM-2). After 14 days of culture, some EPCs were stimulated with 10, 25, 50 microg/ml of oxLDL for 48 hours; some were preincubated with LOX-1 mAb, a blocking antibody of LOX-1, for 24 hours, then exposed to 50 microg/ml oxLDL for 48 hours; others without any further treatment were used as control. The survival of EPC and the ability of adhesion, migration, and tube formation were examined. The levels of LOX-1 protein and mRNA expression were also assayed.

RESULTSIncubation with oxLDL at concentrations of 25 microg/ml or higher resulted in a dose-dependent increase of EPC apoptosis [25 microg/ml: (15.8 +/- 1.1.0%, 50 microg/ml: (18.8 +/- 2.0)% versus control: (9.0 +/- 1.2)%; P < 0.05]. Treated with oxLDL led to a significantly reduced migratry rate [25 microg/ml: (5.7 +/- 1.0)%, 50 microg/ml: (5.1 +/- 0.8)% versus control: (9.5 +/- 0.8)%; P < 0.05]. EPC treated with oxLDL showed a dose-dependent reduction of adhesion to fibronectin (25 Kg/ml: 33 +/- 2, 50 microg/ml: 30 +/- 3 versus control: 37 +/- 5; P < 0.05). Treatment with oxLDL impaired the in vitro vasculogenesis ability of EPCs. The total length of the tube structures in each photograph was decreased [25 microg/ml: (2.9 +/- 0.5) mm, 50 microg/ml: (1.8 +/- 0.5) mm versus control: (5.0 +/- 0.6) mm; P < 0.05]. The tube structure was severely disrupted, resulting in an incomplete and sparse tube network. However, all the detrimental effects on EPC were attenuated by pretreatment of EPC with LOX-1 mAb. In addition, Western blot analysis revealed that oxLDL increased LOX-1 protein expression from 100% to (172 +/- 8)% at a dose of 50 microg/ml. Furthermore, oxLDL caused an increase in LOX-1 mRNA expression from 100% to (174 +/- 39)% at a dose of 50 microig/ml.

CONCLUSIONOxLDL can directly inhibit EPC survival and activity and these effects are mediated by its receptor, LOX-1.

Antigens, CD34 ; metabolism ; Apoptosis ; Cell Adhesion ; Cell Movement ; Cell Survival ; Cells, Cultured ; Endothelial Cells ; drug effects ; physiology ; Fetal Blood ; cytology ; Humans ; Lipoproteins, LDL ; pharmacology ; physiology ; Neovascularization, Physiologic ; Scavenger Receptors, Class E ; biosynthesis ; physiology ; Stem Cells ; drug effects ; physiology

Although empirically well understood in their clinical administration, volatile anesthetics are not yet well comprehended in their mechanism studies. A major conundrum emerging from these studies is that there is no validated model to assess the presumed candidate sites of the anesthetics. We undertook this study to test the hypothesis that the single-celled Paramecium could be anesthetized and served as a model organism in the study of anesthetics. We assessed the motion of Paramecium cells with Expert Vision system and the chemoresponse of Paramecium cells with T-maze assays in the presence of four different volatile anesthetics, including isoflurane, sevoflurane, enflurane and ether. Each of those volatiles was dissolved in buffers to give drug concentrations equal to 0.8, 1.0, and 1.2 EC50, respectively, in clinical practice. We could see that after application of volatile anesthetics, the swimming of the Paramecium cells was accelerated and then suppressed, or even stopped eventually, and the index of the chemoresponse of the Paramecium cells (denoted as I ( che )) was decreased. All of the above impacts were found in a concentration-dependent fashion. The biphasic effects of the clinical concentrations of volatile anesthetics on Paramecium simulated the situation of high species in anesthesia, and the inhibition of the chemoresponse also indicated anesthetized. In conclusion, the findings in our studies suggested that the single-celled Paramecium could be anesthetized with clinical concentrations of volatile anesthetics and therefore be utilized as a model organism to study the mechanisms of volatile anesthetics.
Anesthetics, Inhalation ; administration & dosage ; Biological Assay ; methods ; Cell Movement ; drug effects ; physiology ; Chemotaxis ; drug effects ; physiology ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; methods ; Paramecium tetraurelia ; drug effects ; physiology ; Volatile Organic Compounds ; administration & dosage

OBJECTIVETo explore the influence of oxidized high-density lipoprotein (oxHDL) on the maturation and migration of bone marrow-derived dendritic cells (BMDCs) from C57BL/6J mice.

METHODSThe C57BL/6J mice bone marrow cell suspension was prepared and purified. Recombinant granulocyte-macrophage colony-stimulating factor (rmGM-CSF) and recombinant interleukin-4 (rmIL-4) were used to promote monocytes to differentiate and suppress lymphocytes. Then 50 microg/mL oxHDL was added to stimulate BMDCs, using 50 microg/mL high-density lipoprotein (HDL) as homologous protein control, PBS as negative control, and 1 microg/mL lipopolysaccharide (LPS) as positive control. The CD86 and MHCII expression rates were detected with fluorescence-activated cell sorting (FACS). Liquid scintillation counting (LSC) was used in mixed lymphocyte reactions (MLRs) to reflect the ability of BMDCs in stimulating the proliferation of homologous T cells. Levels of cytokines IL-12 and IL-10 were detected by ELISA. The cell migration was evaluated with the transwell system.

RESULTSCompared with PBS group, the expressions of CD86 and MHCII, counts per minute of MLRs, secretion of IL-12 and IL-10, and number of migrated cells in oxHDL group and LPS group significantly increased (all P<0.05), while the increment was less in oxHDL group than LPS group. The number of migrated cells in oxHDL group was about twice of that in HDL group.

CONCLUSIONOxHDL may promote the maturation and migration of BMDCs in vitro.

Animals ; Bone Marrow Cells ; cytology ; drug effects ; physiology ; Cell Differentiation ; drug effects ; Cell Movement ; drug effects ; Cells, Cultured ; Dendritic Cells ; cytology ; drug effects ; physiology ; Humans ; Lipoproteins, HDL ; metabolism ; pharmacology ; Lipoproteins, LDL ; metabolism ; pharmacology ; Mice ; Mice, Inbred C57BL

OBJECTIVETo explore the effects of different concentrations of putrescine on proliferation, migration, and apoptosis of human umbilical vein endothelial cells (HUVECs).

METHODSHUVECs were routinely cultured in vitro. The 3rd to the 5th passage of HUVECs were used in the following experiments. (1) Cells were divided into 500, 1 000, and 5 000 µg/mL putrescine groups according to the random number table (the same grouping method was used for following grouping), with 3 wells in each group, which were respectively cultured with complete culture solution containing putrescine in the corresponding concentration for 24 h. Morphology of cells was observed by inverted optical microscope. (2) Cells were divided into 0.5, 1.0, 5.0, 10.0, 50.0, 100.0, 500.0, 1 000.0 µg/mL putrescine groups, and control group, with 4 wells in each group. Cells in the putrescine groups were respectively cultured with complete culture solution containing putrescine in the corresponding concentration for 24 h, and cells in control group were cultured with complete culture solution with no additional putrescine for 24 h. Cell proliferation activity (denoted as absorption value) was measured by colorimetry. (3) Cells were divided (with one well in each group) and cultured as in experiment (2), and the migration ability was detected by transwell migration assay. (4) Cells were divided (with one flask in each group) and cultured as in experiment (2), and the cell apoptosis rate was determined by flow cytometer. Data were processed with one-way analysis of variance, Kruskal-Wallis test, and Dunnett test.

RESULTS(1) After 24-h culture, cell attachment was good in 500 µg/mL putrescine group, and no obvious change in the shape was observed; cell attachment was less in 1 000 µg/mL putrescine group and the cells were small and rounded; cells in 5 000 µg/mL putrescine group were in fragmentation without attachment. (2) The absorption values of cells in 0.5, 1.0, 5.0, 10.0, 50.0, 100.0, 500.0, 1 000.0 µg/mL putrescine groups, and control group were respectively 0.588 ± 0.055, 0.857 ± 0.031, 0.707 ± 0.031, 0.662 ± 0.023, 0.450 ± 0.019, 0.415 ± 0.014, 0.359 ± 0.020, 0.204 ± 0.030, and 0.447 ± 0.021, with statistically significant differences among them (χ(2) = 6.86, P = 0.009). The cell proliferation activity in 0.5, 1.0, 5.0, and 10.0 µg/mL putrescine groups was higher than that in control group (P < 0.05 or P < 0.01). The cell proliferation activity in 500.0 and 1 000.0 µg/mL putrescine groups was lower than that in control group (with P values below 0.01). The cell proliferation activity in 50.0 and 100.0 µg/mL putrescine groups was close to that in control group (with P values above 0.05). (3) There were statistically significant differences in the numbers of migrated cells between the putrescine groups and control group (F = 138.662, P < 0.001). The number of migrated cells was more in 1.0, 5.0, and 10.0 µg/mL putrescine groups than in control group (with P value below 0.01). The number of migrated cells was less in 500.0 and 1 000.0 µg/mL putrescine groups than in control group (with P value below 0.01). The number of migrated cells in 0.5, 50.0, and 100.0 µg/mL putrescine groups was close to that in control group (with P values above 0.05). (4) There were statistically significant differences in the apoptosis rate between the putrescine groups and control group (χ(2)=3.971, P=0.046). The cell apoptosis rate was lower in 0.5, 1.0, 5.0, and 10.0 µg/mL putrescine groups than in control group (with P values below 0.05). The cell apoptosis rate was higher in 500.0 and 1 000.0 µg/mL putrescine groups than in control group (with P values below 0.01). The cell apoptosis rates in 50.0 and 100.0 µg/mL putrescine groups were close to the cell apoptosis rate in control group (with P values above 0.05).

CONCLUSIONSLow concentration of putrescine can remarkably enhance the ability of proliferation and migration of HUVECs, while a high concentration of putrescine can obviously inhibit HUVECs proliferation and migration, and it induces apoptosis.

Apoptosis ; drug effects ; Biological Products ; Cell Line ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Flow Cytometry ; Human Umbilical Vein Endothelial Cells ; cytology ; drug effects ; Humans ; Putrescine ; administration & dosage ; adverse effects ; pharmacology ; physiology ; Skin ; cytology ; Wound Healing

BACKGROUNDMany studies on periostin have focused on its role in tumors and vascular reconstruction. However, the effect of periostin on stem cell function remains unclear. The aim of this study was to enhance vitality in adipose-derived stem cells (ADSCs), the effect of periostin on the function of ADSCs was observed.

METHODSHuman ADSCs (hADSCs) were isolated from human adipose tissue by collagenase I digestion and collected in multi-periods for in vitro culture. CD29, CD34, CD44, CD45 and CD105 were detected by flow cytometry. In addition, directed differentiation of hADSCs was induced using adipogenic, osteogenic and chondrogenic induction mediums. The induced morphological changes were observed using oil red O, Alizarin red and alcian blue staining. Periostin was administered to hADSCs in an acidic environment. The treatments of cells were divided into three groups: a periostin group (P); an acidic control group (A); a normal group (N). Then the resulting cell proliferation and migration were detected using a Cell Counting Kit-8 (CCK-8) and a transwell chamber assay, respectively.

RESULTSThe detection rates of CD29, CD44, CD105, CD34 and CD45 were 98.89%, 93.73%, 86.99%, 0.19% and 0.16%. The specific staining of cells was positive after induction culture. The mean absorbance of the cells in group P and A at 12 hours were 16.67% and 22.22% greater than group N, respectively (P < 0.01). The mean absorbance of cells from group P was 20.00% greater than that of group A at 48 hours (P < 0.05). The mean number of migratory cells per visual field in group A was 50.38% lower than that in group N (P < 0.05). The migratory cell number in group P was 119.98% greater than that in group A (P < 0.05).

CONCLUSIONSThe acidic environment impacted hADSC proliferation and inhibited cell migration. However, periostin was able to promote the proliferation and migration of hADSCs despite the acidic environment.

Adipose Tissue ; cytology ; Adult ; Antigens, Surface ; analysis ; Cell Adhesion Molecules ; pharmacology ; Cell Differentiation ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Female ; Humans ; Stem Cells ; drug effects ; physiology