The identification and characterization of stem cells is a major focus of developmental biology and regenerative medicine. The advent of genetic inducible fate mapping techniques has made it possible to precisely label specific cell populations and to follow their progeny over time. When combined with advanced mathematical and statistical methods, stem cell division dynamics can be studied in new and exciting ways. Despite advances in a number of tissues, relatively little attention has been paid to stem cells in the oral epithelium. This review will focus on current knowledge about adult oral epithelial stem cells, paradigms in other epithelial stem cell systems that could facilitate new discoveries in this area and the potential roles of epithelial stem cells in oral disease.
Adult Stem Cells ; cytology ; physiology ; Animals ; Asymmetric Cell Division ; Biomarkers ; Cell Proliferation ; Clone Cells ; Epithelial Cells ; cytology ; Genetic Drift ; Humans ; Mouth Mucosa ; cytology ; Mouth Neoplasms ; pathology ; Neoplastic Stem Cells

A recent study has proposed that dimethyl sulfoxide (DMSO) increases the number of HL-60 cells in high cell density conditions by inhibiting cell density-dependent apoptosis. We observed that dimethylformamide (DMF), a DMSO-related polar compound, also increased the concentration of HL-60 cells. The effective dose range of DMSO and DMF was 0.5-1% and 0.2-0.6% respectively. DMF, like DMSO, inhibited density-dependent apoptosis of HL-60 cells. The flow cytometric PKH26 cell proliferation assay showed DMSO and DMF actively increased cell division. However, the difference in the distribution of cell cycle phase was not noted between the control and the DMSO- or DMF-treated HL-60 cultures. Finally, DMSO and DMF stimulated HL-60 growth even in low density conditions. These results suggest that DMSO and OMF at appropriate concentrations increase the number of HL-60 cells by both apoptosis inhibition and cell division augmentation.
Apoptosis ; Cell Count ; Cell Cycle ; Cell Division ; Cell Proliferation ; Dimethyl Sulfoxide* ; Dimethylformamide* ; HL-60 Cells* ; Humans*

OBJECTIVETo study the effects of Saccharomyces albicans (S. albicans) on the cell cycle distribution and proliferation of human umbilical vein endothelial cell ECV304 cells in vitro.

METHODSThe line of ECV304 cultured in vitro were divided into four groups which were treated by S. albicans supernatant, S. albicans inactivated bacilli, supernatant and inactivated bacilli mixture, normal culture medium. The proliferous effect of ECV304 induced by supernatant, inactivated bacilli, supernatant and inactivated bacilli mixture using the methods of MTT, cell count, microscope and flow cytometry were conducted.

RESULTSIn the condition of different times and different culture concentrations, ECV304 cells incubated with 4-fold diluted S. albicans supernatant for 48 h increased the proliferation rate. The S and G2/M population of ECV304 cells increased after incubated with S. albicans supernatant for 40 h, which showed significant increasing cell proliferation index (PI) (P < 0.05). The PI of the cells treated by inactivated bacilli showed no significant change (P > 0.05).

CONCLUSIONS. albicans could induce ECV304 cell proliferation which depends on the release of metabolic products of S. albicans.

Cell Cycle ; Cell Division ; Cell Proliferation ; Human Umbilical Vein Endothelial Cells ; Humans ; Saccharomyces ; Umbilical Veins

OBJECTIVETo evaluate the effects of non-Saccharomyces albicans metabolic products on the cell cycle distribution and proliferation of human umbilical vein endothelial cell ECV304 cells in vitro.

METHODSThe parallel dilution supernatant of Saccharomyces tropicalis, Saccharomyces krusei and Saccharomyces glabrata were prepared, and 1, 4, 16-fold(s) diluted concentration and control group were set up. The line of human umbilical vein endothelial cell ECV304 was cultured in vitro and treated by non-Saccharomyces albicans supernatant. The proliferous effect of ECV304 induced by non-Saccharomyces albicans supernatant after 24, 48, 72 h was detected by the methods of MTT, and the changes of cell density and cycle after 48 h were investigated by inverted microscope and flow cytometry.

RESULTSAt the 24th hour, all of the higher concentration (1-fold) of non-Saccharomyces albicans supernatant and the 4-folds diluted Saccharomyces krusei could promote ECV304 proliferation(P < 0.05). After adding various non-Saccharomyces albicans supernatant at 48h and 72th hour, Saccharomyces krusei supernatant and Saccharomyces glabrata supernatant significantly increased proliferation rate of ECV304, while Saccharomyces tropicalis supernatant group showed no significant change no matter which concentration was tested. At 48th hour after adding the non-Saccharomyces albicans supernatant, the ECV304 cells density treated by Saccharomyces krusei supernatant and Saccharomyces glabrata supernatant were significantly higher under the inverted microscope. The G0/G1 population of ECV304 cells decreased while cell proliferation index (PI) increased after incubated with Saccharomyces krusei supernatant and Saccharomyces glabrata supernatant for 48 hours (P < 0.05). Saccharomyces tropicalis group showed no significant change (P > 0.05).

CONCLUSIONThe metabolic products of Sacharoymces krusei and Saccharomyces glabrata could induce proliferation of ECV304 cell, which suggests non-Saccharomyces albicans should be undergone more attention clinically in detection and treatment.

Cell Cycle ; Cell Division ; Cell Proliferation ; Human Umbilical Vein Endothelial Cells ; Humans ; Saccharomyces ; Umbilical Veins

OBJECTIVETo approach the effects on induction of differentiation of Tca8113 cells affected by abscisic acid.

METHODSThe changes of surface differentiation markers, cell configuration, restrain of cell growth and the expression of Caspase-3 mRNA were examined by using inverted-phase contrast microscope, immunohistochemistry (IHC) and in situ hybridization in vitro. The dependablity between the surface differentiation markers and Caspase-3 mRNA was analysed.

RESULTSThe restraint of cell growth in ABA groups was higher than that of the control group (P<0.05). There was a trend that the tumor cell had transformed the normal cell. Furthermore, the time-dosage dependent relationship existed in the inhibition rate of tumor cells. The results showed that the expressions of Involucrin protein, retinoic acid receptor beta (RARbeta) and Caspase-3 mRNA in experimental group had been higher than that of control group. There was a significance between the different concentration experimental groups at 24 h (P<0.05). Moreover, the positive correlation existed among the Involucrin, RARbeta and Caspase-3 mRNA at the time of 12 hour and 24 hour (P<0.05).

CONCLUSIONThe possible mechanism is that abscisic acid acted on the tumor cell and raised the level of RARbeta gene through combining the correlative receptors so that increased the expression of Involucrin protein and promoted the activity of Caspase-3 and resulted in apoptosis of tumor cell.

Abscisic Acid ; Apoptosis ; Cell Differentiation ; Cell Division ; Cell Proliferation ; In Vitro Techniques ; RNA, Messenger ; Receptors, Retinoic Acid

OBJECTIVEThis study was to explore the expression of CD71, as a proliferation indicator, on cell proliferaration in hematologic malignancy and its correlation with Ki-67, so as to assess the feasibility of CD71 instead of Ki-67 for assaying cell proliferation by flow cytometry (FCM).

METHODS(1) Compared with mature B lymphoctyes during stationary phase in peripheral blood from healthy people, the cell cycle and the expression of CD71 and Ki-67 of cell lines from patients with leukemia and lymphoma were examined, the correlation among CD71, S-phase cell fraction (SPF) and Ki-67 were analyzed; (2) Compared with mature B lymphoctyes in bone marrow from non-hematologic disease patients, the expression and correlation of CD71 and Ki-67 of all kinds of leukemic cells and myeloma cells from bone marrow were analyzed by using Ki-67/CD71/CD45/CD123, Ki-67/CD71/CD45/CD20 or Ki-67/CD71/CD45/CD138.

RESULTS(1) in respect to the expression rate of CD71 on tumor cell lines, the expression rate of CD71 on HL-60 cells was (99.77 ± 0.064)%, the expression rate of CD71 on NB4 cells was (99.23 ± 0.12)%, the expression rate on THP-1 cells was (98.90 ± 0.30)% and the expression rate on K562 cells was (97.03 ± 0.15)% in myelogenous leukemia cell lines, the expression rate of CD71 on Raji cells was (99.35 ± 0.21)% and the expression rate on Mino cell was (96.95 ± 0.42)% in lymphoma cell lines, which were also obviously higher than that on cells of the control group (P < 0.05); (2) in respect to the expression rate of CD71 on tumor cells in bone marrow, the expression rate of CD71 on poorly differentiated AML(M1 and M2) cells was (51.50 ± 19.31)%, the expression rate of CD71 on acute promyelocytic leukemia (AML-M3) cells was (35.71 ± 14.02) %, the expression rate of CD71 on acute monocytic leukemia (AML-M5) cells was (30.54 ± 14.38)%, the expression rate of CD71 on acute T lymphoblastic leukemia cells was (68.40 ± 20.83)%, the expression rate of CD71 on acute B lymphoblastic leukemia was (39.67 ± 18.27)%, the expression rate of CD71 on multiple myeloma (MM) cells was (55.49 ± 18.15%), the expression rate of CD71 on chronic lymphocytic leukemia(CLL) was (1.32 ± 0.33%), which were also higher than that on cells in the control group(P < 0.05) except for CLL cells (P > 0.05); (3) CD71 had a positive linear corrlation with SPF in cell lines (r = 0.914, P < 0.05), and also had a positive linear corrlation with Ki-67 in cell lines and carcinoma cells from bone marrow (r = 0.894,r = 0.904, P < 0.05).

CONCLUSIONThe CD71 can take the place of Ki-67 as an indicator of cell proliferation activity of hematologic malignancies and the determination CD71 by FCM is simpler and better than that of Ki-67 in respest of methodology.

Antigens, CD ; Cell Division ; Cell Proliferation ; Flow Cytometry ; Hematologic Neoplasms ; Humans ; Ki-67 Antigen ; Receptors, Transferrin

OBJECTIVETo investigate whether Echinococcus granulosus cyst fluid-infected host liver cells had differential expression of mitogen-activated protein kinases (MAPKs) or differential cell cycle activity.

METHODSHuman liver cells cultured with different concentrations of hydatid cyst fluid (HCF) were tested by the MTT method to determine effects on proliferation. The cell cycle was assessed by flow cytometry. Western blotting was used to detect changes in protein expressions of p-ERK, PCNA, cyclin-A, cyclin-B1, cyclin-D1, and cyclin-E.

RESULTSForty-eight, 72 and 96 h of HCF at 15%, 30% and 60% concentrations in the cell media significantly promoted cell proliferation (F=67.845, P less than 0.01) and compared to controls (P less than 0.05). Cells exposed to 15% HCF for 48 h showed significantly induced expression of p-ERK (F=1.916, P less than 0.01), higher than controls (P less than 0.01). Cells exposed to 15% HCF for 24 h showed significantly induced expression of cyclin-Dl (F=3.901, P less than 0.01), higher than controls (P less than 0.01). Cells exposed to 15% HCF for 48 h or 30% HCF for 72 h showed significantly induced expression of PCNA (F=91.140, P less than 0.01), higher than controls (P less than 0.01). Cells exposed to 15% HCF for 48 h or 30% HCF for 72 h shed significantly induced expression of cyclin-A (F=18.587, P=0.002), higher than controls (P less than 0.01). Cells exposed to 15% HCF for either 48 h or 72 h showed significantly induced expression of cyclin-B1 (F=2.064, P less than 0.01), higher than controls (P less than 0.01). Cells exposed to 30% HCF for 96 h showed significantly induced expression of cyclin-E (F=1.068, P less than 0.01), higher than controls (P less than 0.01).

CONCLUSIONHydatid cyst fluid exerts no inhibitory effect on primary cultured host liver cells, but may promote cellular proliferation.

Animals ; Cell Cycle ; Cell Division ; Cell Proliferation ; Cyst Fluid ; chemistry ; Echinococcosis ; Echinococcus granulosus ; Flow Cytometry ; Hep G2 Cells ; Humans

Endogenous electric fields (EFs) have been detected at wounds and damaged tissues. The potential roles of EFs in tissue repair and regeneration have been an intriguing topic for centuries. Recent researches have provided significant insights into how naturally occurring EFs may participate in the control of tissue repair and regeneration. Applied EFs equivalent to the size of fields measured in vivo direct cell migration, cell proliferation and nerve sprouting at wounds. More remarkably, physiological EFs are a guidance cue that directs cell migration which overrides other well accepted directional signals including initial injury stimulation, wound void, contact inhibition release, population pressure and chemotaxis. EFs activate many intracellular signaling pathways in a directional manner. Modulation of endogenous wound EFs affects epithelial cell migration, cell proliferation, and nerve growth at cornea wounds in vivo. Electric stimulation is being tested clinically for the treatments of bone fracture, wound healing and spinal cord injury. EFs thus may represent a novel type of signaling paradigm in tissue repair and regeneration. Combination of the electric stimulation and other well understood biochemical regulatory mechanisms may offer powerful and effective therapies for tissue repair and regeneration. This review introduces experimental evidence for the existence of endogenous EFs and discusses their roles in tissue repair and regeneration.
Cell Division ; Cell Movement ; Cell Proliferation ; Electric Stimulation ; Electromagnetic Fields ; Humans ; Neurons ; physiology ; Regeneration ; Wound Healing ; Wounds and Injuries ; physiopathology

OBJECTIVE: To investigate the effect of small interfering RNA (siRNA) targeting c-myc gene in Hep-2 cells. METHOD: siRNA targeting c-myc mRNA was designed and synthesized. In vitro cultured Hep-2 cells were transfected with lipofectamine 2000 and the inhibitory effect was detected by MTT, morphology, real time PCR assay. RESULT: 1) The MTT result showed the c-myc siRNA to be able effectively to suppress the Hep-2 cell multiplication; 2) The real time PCR result showed c-myc at mRNA level inhibition ratio at 94% in group S3; 3) The morphology result showed the c-myc siRNA to be able effectively to suppress the Hep-2 cell multiplication, the cell heteromorphism was diminished. CONCLUSION siRNA targeting c-myc can remarkably suppress the Hep-2 cell growth and multiplication.
Apoptosis ; Cell Division ; Cell Line, Tumor ; Cell Proliferation ; Gene Targeting ; Genes, myc ; genetics ; Humans ; RNA, Small Interfering ; genetics ; Transfection

OBJECTIVETo investigate the effects of β-elemene in suppressing the proliferation and apoptosis of SGC7901 gastric cancer cells in vitro and explore the underlying mechanisms.

METHODSUsing MTT assay, flow cytometry, and clonogenic survival assay, we assessed the effects of β-elemene on the viability, apoptosis, cell cycle distribution, and clonogenic survival of gastric cancer SGC7901 cells and gastric mucosal epithelial GES-1 cells. Western blotting was employed to determine the changes in the protein expression profiles in SGC7901 cells in response to β-elemene treatment.

RESULTSβ-elemene significantly suppressed the cell viability and increased the apoptosis of SGC7901 cells, and these effects were less obvious in GES-1 cells. β-elemene decreased clonogenic survival of SGC7901 cells, increased the proportion of G2/M phase cells, decreased the expression of Bcl-2, and increased the expression of Bax and cleaved caspase-3. β-elemene did not obviously affect the expression of total p21-activated protein kinase 1 (Pak1) but decreased the level of phospho-Pak1 (Thr423) and phospho-ERK1/2 (Thr202/Tyr204) in SGC7901 cells.

CONCLUSIONβ-elemene inhibits the proliferation and induces apoptosis of gastric cancer cells possibly by inhibiting Pak1/ERK signaling and regulating apoptosis-associated proteins such as Bcl-2 and Bax.

Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Cell Cycle ; Cell Division ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; Cell Survival ; Humans ; Sesquiterpenes ; pharmacology ; Signal Transduction ; Stomach Neoplasms ; pathology