All-trans retinoic acid (ATRA) is a vitamin A derivative and plays an important role in the regulation of cell aggregation, differentiation, apoptosis, proliferation, and inflammatory response. In recent years, some progress has been made in the role of ATRA in renal diseases, especially its protective effect on podocytes. This article reviews the research advances in podocyte injury, characteristics of ATRA, podocyte differentiation and regeneration induced by ATRA, and the protective effect of ATRA against proliferation, deposition of fibers, and apoptosis.
Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cytoprotection ; Humans ; Podocytes ; drug effects ; physiology ; Tretinoin ; pharmacology

OBJECTIVE: To explore the proliferation and differentiation-inducing effects of aminosteroid H42648 on K562 leukemia cells. METHODS: The effects of H42648 on K562 cell proliferation were determined by cell count, colony count and MTT assay, and the differentiation by morphology, benzidine stain and flow cytometry. RESULTS: The growth of K562 cells was inhibited after the treatment with H42648 for 5 days. The inhibition rates for K562 cells in MTT assay were (26.90+/-3.18)% and (43.26+/-2.54)% after the treatment by 10(-8)mol/L and 10(-6)mol/L H42648. The inhibitions for K562 cells in colony culture assay were (22.21+/-9.20)% and (48.71+/-8.24)% at 10(-8)mol/L and 10(-6)mol/L H42648, respectively. H42648 also induced K562 cells toward erythroid differentiation. It was verified by benzidine stain that the OD value at 10(-8)mol/L H42648 was increased by (153+/-17.65)% compared with the control, and at 10(-6)mol/L H42648 the OD value was increased by (250+/-4.60)% compared with the control. The morphology showed the differentiation tendency of K562 cells after the treatment. Data from flow cytometry showed that after the treatment with 10(-6)mol/L H42648 for 4 days, positive CD71 expression in differentiated K562 cells was 89.91%. CONCLUSION H42648 can inhibit the proliferation of K562 cell lines and induce toward erythroid differentiation. H42648 may become a new lead for the differentiation-inducing therapy for leukemia.
Antineoplastic Agents ; pharmacology ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Humans ; K562 Cells ; Steroids ; pharmacology

OBJECTIVETo study the maturation effect of CpG2006 and phosphodiester oligonucleotides on leukemia-derived dendritic cells.

METHODSLeukemia cells K562/A02 were induced into dendritic cells by rhGM-CSF and rhIL-4. After 7 days induction, the cell-morphology was observed, the immunophenotype of cells was detected by flow cytometry and the cell function was evaluated by allogeneic mixed lymphocyte reactions, CTL responses and secretion of IL-12 and IL-6. Then a CpG oligonucleotide CpG2006, two synthetic bacterial phosphodiester oligonucleotides A-ODN and T-ODN were added to these leukemia-derived DCs. Three days later, the DCs were re-detected by the above-mentioned methods.

RESULTSAfter induced by CpG2006, A-ODN or T-ODN, the leukemia-derived DCs with typical dendritic morphology were increased. The expressions of CD83, HLA-DR and CD86 were (65.5 +/- 8.4)%, (32.0 +/- 4.3)% and (18.6 +/- 3.2)% respectively in day 7 leukemia-derived DCs, raised to (88.9 +/- 3.6)%, (53.9 +/- 3.2)% and (39.9 +/- 7.3)% respectively after exposing CpG2006 for 3 days; increased to (97.0 +/- 5.3)%, (63.9 +/- 7.3)% and (40.2 +/- 7.4)% respectively after treated by A-ODN; and further increased to (93.26 +/- 4.65)%, (58.3 +/- 5.6)% and (36.2 +/- 6.8)% respectively after treated by T-ODN. These results was markedly different than unaffected cells did. These DCs induced by the above-mentioned three oligonucleotides could upregulate significantly the capacity for stimulating allogeneic T cells. They could also induce CTL to generate specific cytotoxic activity against K562/A02 cells. The secretion of IL-6 and IL-12 was increased remarkably.

CONCLUSIONCpG2006, as well as two phosphodiester oligonucleotides can induce leukemia-derived DCs maturation.

Cell Differentiation ; drug effects ; Cell Survival ; drug effects ; Dendritic Cells ; cytology ; drug effects ; Humans ; K562 Cells ; Oligodeoxyribonucleotides ; pharmacology ; Oligonucleotides ; pharmacology

OBJECTIVETo analyze the influence of retinoic acid (RA) on the undifferentiated state and EB formation abilities of human embryonic stem cells.

METHODSThe biological characteristics of H9 ESCs after RA treatment were characterized by real-time PCR, MTS proliferation assay and immunofluorescence staining. The expression of three germ layers markers, osteogenic differentiation markers and adipogenic differentiation markers in H9-differentiated embryoid bodies (EBs) with RA treatment were quantified by real time PCR.

RESULTSThe proliferation of H9 ESCs in the early logarithmic growth phase was accelerated by RA treatment. In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level. RA induced formation of cavities in EBs. Real time PCR results showed that the expressions of ectodermal markers: NeuroD1, Noggin; mesodermal markers: Brachyury, Twist and endodermal markers: AFP, GATA-4 were significantly increased (P < 0.05), especially for AFP (P < 0.01), by RA treatment in a dose-dependent manner. In addition, the expression of adipogenic differentiation marker C/EBPalpha was increased while the osteogenic differentiation marker OPN was decreased in EBs after RA treatment for 5 days.

CONCLUSIONSHigh concentrations of RA induced the loss of stemness in H9 ESCs and excessive differentiation in EBs, and damaged the balance between osteogenic and adipogenic differentiation during early EB differentiation, which may be relevant to the congenital malformations.

Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Embryonic Stem Cells ; cytology ; drug effects ; Humans ; Tretinoin ; pharmacology

OBJECTIVETo study the effect of embelin on proliferation, differentiation and apoptosis of HL-60 cells and explore its possible mechanism.

METHODSDifferent concentration of embelin were used to treat HL-60 cells. Cell growth curve was analysed by MTT assay, cell apoptosis by Annexin V/PI double staining and JC-1 dye. The differentiation of HL-60 cells was evaluated by expression of CD33, CD34, CD11b and CD14. Bone marrow cells (BMC) from nine patients with acute nonlymphocytic leukemia (ANML) were also studied.

RESULTSEmbelin induced differentiation of HL-60 cells with significant increase of CD14 and CD11b expression at 33.97µmol/L for 3 days (P < 0.01). Embelin induced apoptosis of HL-60 cells in a time- and dose-dependent manner, the apoptosis rates were (9.23 ± 0.05)%, (25.86 ± 0.30)% and (39.03 ± 0.07)% respectively at 339.67 µmol/L of embelin for 12-, 24- and 48-hours treatment (P < 0.05); the apoptosis rates were (0.07 ± 0.03)%, (7.43 ± 0.30)%, (14.01 ± 0.01)%, (25.52 ± 0.03)% and (39.15 ± 0.01)% respectively at 10.19, 33.97, 101.90, 339.67 and 1019.02 µmol/L of embelin for 24-hours culture (P < 0.05). Clusters of differentiation antigen on BMC from three acute promyelocytic leukemia patients showed significant changes at 33.97 µmol/L of embelin treatment for 3 days. Embelin induced apoptosis of BMCs from all the nine ANML patients at 33.97 µmol/L for 24 hour.

CONCLUSIONEmbelin can inhibit proliferation and induce differentiation and apoptosis of HL-60 cells. The mechanism may be related to mitochondrial apoptosis pathway. Embelin at subtoxic concentration doesn't promote leukemia BMC differentiation, but at 339.67 µmol/L induces apoptosis of these cells.

Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; HL-60 Cells ; Humans ; Leukemia, Promyelocytic, Acute ; metabolism

OBJECTIVETo study the effect of macrocalyxin A (MA) on proliferation, differentiation and apoptosis in HL-60 cells and explore its possible mechanisms.

METHODSDifferent concentration of MA were used to treat HL-60 cells. Proliferation inhibition was analyzed by Trypan blue staining and MTT assay, cell apoptosis by cell morphology, DNA content, cell cycle analysis, Annexin-V/PI and Hoechst 33258 fluorescence staining. The differentiation of HL-60 cells was evaluated by cell morphology, NBT tests and expression of CD11b, CD13, CD14. The expressions of bcl-2, bax, Fas, P53, mitochondrial transmembrane-potential (DeltaPsim) and mitochondrial membrane protein were analyzed by flow cytometry.

RESULTSMA could inhibit HL-60 cells proliferation capacity in a time-and dose-effect, with a 24 h IC50 value of 8.76 microg/ml, 48 h of 7.17 microg/ml and 72 h of 7.14 microg/ml. The HL-60 cells apoptosis was confirmed by cell morphology, sub-G1 phase and Annexin-V/PI labeling in a time and dose dependent manner. The more mature HL-60 cells were a with higher positivity of NBT and expressions of CD11b than those cultured without MA. The expression of bax was increased, while bcl-2, P53, Fas were unchanged on the MA treatment. MA could increase the expression of mitochondrial membrane protein in a dose-dependent manner while the DeltaPsim was reduced.

CONCLUSIONMA can inhibit proliferation and induce differentiation and apoptosis of the HL-60 cells. The mechanism may be related with up-regulating bax, opening the mitochondrial permeability transition pore and reducing DeltaPsim.

Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Diterpenes ; pharmacology ; HL-60 Cells ; Humans

Chitosan is a natural biopolymer and is made up of D-glucosamine subunits linked by beta-(1,4) glycosidic bond. In recent years, the application of chitosan has attracted more and more attention because of its good biological function in cell biology. The properties of chitosan-based biomaterial are attributed to the physical properties and chemical composition of chitosan. The author of this paper summarized recent related studies and progresses of the influence of physical properties of chitosan on cell activity and cell mechanics property at home and abroad. The findings show that most studies mainly focused on the influence of chitosan and cell activity, while few were on cell mechanics property. The related studies of the influence of chitosan on cell will contribute to the explanation for the mechanism of the interaction between chitosan and cell, and provide the theoretical support for the further study.
Animals ; Cell Adhesion ; drug effects ; Cell Differentiation ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Chemical Phenomena ; Chitosan ; chemistry ; pharmacology ; Humans ; Tissue Engineering ; Tissue Scaffolds ; chemistry

OBJECTIVETo study the effect of emodin on the differentiation, maturation and function of human dendritic cells (DC) in vitro.

METHODSCells isolated from human peripheral blood mononuclear cells (PBMCs) were induced to dendritic cells (DC) with recombinant interleukin-4 and recombinant granulocyte-macrophage colony stimulating factor (GM-CSF). Lipopolysaccharide (LPS) and different concentrations of emodin were added respectively in the cultured cells on the 5th and the 7th to obtain mature or immature DCs. The phenotype of DCs ( HLA-DR, CD80, CD86, CD83, CD14, CD11c) and the secretion of interleukin-12 (IL-12) were analyzed by flow cytometry, and the immune-stimulating function of DCs was evaluated by co-culture of DCs and self-T-lymphocytes.

RESULTSThe expression rate of CD80 and CD83 in the emodin group were 13.4% +/- 6.6% and 9.3% +/- 2.2% respectively; which were significantly lower than those in the control group (39.3% +/- 8.6% and 30.7% +/- 5.6%), respectively (P<0.05). IL-12 secretion of DCs was lower (1700.44 +/- 1000.21 microg/L vs 4500.60 +/- 1200.6 microg/L) but IL-10 secretion was higher (350.6 +/- 150.2 microg/L vs 230.7 +/- 90.1 microg/L) in the emodin group than in the control group (P<0.05). Mixed lymphocyte culture (MLR) examination showed that emodin could significantly inhibit the stimulation of DCs on self-T-lymphocyte proliferation.

CONCLUSIONEmodin could evidently suppress the maturation and immune stimulating function of DCs during their in vitro conversion process.

Cell Differentiation ; drug effects ; Cells, Cultured ; Dendritic Cells ; cytology ; drug effects ; Emodin ; pharmacology ; Humans

OBJECTIVEThis study aimed to explore the effects of hyperoxia on the development of fetal lung by investigating the changes of morphological and cell proliferation induced by hyperoxia in cultured fetal lungs as well as the effects of dexamethasone on hyperoxia-exposed lungs.

METHODSHuman fetal lung explants at the pseudoglandular stage of development were cultured randomly either in normoxia (21% O2/5% CO2) or hyperoxia (95% O2/5% CO2) for 72 hrs. Dexamethasone was added into the feeding medium at the concentration of 10(-6)M. Harvested tissues were stained for pancytokeratin to identify epithelial cells, with Ki-67 as a marker of proliferation. The effects of lung morphometry were analyzed using computer assisted image analysis. The mean airway thickness, the proportion of the surface area occupied by airways, the mean airway surface area and the index of the epithelium proliferation were measured.

RESULTSThe lung architectures remained unchanged after 72 hrs normoxia culture, whereas hyperoxia culture resulted in significant dilation of airways and thinning of epithelium, with the surface area of airways of 6662 microm(2) vs 2728 microm(2) and the thickness of airways of 7.8 microm vs 8.1 microm (P < 0.05). Hyperoxia culture also resulted in an increase in the proportion of the surface area occupied by airways than normoxia culture (35.2% vs 23.4%; P < 0.05). The surface area of airways (3174 microm(2)) and the proportion of the surface area occupied by airways (23.9%) decreased significantly in hyperoxia-cultured lungs after dexamethasone administration (P < 0.05). The epithelium proliferation index in hyperoxia-cultured lungs (21.8%) was higher than that in normoxia-cultured lungs (5.1%) and dexamethasone-treated hyperoxia-cultured lungs (7.4%) (P < 0.05).

CONCLUSIONSThe exposure of pseudoglandular lungs to hyperoxia modulates the lung architecture to resemble saccular lungs with higher epithelium proliferation index. Dexamethasone may inhibit the effects induced by hyperoxia.

Cell Differentiation ; drug effects ; Dexamethasone ; pharmacology ; Female ; Humans ; Hyperoxia ; pathology ; Lung ; drug effects ; embryology ; pathology ; Pregnancy

In kidney, the role of cell proliferation, differentiation, apoptosis, inflammatory mediators and cytokines expression is closely related with cell signaling pathways, including tyrosine kinase pathway, transforming growth factor-beta/Smad pathway, Rho/Rho-associated coiled-coil forming protein kinase pathway, phosphoinositol pathway, cyclic nucleotide pathway, nuclear factor kappaB pathway and so on. Some Chinese herbs and their extracts, such as rhubarb and triptolide, as well as some Chinese herbal prescriptions, such as astragalus-angelica mixture and Chailing decoction, not only could ameliorate proliferation, differentiation and apoptosis of renal cell by regulating cell signaling pathways, but also could control target gene transcription, expression and its biological effects through inhibiting the phosphorylation of key signaling molecules.
Animals ; Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Humans ; Kidney ; cytology ; drug effects ; metabolism ; Signal Transduction ; drug effects