Schwann cells (SCs), a type of glial cell in the peripheral nervous system, can serve as a source of mesenchymal stem cells (MSCs) to repair injured pulp. This study aimed to investigate the role of SCs in tooth germ development and repair of pulp injury. We performed RNA-seq and immunofluorescent staining on tooth germs at different developmental stages. The effect of L-type calcium channel (LTCC) blocker nimodipine on SCs odontogenic differentiation was analyzed by real-time polymerase chain reaction and Alizarin Red S staining. We used the PLP1-CreERT2/ Rosa26-GFP tracing mice model to examine the role of SCs and Cav 1.2 in self-repair after pulp injury. SC-specific markers expressed in rat tooth germs at different developmental stages. Nimodipine treatment enhanced mRNA levels of osteogenic markers (DSPP, DMP1, and Runx2) but decreased calcium nodule formation. SCs-derived cells increased following pulp injury and Ca v 1.2 showed a similar response pattern as SCs. The different SCs phenotypes are coordinated in the whole process to ensure tooth development. Blocking the LTCC with nimodipine promoted SCs odontogenic differentiation. Moreover, SCs participate in the process of injured dental pulp repair as a source of MSCs, and Cav 1.2 may regulate this process.

Schwann cells (SCs), a type of glial cell in the peripheral nervous system, can serve as a source of mesenchymal stem cells (MSCs) to repair injured pulp. This study aimed to investigate the role of SCs in tooth germ development and repair of pulp injury. We performed RNA-seq and immunofluorescent staining on tooth germs at different developmental stages. The effect of L-type calcium channel (LTCC) blocker nimodipine on SCs odontogenic differentiation was analyzed by real-time polymerase chain reaction and Alizarin Red S staining. We used the PLP1-CreERT2/ Rosa26-GFP tracing mice model to examine the role of SCs and Cav 1.2 in self-repair after pulp injury. SC-specific markers expressed in rat tooth germs at different developmental stages. Nimodipine treatment enhanced mRNA levels of osteogenic markers (DSPP, DMP1, and Runx2) but decreased calcium nodule formation. SCs-derived cells increased following pulp injury and Ca v 1.2 showed a similar response pattern as SCs. The different SCs phenotypes are coordinated in the whole process to ensure tooth development. Blocking the LTCC with nimodipine promoted SCs odontogenic differentiation. Moreover, SCs participate in the process of injured dental pulp repair as a source of MSCs, and Cav 1.2 may regulate this process.

Schwann cells (SCs), a type of glial cell in the peripheral nervous system, can serve as a source of mesenchymal stem cells (MSCs) to repair injured pulp. This study aimed to investigate the role of SCs in tooth germ development and repair of pulp injury. We performed RNA-seq and immunofluorescent staining on tooth germs at different developmental stages. The effect of L-type calcium channel (LTCC) blocker nimodipine on SCs odontogenic differentiation was analyzed by real-time polymerase chain reaction and Alizarin Red S staining. We used the PLP1-CreERT2/ Rosa26-GFP tracing mice model to examine the role of SCs and Cav 1.2 in self-repair after pulp injury. SC-specific markers expressed in rat tooth germs at different developmental stages. Nimodipine treatment enhanced mRNA levels of osteogenic markers (DSPP, DMP1, and Runx2) but decreased calcium nodule formation. SCs-derived cells increased following pulp injury and Ca v 1.2 showed a similar response pattern as SCs. The different SCs phenotypes are coordinated in the whole process to ensure tooth development. Blocking the LTCC with nimodipine promoted SCs odontogenic differentiation. Moreover, SCs participate in the process of injured dental pulp repair as a source of MSCs, and Cav 1.2 may regulate this process.

Background and Objectives: Dental pulp stem cells (DPSCs) play an important role in the repair of tooth injuries. Electrogenic sodium bicarbonate cotransporter 1 (NBCe1) is a Na＋ -coupled HCO3− transporter encoded by the solute carrier 4A4 (SLC4A4) gene and plays a crucial role in maintaining the pH of DPSCs. Our previous research confirmed that NBCe1 is highly expressed in odontoblasts during the development of the tooth germ. Therefore, in this study, we aimed to investigate the effect of NBCe1 on odontogenic differentiation of DPSCs and further clarify the underlying mechanisms. Methods: and Results: DPSCs were isolated and identified, and the selective NBCe1 inhibitor S0859 was used to treat DPSCs. We used a cell counting Kit-8 assay to detect cell proliferative ability, and intracellular pH was assessed using confocal microscopy. Odontogenic differentiation of DPSCs was analyzed using real-time PCR and Alizarin Red S staining, and the NF-κB pathway was assessed using western blotting. Our results indicated that 10 μM S0859 was the optimal concentration for DPSC induction. Intracellular pH was decreased upon treatment with S0859. The mRNA expressions of DSPP, DMP1, RUNX2, OCN, and OPN were upregulated in the NBCe1 inhibited group compared to the controls. Moreover, NBCe1 inhibition significantly activated the NF-κB pathway, and a NF-κB inhibitor reduced the effect of NBCe1 on DPSC differentiation. Conclusions NBCe1 inhibition significantly promotes odontogenic differentiation of DPSCs, and this process may be regulated by activating the NF-κB signaling pathway.

Objective To establish the MCF-7 cell models of Beclin 1 over-and low-expressions,and to detect the autophagic and apoptotic changes after 4 Gy irradiation,and to explore their molecular regulation mechanisms. Methods MCF-7,MCF-7 + 4Gy,MCF-7-Beclin 1 + 4Gy and MCF-7-Belcin 1 RNAi+ 4Gy groups were set up. Molecular biology method was used to construct Beclin 1 over-expression vector pcDNA3.1-Beclin 1,and to estabilish the Beclin 1 over- and low-expression cell models.After the cells were irradiated with 4 Gy, the autopahgic cell percentages were measured by fluorescence microscope with MDC staining, the apoptotic cell percentages were measured by FCM with AnnexinⅤ-FITC and PI staining,and the expressions of Beclin1,P53, Bcl-2 and Bax proteins were measured by Western blotting method.Results Compared with MCF-7 group,the autophagic and apoptotic cell percentages in MCF-7+4 Gy,MCF-7 Beclin 1 +4 Gy and MCF-7-Beclin 1 RNAi+4 Gy groups were significantly increased (P <0.05 or P <0.001 ),especially in MCF-7 Beclin 1+4 Gy group which was significantly higher than those in MCF-7 + 4 Gy (P < 0.05);while there was significant difference in the necrotic cell percentages between various groups. After 4 Gy irradiation, compared with MCF-7 group, the expression levels of Beclin 1,P53 and Bax proteins in MCF-7 + 4 Gy and MCF-7-Beclin 1 + 4 Gy groups were increased,but the expression levels of Bcl-2 protein were decreased,especially in MCF-7-Beclin 1 + 4 Gy group. Conclusion The MCF-7 cell models of Beclin 1 over-and low-expressions are successfully established,and ionizing radiation could induce the autophagy and apoptosis of MCF-7 cells,which is more obvious in Beclin 1 over-expression MCF-7 cells.Beclin 1 can activate P53,inhibit Bcl-2 and activate Bax,which forms the regulation of autophagy and apoptosis by P53 .

Objective To explore the mechanism of radio-resistance of breast cancer stem cells by investigating the effects of ionzing radiation on the reactive oxygen species (ROS),apoptosis and cycle distribution.Methods The breast cancer MCF-7 cells were suspension cultured in serum-free medium containing a variety of growth factors. There were MCF-7 (breast cancer cells),MCF-7-S (breast cancer stem cells),MCF-7+8 Gy and MCF-7-S+8 Gy groups in the experiment. 4-24 h after 8 Gy irradiation, the ROS levels, percentages of apoptotic cells and percentages of the cells at each cycle phage were measured by FCM with 2′, 7′-dichlorodihydrofluorescin diacetate (DCFH-DA ), Annexin Ⅴ-FITC/PI and PI staining, respectively. Results The breast cancer stem cell microsphere accumulated hundreds of cells were obtained successfully at 7 d after suspension culture with serum-free medium containing a variety of growth factors;the FCM results showed that CD44+CD24- phenotype breast stem cells were up to 75.20%.With the time prolongation,the ROS levels and apoptosis in MCF-7 group and MCF-7-S group showed increasing trendency, and reached for the maximum values at 12 and 24 h;the ROS levels in MCF-7-S group were significantly lower than those in MCF-7 group at 4,8,12 and 24 h (P<0.05 or P<0.01), and the percentage of apoptotic cells in MCF-7-S group was significantly higher than that in MCF-7 group only at 8 h(P<0.05);the ROS levels (4,8,12 and 24 h)and percentage of apoptotic cells(12 h)were significantly increased in MCF-7+8 Gy group (P<0.05),and the percentages of apoptotic cells (4,8,12 and 24 h)in MCF-7-S +8 Gy group were significantly decreased (P<0.05 or P<0.01),but the ROS levels had no obvious change in MCF-7-S+8 Gy.At 12 h,as compared with MCF-7 group,the percentages of the cells at G0/G1 phase and G2/M phase in MCF-7-S group were significantly decreased (P<0.05),and the percentage of the cells at S phase was significantly increased (P<0.05 );the percentage of the cells at G2/M phase in MCF-7+8 Gy group was significantly increased (P<0.05 ), but there were no significant changes in MCF-7-S+ 8 Gy group. Conclusion Ionizing irradiation can cause the increasing of ROS level and apoptosis and G2/M phase arrest in breast cancer cells,but has no obvious effects on the breast cancer stem cells;it indicates that radio-resistance might be related to ROS level,apoptosis and G2/M phase arrest.

Objective To explore the effects of 75 mGy irradiation on the apoptosis of spermatogenic cells and antioxidant capacity of serum and testis and hormone levels in male rats with diabetes mellitus(DM).Methods Rats were injected intraperitoneally with streptozotocin(STZ)to develop diabetes.The diabetic rats were irradiated with 75 mGy X-rays every other day for 4 weeks.Their survival rate and body weight were recorded 12 weeks after development of diabetes.The apeptosis percentage of germ cells was measured with flow cytometry and TUNEL method.The changes of anti-oxidation and gonadal hormone levels in serum and testis were measured with kits.Results After the rats suffered from diabetes for 12 weeks,the survival rate in DM group was 25%(6/24),100% in normal control group(16116).The survival rate in 75 mGy + DM group(9/16,56.25%)was obviously higher than that in the DM group(X2= 4.00,P < 0.05).Meanwhile,the percentage of apaptotic spermatogenic cells in the diabetic rats was significantly larger than those in the normal control and irradiation groups(F = 5.496,P < 0.05).MDA and NO levels in serum and testis of diabetic rats were higher in varying degrees than that in the normal control,while the serum and testis MDA content in the 75 mGy + DM group were lower than those in the DM group especially in the testis(F = 10.644,P < 0.01).75 mGy X-ray irradiation decreased NO content in the diabetic rats serum significantly(F = 14.379,P < 0.05)and increased NOS activity and TS,FSH level(F = 9.676,43.194 and 5.282,respectively,P < 0.05 and P < 0.01).Conclusions LDR could decrease the MDA level and NO content,and increase the antioxidant enzyme activity and TS and FSH levels in testis and serum of diabetic rats.

Objective To study the changes of apoptosis and cell cycle progression of Hela cells after the poly(ADP-ribose) polymerase(PARP) was inhibited by its inhibitor 3-aminobenzamid(3-AB) and the mechanisms of PARP interaction with Hela cells damaged by irradiation.Methods Hela cell line was used.Flow cytometry(FCM) was used to examine the PARP expression of control and 3-AB groups at 0,2,4,8,12 h after administration with 5 mmol?L-1 3-AB.The percentage of apoptotic cells and cell cycle progression of control,irradiation,3-AB plus irradiation groups were measured with FCM at 2,8,12,24 h after exposure to 2 Gy irradiation following administration with 5 mmol?L-1 3-AB.Results The percentage of Hela cells with positive expression of PARP protein decreased after administration with 3-AB and there was significant difference between 3-AB plus irradiation group and control group(P

Diabetes is a metabolic disease caused by complicated factors, and its damage to the male reproductive system is threatening men's health. This article reviews the pathophysiological changes in the diabetes-damaged male reproductive system and the mechanism of these changes. Oxidative stress induced by hyperglycemia plays an important role in working damage to the reproductive system of diabetic males, for which some anti-oxidative substances may prove to be an effective cure.
Androgen-Binding Protein ; biosynthesis ; Animals ; Diabetes Mellitus ; pathology ; physiopathology ; Free Radicals ; Humans ; Leydig Cells ; metabolism ; Male ; Oxidative Stress ; Rats ; Sertoli Cells ; secretion ; Testis ; pathology ; Testosterone ; biosynthesis

OBJECTIVETo investigate more deeply the function and mechanism of DSPP during tooth development.

METHODSExplants of tooth germs from embryonic 17th day mice were divided into two groups. In the control experiment, explants were cultured in agarose semi-solid medium under serum-free and chemically defined conditions, while explants in the other group were cultured with 30 mumol/L, 15 bp antisense oligodeoxynucleotide targeted to DSPP mRNA. After 10 ds, the explants were examined by transmission electron microscope. The width of dentin matrix at the tip of the cusps were then measured and statistically analyzed with Student t-test.

RESULTSUltrastructure analyses showed that large cisternae of the rough endoplasmic reticulum (RER) existed in the odontoblasts at the tip of the cusps of antisense-treated explants and the average thickness of dentin matrix (2.5 microns) was thinner compared to the control ones (3 microns, P < 0.001). In addition, the collagen fibers in extracellular matrix were disorganized.

CONCLUSIONThese findings indicated that DSPP played an important role in keeping tooth normal development, as well as in dentin mineralization by maintaining odontoblasts' secreting ability and controlling fiber structure and orientation.

Animals ; Embryo, Mammalian ; Extracellular Matrix Proteins ; Mice ; Mice, Inbred BALB C ; Microscopy, Electron ; Molar ; Oligoribonucleotides, Antisense ; pharmacology ; Phosphoproteins ; Protein Precursors ; pharmacology ; Sialoglycoproteins ; Tooth Germ ; ultrastructure