Effect of Notch ligand Delta-1 on the differentiation and maturation of erythroid progenitors in humans / 中华血液学杂志

<p><b>OBJECTIVE</b>To explore the biological effect of Notch ligand Delta-1 (Notch L delta-1) on the sIL-6R during the differentiation of erythroid hematopoiesis.</p><p><b>METHODS</b>Mononuclear cells (MNCs) was isolated from the normal cord blood using Ficoll graduation solution. MNCs were enriched for CD34(+) CD38(-) cells by CD34 immunomagnetic beads and a FACS Vantage. CD34(+) CD38(-) cells was cultured for 7 days in the presence of SCF, Flt3L, TPO and IL-3 (4GFs). The cultured cells was detected for the expression of IL-6R and GPA. The subsequently enriched CD36(+) erythroid progenitors were sorted for cells with IL-6R(+) and IL-6R(-) using FACS Vantage. The CD36(+) GPA(-) IL-6R(-) cells were respectively cultured in the 4GFs, 4GFs + IL-6 or 4GFs + FP6 containing medium in the presence or absence of Notch L delta-1 for 14 days and CD36(+) GPA high red cells were counted.</p><p><b>RESULTS</b>IL-6R cells accounted for 95% of CD36(+) GPA(+) cells. The CD36(+) GPA(-) cells was clearly divided into IL-6R(+) (46%) and IL-6R(-) (54%) subpopulations, the IL-6R(+) cell subpopulation formed only a few GM colonies (2.1 +/- 1.8) and a greater number of BFU-E colonies were generated from the IL-6R(-) subpopulation (58.2 +/- 18.1) (P < 0.05). The number of CD36(+) GPA high cell was (1.400 +/- 0.180) x 10(6) in the presence of FP6, lower than that [(2.460 +/- 0.190) x 10(6)] in the presence of FP6 + Notch L delta-1 (P < 0.05).</p><p><b>CONCLUSION</b>Notch L delta-1 enhances the sIL-6R-mediated effects of IL-6 on the generation of erythroid cells.</p>

Effects of blood serum from rats with combined radiation-thermal injury on the bone marrow hematopoietic progenitor cells growth / 中国实验血液学杂志

To observe the effects of blood serum from rats with radiation injury, thermal injury and combined radiation-thermal lesions on growth of hematopoietic progenitor cells and the change of their serum cytokine levels, total body irradiation of rats was performed with 12 Gy gamma ray from a (60)Co source, and 30% total body surface area III degree thermal lesion on the back was inflicted with a 5 kW bromotungsten lamp. The blood serum from these animals was collected at 3, 12, 24, 48, 72 and 96 hours after injury. Then the blood serum was added to the culture medium of erythrocyte progenitor cells (CFU-E, BFU-E) or granulocyte-macrophage progenitor cells (CFU-GM) at final concentration of 10 microg/ml. The results showed that the colony number of CFU-E, BFU-E and CFU-GM formed after addition of the blood serum from rats with thermal or combined radiation-thermal injury was significantly higher than that from normal rats at 3, 12, 24, 48, 72 and 96 hours after injury and reached its peak value at 24 hours after injury (342.8, 261.6 and 228.4% respectively from burned rats, 252.4, 205.1 and 174.2% respectively from rats with combined radiation-thermal injury as compared with that of normal rats). However, a few CFU-E, BFU-E or CFU-GM formation was found after addition of the blood serum from irradiated rats. At the same time, the level of TNF alpha and IL-6 in serum of burn group and combined radiation-thermal injury group was markedly higher than that of normal group, even more higher than that of irradiation injury group (P < 0.01). It is concluded that the blood serum from rats with thermal lesion or combined radiation-thermal injury improves the growth of erythrocyte and granulocyte progenitor cells. On the contrary, the blood serum from the irradiated rats shows the inhibiting effects, definitely related to their serum cytokines changes.

Changes of glucocorticoid receptor in hepatic cytoplasm in scalded rats and its regulation by α-MSH and KPV peptide / 第三军医大学学报

Objective　To observe the changes of glucocorticoi d receptor (GR) in hepatic cytoplasm in rats after scalding-induced pathologic al stress and its regulation. Methods　The receptor binding capa city (R0) and the apparent dissociation constant (Kd) of GR in hepatic cytopla sm of normal, low-degree and heavy-degree scalded rats were measured with rad io-ligand binding assay, with ［3H］ dexamethasone as ligand. The changes of R0 and Kd of GR were regulated by injections of anti-rat TNFα, IL-1β a ntibodies, α-melanocyte-stimulating hormone (α-MSH), and KPV peptide( Ac- D-Lys-L-Pro-D-Val) respectively in vivo. Results　The R 0 of GR in hepatic cytoplasm in rats 12 h after heavy-degree scalding ［Mass action robust: （205.52±30.14） fmol/mg; Scatchard: （208.45±30.78） fmol/mg ］were significantly lower than that of control group ［Mass action robust:（307 .86±24.22） fmol/mg;Scatchard:（306.71±27.96） fmol/mg］(P<0.01), but no s ignificant difference was found in the R0 of GR between the control and the ra ts 12 h after low-degree scalding ［Mass action robust: （285.19±16.62） fmol/ mg ; Scatchard: （296.64±16.06） fmol/mg］. The injection of anti-rat TNFα, IL-1β antibodies, α-MSH and KVP all prevented the decline of R0 of GR in h epatic cytoplasm in rats with severe scalding. Conclusion　The injections of anti-rat TNFα, IL-1β antibodies, α-MSH or KPV can attenuate the reduction of GR in rat hepatic cytoplasm caused by severe scalding-induced pathological stress to some extent.

Changes of glucocorticoid receptor in hepatic cytoplasm in scalded rats and its regulation by α-MSH and KPV peptide / 第三军医大学学报

Objective　To observe the changes of glucocorticoi d receptor (GR) in hepatic cytoplasm in rats after scalding-induced pathologic al stress and its regulation. Methods　The receptor binding capa city (R0) and the apparent dissociation constant (Kd) of GR in hepatic cytopla sm of normal, low-degree and heavy-degree scalded rats were measured with rad io-ligand binding assay, with ［3H］ dexamethasone as ligand. The changes of R0 and Kd of GR were regulated by injections of anti-rat TNFα, IL-1β a ntibodies, α-melanocyte-stimulating hormone (α-MSH), and KPV peptide( Ac- D-Lys-L-Pro-D-Val) respectively in vivo. Results　The R 0 of GR in hepatic cytoplasm in rats 12 h after heavy-degree scalding ［Mass action robust: （205.52±30.14） fmol/mg; Scatchard: （208.45±30.78） fmol/mg ］were significantly lower than that of control group ［Mass action robust:（307 .86±24.22） fmol/mg;Scatchard:（306.71±27.96） fmol/mg］(P<0.01), but no s ignificant difference was found in the R0 of GR between the control and the ra ts 12 h after low-degree scalding ［Mass action robust: （285.19±16.62） fmol/ mg ; Scatchard: （296.64±16.06） fmol/mg］. The injection of anti-rat TNFα, IL-1β antibodies, α-MSH and KVP all prevented the decline of R0 of GR in h epatic cytoplasm in rats with severe scalding. Conclusion　The injections of anti-rat TNFα, IL-1β antibodies, α-MSH or KPV can attenuate the reduction of GR in rat hepatic cytoplasm caused by severe scalding-induced pathological stress to some extent.