Previous studies have indicated that regulatory T cells serve essential roles in maintaining intestinal homeostasis, however, the role of different Treg subsets in modulating inflammatory bowel disease has still not been addressed clearly. In the present study, the authors measured the percentage of Foxp3+ IL‑10+ TGF‑β+ natural Tregs, Foxp3‑ IL‑10+ TGF‑β‑ induced Tregs, CD127‑ induced Tregs and CD8+ Tregs at different time points in DSS‑induced experimental colitis model in murine lamina propria lymphocytes, mesenteric lymph node and peripheral blood. In addition, the authors compared the frequency of four Treg subsets in patients diagnosed of ulcerative colitis at different stages with enrolled healthy controls. The percentage of Foxp3+ IL‑10+ TGF‑β+ natural Tregs decreased in acute stage of both human and mice was observed, but proliferated significantly during remittent stage. Foxp3‑ IL‑10+ TGF‑β‑ inducible (i) Treg and CD127‑ iTreg was observed as being significantly decreased percentage in LPL at 4 and 7 days, the frequency of Foxp3‑ IL‑10+ TGF‑β‑ iTreg cells became decreased and CD127‑ iTreg only slightly increased at the chronic stage following DSS induction. However, the proportion of both Foxp3‑ IL‑10+ TGF‑β‑ iTreg and CD127‑ iTreg was nearly unchanged in human IBD. Although intestinal inflammation decreased the percentage of CD8+ Tregs, it remained lower in the remittent stage of human IBD. Only enhanced proliferation of lamina propria lymphocytes‑derived CD8+ Treg was reported at 7 days in dextran sodium sulfate‑induced murine colitis. The results demonstrated that Foxp3+ IL‑10+ TGF‑β+ natural Tregs may serve an essential role in exhibiting suppressive and protecting from immune‑related mucosal injury during chronic stage in inflammatory bowel disease.

Regulator of G-protein signaling 7 (RGS7) is predominately present in the nervous system and is essential for neuronal signaling involving G-proteins. Prior studies in cultured cells showed that RGS7 is regulated via proteasomal degradation, however no protein is known to facilitate proteasomal degradation of RGS7 and it has not been shown whether this regulation affects G-protein signaling in neurons. Here we used a knockout mouse model with conditional deletion of arginyltransferase (Ate1) in the nervous system and found that in retinal ON bipolar cells, where RGS7 modulates a G-protein to signal light increments, deletion of Ate1 raised the level of RGS7. Electroretinographs revealed that lack of Ate1 leads to increased light-evoked response sensitivities of ON-bipolar cells, as well as their downstream neurons. In cultured mouse embryonic fibroblasts (MEF), RGS7 was rapidly degraded via proteasome pathway and this degradation was abolished in Ate1 knockout MEF. Our results indicate that Ate1 regulates RGS7 protein level by facilitating proteasomal degradation of RGS7 and thus affects G-protein signaling in neurons.

These data demonstrate an important role for COX-2 activity in nephrogenesis in the rodent, and define a specific time period of susceptibility to these effects.

An easily self-assembled and gelated octa-peptide FHFDFHFD was chosen as a novel drug delivery system (DDS) for both tanshinone IIA and total tanshinone extract. The DDS showed increased loading capacity, sustained drug release and better anticancer capability. Our research proved that a hydrogel DDS of other traditional Chinese medicines is possible.