[Effects of Biochar on Soil Organic Carbon of Eroded Cultivated Layer of Slope Farmland in Purple Hilly Area].

Soil organic carbon (SOC) is the largest carbon pool in the terrestrial ecosystem. It is not only the core index of cultivated land soil quality evaluation but also an important part of the global carbon cycle. In order to understand the response characteristics of SOC in the cultivated layer to the interaction of soil erosion and management measures, the eroded cultivated layer of typical purple soil slope farmland in the Three Gorges Reservoir area was the research object. The in-situ tests of five erosion degrees on sloping farmland were established using the shovel erosion simulation test method; taking no fertilizer (CK) as a control measure, two types of restorative management measures were set up, namely chemical fertilizer (F) and biochar+chemical fertilizer (BF), to clarify the differences in SOC content under different erosion degrees and management measures and to analyze the variation characteristics and interannual variation trend of SOC along the cultivated-layer profile. The results showed that:① BF significantly increased the soil organic carbon content in the cultivated layer of purple soil slope farmland; the SOC of BF was 90.25% and 23.84% higher than that of CK and F on average, respectively. Soil erosion significantly reduced the content of SOC (12.25%-27.74%) under CK measures, but there was no significant difference in the profile distribution of SOC under different erosion degrees. ② The SOC content in the surface layer (0-10 cm) of slope farmland was the highest, and the two measures had the most obvious effect on improving the SOC contents, which were 120.59% and 66.90%, respectively. ③ After three consecutive years of experiments, the SOC content in the cultivated-layer of slope farmland changed significantly. Under CK, the average annual loss of SOC was 12.52%, whereas under BF, the average annual increase in SOC content was 9.31%. ④ The correlation between SOC and soil physical and chemical properties was different in the various soil layers; the deeper the soil layer was, the weaker the correlation was. Therefore, biochar combined with chemical fertilizer (BF) was an important management measure to improve the erosive cultivated layer and enhance soil fertility for slope farmland in the purple hilly area. The results of this study can provide basic parameters for the rational regulation of cultivated layers and the improvement of soil fertility.

The orphan receptor TR3 participates in angiotensin II-induced cardiac hypertrophy by controlling mTOR signalling.

Angiotensin II (AngII) induces cardiac hypertrophy and increases the expression of TR3. To determine whether TR3 is involved in the regulation of the pathological cardiac hypertrophy induced by AngII, we established mouse and rat hypertrophy models using chronic AngII administration. Our results reveal that a deficiency of TR3 in mice or the knockdown of TR3 in the left ventricle of rats attenuated AngII-induced cardiac hypertrophy compared with the respective controls. A mechanistic analysis demonstrates that the TR3-mediated activation of mTORC1 is associated with AngII-induced cardiac hypertrophy. TR3 was shown to form a trimer with the TSC1/TSC2 complex that specifically promoted TSC2 degradation via a proteasome/ubiquitination pathway. As a result, mTORC1, but not mTORC2, was activated; this was accompanied by increased protein synthesis, enhanced production of reactive oxygen species and enlarged cell size, thereby resulting in cardiac hypertrophy. This study demonstrates that TR3 positively regulates cardiac hypertrophy by influencing the effect of AngII on the mTOR pathway. The elimination or reduction of TR3 may reduce cardiac hypertrophy; therefore, TR3 is a potential target for clinical therapy.

Orphan receptor TR3 enhances p53 transactivation and represses DNA double-strand break repair in hepatoma cells under ionizing radiation.

In response to ionizing radiation (IR)-induced DNA double-strand breaks (DSB), cells elicit an evolutionarily conserved checkpoint response that induces cell cycle arrest and either DNA repair or apoptosis, thereby maintaining genomic stability. DNA-dependent protein kinase (DNA-PK) is a central enzyme involved in DSB repair for mammalian cells that comprises a DNA-PK catalytic subunit and the Ku protein, which act as regulatory elements. DNA-PK also functions as a signaling molecule to selectively regulate p53-dependent apoptosis in response to IR. Herein, we demonstrate that the orphan nuclear receptor TR3 suppresses DSB repair by blocking Ku80 DNA-end binding activity and promoting DNA-PK-induced p53 activity in hepatoma cells. We find that TR3 interacts with Ku80 and inhibits its binding to DNA ends, which then suppresses DSB repair. Furthermore, TR3 is a phosphorylation substrate for DNA-PK and interacts with DNA-PK catalytic subunit in a Ku80-independent manner. Phosphorylated TR3, in turn, enhances DNA-PK-induced phosphorylation and p53 transcription activity, thereby enhancing IR-induced apoptosis in hepatoma cells. Together, our findings reveal novel functions for TR3, not only in DSB repair regulation but also in IR-induced hepatoma cell apoptosis, and they suggest that TR3 is a potential target for cancer radiotherapy.