bfc, a novel serpent co-factor for the expression of croquemort, regulates efferocytosis in Drosophila melanogaster.

Efferocytosis is the process by which phagocytes recognize, engulf, and digest (or clear) apoptotic cells during development. Impaired efferocytosis is associated with developmental defects and autoimmune diseases. In Drosophila melanogaster, recognition of apoptotic cells requires phagocyte surface receptors, including the scavenger receptor CD36-related protein, Croquemort (Crq, encoded by crq). In fact, Crq expression is upregulated in the presence of apoptotic cells, as well as in response to excessive apoptosis. Here, we identified a novel gene bfc (booster for croquemort), which plays a role in efferocytosis, specifically the regulation of the crq expression. We found that Bfc protein interacts with the zinc finger domain of the GATA transcription factor Serpent (Srp), to enhance its direct binding to the crq promoter; thus, they function together in regulating crq expression and efferocytosis. Overall, we show that Bfc serves as a Srp co-factor to upregulate the transcription of the crq encoded receptor, and consequently boosts macrophage efferocytosis in response to excessive apoptosis. Therefore, this study clarifies how phagocytes integrate apoptotic cell signals to mediate efferocytosis.

[Enhancement of thrombolytic activities of Carthamus tinctorius processed with fermentation with a bacillus sp. C2-13].

A processing method to enhance thrombolytic effect of Carthamus tinctorius using a fermentation technology with bacillus sp. C2-13 was investigated. The fibrinolysis and anticoagulation activity of thrombolytic extracts from an optimized fermentation process was studied using a carrageenan induced mice model. The fermented extracts resulted in significantly better thrombolytic activity, suggesting that the process was promising for use in the study and preparation of nature medicines.

Role of thymic stromal cell dysfunction in the thymic involution of mammary tumor-bearing mice.

The growth of D1-DMBA-3 mammary tumors leads to a profound thymic atrophy in the hosts. In previous studies we have shown a minor increase in thymic apoptosis in tumor bearers and an early block in the maturation of double negative cells was observed in the thymuses of tumor-bearing mice. We now present evidence that in tumor bearers there is no increased apoptosis in the periphery that may enhance the migration of thymic precursors. Furthermore, using direct fluorescein labeling of thymocytes in vivo, no increased numbers of recent thymic emigrants could be detected. In addition, the thymic atrophy did not affect all thymus functions since the integrity of negative selection was preserved in tumor-bearing mice. Stromal cells derived from the thymuses from normal mice and tumor-bearers had decreased proliferation in the presence of culture supernatants from DA-3 cells, derived from the in vivo D1-DMBA-3 mammary tumors. Addition of known tumor derived factors to normal thymic stromal cells showed that, while granulocyte-macrophage colony stimulating factor and prostaglandin E2 did not cause any effects, phosphatidyl serine severely inhibited their proliferation. Importantly, we demonstrated that tumor bearers' stromal cells could not support the proliferation of thymuses from either normal or tumor-bearing mice, indicating that functional changes in the stromal cells may be involved in the abnormal thymic development occurring during mammary tumor development.