Further analysis revealed the response of FBR monocytes/ macrophages specific after binding with FG and again showed the importance of TGF-b signaling during the early FBR, as several TGF-b inducible genes were upregulated. Heme oxygenase 1 induces the alternate activation of classically activated macrophages and confirmed the progressive switch from the pro-inflammatory to anti-inflammatory effects of macrophages during the early FBR. During the FBR, primitive cells were attracted and shown to differentiate into myofibroblasts, the main cell population of mature FBR-tissue. However, it has been shown that macrophages from FBR-tissue possess myofibroblast differentiation potential, yet they are potentially confounded with fibrocytes. Fibrocytes, of myeloid origin, express hematopoietic markers such as CD34, CD45 and monocyte/macrophage markers, and are known to express ASMA, vimentin and collagen upon TGF-b stimulation. This cell population could also be mistaken for myeloid precursors of macrophages. So alternatively, these monocytes/macrophages attract macrophage precursors expressing C-fms and make them differentiate into myofibroblast, thus combining these findings with those of the Campbell et al. However, due to the different used techniques to isolate and describe the cells, it could also be possible that the cells in the different studies come from a common origin and only differ by their differentiation stage. TGF-b has been shown to induce differentiation of fibrocytes. It was remarkable that the small round cells in culture showed much stronger signals than the larger cells, possibly because these larger, more differentiated cells didn’t need signaling anymore. The survival and function of the pancreatic beta-cell is critical in the pathogenesis of all forms of diabetes mellitus. Increased beta-cell apoptosis and decreased beta-cell function are also major complicating factors in clinical islet transplantation. Thus, efforts to generate new beta-cells or increase the function and survival of beta-cells are critical. To date, significant progress has been made in understanding the control of beta-cell function and fate by focusing on specific candidate genes and pathways. Similarly, high throughput screens for novel compounds affecting beta cell function have relied on GSK1363089 single reporters typically transfected in non beta-cell lines. High throughput screening has recently been employed to direct embryonic stem cells towards a beta-cell lineage, to increase insulin expression in an alpha-cell line and to increase beta-cell survival. As a step towards the goal of increasing beta-cell function, proliferation or survival, we designed a multi-parameter, high content screening platform that enabled us to screen a library containing 1319 unique natural marine invertebrate extracts. We simultaneously examined four parameters for each compound, including insulin promoter activity, pdx1 promoter activity, nuclear morphology, and cell number. Insulin was chosen as a primary parameter because it defines the fitness and maturity of pancreatic beta-cells.