To our knowledge, this is the first report showing the role played by this peptide in the regulation of global respiration for glioblastoma cells. Our results show that disrupting a microtubule network affects the mitochondrial network distribution, thus confirming the close relationship between these two networks. Pulmonary fibrosis is a progressive lung disease characterized by the irreversible formation of scar tissue throughout the lungs, which ultimately leads to respiratory failure. The etiologies of pulmonary fibrosis are diverse and in some cases the Psora 4 causes are unknown. Pulmonary fibrosis is currently irreversible, and patients only have 2�C6 years�� life expectancy after diagnosis. Much of our understanding of the molecular and cellular mechanisms governing pulmonary fibrosis is derived from in vivo mouse studies using the BIPF model, in which lung fibrosis is induced with a single administration of bleomycin. Development of BIPF involves a complex ballet between the coagulation cascade, inflammatory response, and lung tissue remodeling. Over the years a strong effort has been devoted to clarifying the immunological response during BIPF. As a result the list of leukocytes and secreted cytokines and growth factors involved in the progression of pulmonary fibrosis is extensive. However, not all of the inflammatory cells that migrate to the lungs and airways during BIPF are thought to be pathogenic. NK cells, for example have been hypothesized to dampen pulmonary fibrosis. NK cells may induce anti-fibrotic signals in liver and in lung through two independent mechanisms: 1) contact dependent interactions where NK cells can block liver fibrosis by directly killing activated liver collagen producing fibroblasts or 2) through the release of soluble anti-fibrotic mediators such as putative anti-fibrotic cytokine IFN-c. In pulmonary fibrosis, NK cells are thought to provide protection against bleomycin induced injury through the production IFN-c, which is believed to counteract the profibrotic activities of TGF-b. To decipher the contribution of NK cells to the development of pulmonary fibrosis, we opted to systemically deplete NK cell over the course of the disease using an antibody based approach. Systemic depletion of NK cells was achieved using the anti-asialo GM1 antibody, which was injected at PS 1145 dihydrochloride different times during the BIPF model, both immediately before and throughout the acute inflammatory phase or before the fibrotic phase of disease, or only during the fibrotic phase. Anti-asialo GM1 is a rabbit polyclonal antibody from that reacts with a neutral glycosphingolipid expressed on the surface of numerous hematopoietic cells including NK, NKT, CD8+T, cdT, some CD4+T cells, macrophages, eosinophils and basophils.