Date of Report (Date of earliest event reported): January 19, 2011
Registrants telephone number, including area code: (216) 431-9900
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:
o Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
Item 8.01 Other Events.
On January 19, 2011, Athersys, Inc. (the Company), with Case Western Reserve University School of Medicine (the School of Medicine), announced that a joint scientific study on spinal cord injury was published in the January issue of The Journal of Neuroscience. The study, by researchers from the Department of Neurosciences at the School of Medicine and scientists at the Company, presents data supporting the potential therapeutic benefit of the Companys MultiStem® program for spinal cord injury. Researchers observed that administration of Multipotent Adult Progenitor Cells (MAPC) following spinal cord injury in rodent models prevented the retraction of neurons, a process referred to as axonal dieback, reduced inflammation in the region of injury, and also promoted the regrowth of neurons.
According to the study, Multipotent Adult Progenitor Cells Prevent Macrophage-Mediated Axonal Dieback and Promote Regrowth after Spinal Cord Injury, demonstrates how the administration of MAPC potently affects immune cells responding to the initial injury in a number of ways. First, MAPC significantly decrease the release of a harmful protein called MMP-9 (matrix metalloproteinase-9), made by certain cells of the immune system known as macrophages, that is known to induce axonal dieback. The study also provides that MAPC induce a shift in macrophages from an M1, or classical activated pro-inflammatory state, to an M2, or alternatively activated anti-inflammatory state. In addition to these effects on macrophages, the study also states that MAPC promote sensory neurite outgrowth beyond the site of the injury, induce sprouting, and further enable axons to overcome the negative effects of macrophages as well as inhibitory molecules in their environment by increasing their intrinsic growth capacity.
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
Date: January 25, 2011
By: /s/ Laura K. Campbell