Sandbox Reserved 484: Difference between revisions

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One very crucial function of cathepsin B that I would like to emphasize on is its ability to break down the proteins that cause amyloid plaque, the root cause of Alzheimer’s systems. So, Cathepsin B has a built in protective mechanism against Alzheimer’s disease.  Cathepsin B functions by “snipping” apart proteins which are closely associated with the amyloid protein that forms the amyloid plaques. Once, Cathepsin B breaks down these amyloid plaques, it signals other enzymes to further degrade the protein.  An experiment was conducted in which a group of researchers found that cutting out the Cathepsin B gene increased the plaque deposition in mice with Alzheimers disease symptoms.  The mice showed the human form of  amyloid precursor protein (APP).  These researchers also discovered that Cathepsin B piled up within the amyloid plaques and that it acted to decrease levels in neurons.  The researchers also found that introducing a pathological form APP called APP1-42 into the neurons drastically increased cathepsin B in young and middle aged mice with human APP, but not old mice.  From this observation, the researchers concluded that the upregulation of Cathepsin B could represent a protective mechanism that fails with  aging and a failure like this could mean that it plays a role in late-onset sporadic Alzheimer’s disease.   

Another function of Cathepsin B that I would like to highlight is its function to regulate angiogenic threshold of endothelial cells.  Cathepsin B has the ability to suppress the intrinsic angiogenic switch.  When BRECS are cultured between two layers of collagen, the BRECS cane produce both proangiogenic factors (VEGF) and antioangiogenic factors (endostatin).  Cathepsin B can suppress the production of VEGF and increase the levels of endostatin.  Under these specific conditions the tube formation is low, but it can be induced by adding VEGF.  By blocking Cathepsin B activity allows for the release of endogenous control mechanism and VEGF levels increase and the endostatin levels decrease.  A diagram representation of how Cathepsin B allows for this mechanism to occur can be seen to the right.