Sandbox Reserved 484: Difference between revisions

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Another mechanism of action that Cathepsin B takes on is its function to regulate [http://en.wikipedia.org/wiki/Angiogenesis angiogenic] threshold of [http://en.wikipedia.org/wiki/Endothelium endothelial] cells. Cathepsin B has the ability to suppress the [http://en.wikipedia.org/wiki/Intrinsic_and_extrinsic_properties intrinsic] angiogenic switch. When bovine retinal endothelial cells (BREC) are cultured between two layers of collagen, the BRECS can produce both proangiogenic factors ([http://en.wikipedia.org/wiki/Vascular_endothelial_growth_factor cascular endothelial growth factor]) and antioangiogenic factors ([http://en.wikipedia.org/wiki/Endostatin 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. 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 is shown.

[[Image:Cathepsin B VEGF.gif ]]

== Medical Implications ==

Cathepsin B has been very involved in the field of medicine. It has been implicated in diseases such as invasive cancers, neurodegenerative diseases, and cardiovascular diseases. In invasive cancers, the over-expression of cathepsin B messenger Ribonucleic acid (mRNA) has been seen in many human tumours such tumors in brain, colon, prostate, and thyroid. Studies have found that the increased expression of Cathepsin B in premalignant lesions suggests that the enzyme has a significant role in the transformation of pre-malignant lesions to malignant tumours. Also, Cathepsin B has been shown to be involved in the processes of tumour growth, vascularisation, invasion, and metastasis [http://en.wikipedia.org/wiki/Metastasis metastasis]. The tumour tissue extracts can provide useful clinical information to predict disease free and survival in breast, prostate, lung, colorectal and other cancer patients. In neurodegenerative diseases, Cathepsin B can act as an inhibitor to the amyloid plaques which form in Alzheimer's disease. Inhibitors of Cathepsin B can be used as therapeutic agents to reduce the dangerous beta-amyloid plaques in Alzheimer's patients. Cathepsin B plays a major role in cardiovascular diseases such as [http://en.wikipedia.org/wiki/Restenosis], [http://en.wikipedia.org/wiki/Neointima neointima] formation,[http://en.wikipedia.org/wiki/Aneurysm aneurysm] formation, and atherosclerosis. Cathepsin B is expressed in macrophages, but it can also be expressed in smooth muscle cells and human umbilical venous endothelial cells. Research has shown that the relocation of Cathepsin B from the lysosome into the cytosol, where it may act as cleavage enzymes in [http://en.wikipedia.org/wiki/Apoptosis apoptosis], can lead to the formation of the necrotic core and can be involved in an atherosclerosis-stimulating role. Inhibition of Cathepsin B reduces lysosomal degradation of modified LDL, therefore allowing [http://en.wikipedia.org/wiki/Foam_cell foam cell] formation, which can be important as an atherosclerosis-protective role for cathepsin B. Also, Cathepsin B has been involved in the degradation [http://en.wikipedia.org/wiki/Myofibril myofibrillar proteins] in [http://en.wikipedia.org/wiki/Myocardial_infarction myocardial infarction].

Cathepsin B has been very involved in the field of medicine. It has been implicated in diseases such as invasive cancers, neurodegenerative diseases, and cardiovascular diseases. In invasive cancers, the over-expression of cathepsin B messenger Ribonucleic acid (mRNA) has been seen in many human tumours such tumors in brain, colon, prostate, and thyroid. Studies have found that the increased expression of Cathepsin B in premalignant lesions suggests that the enzyme has a significant role in the transformation of pre-malignant lesions to malignant tumours. Also, Cathepsin B has been shown to be involved in the processes of tumour growth, vascularisation, invasion, and metastasis [http://en.wikipedia.org/wiki/Metastasis metastasis]. The tumour tissue extracts can provide useful clinical information to predict disease free and survival in breast, prostate, lung, colorectal and other cancer patients. In neurodegenerative diseases, Cathepsin B can act as an inhibitor to the amyloid plaques which form in Alzheimer's disease. Inhibitors of Cathepsin B can be used as therapeutic agents to reduce the dangerous beta-amyloid plaques in Alzheimer's patients. Cathepsin B plays a major role in cardiovascular diseases such as [http://en.wikipedia.org/wiki/Restenosis restenosis], [http://en.wikipedia.org/wiki/Neointima neointima] formation,[http://en.wikipedia.org/wiki/Aneurysm aneurysm] formation, and atherosclerosis. Cathepsin B is expressed in macrophages, but it can also be expressed in smooth muscle cells and human umbilical venous endothelial cells. Research has shown that the relocation of Cathepsin B from the lysosome into the cytosol, where it may act as cleavage enzymes in [http://en.wikipedia.org/wiki/Apoptosis apoptosis], can lead to the formation of the necrotic core and can be involved in an atherosclerosis-stimulating role. Inhibition of Cathepsin B reduces lysosomal degradation of modified LDL, therefore allowing [http://en.wikipedia.org/wiki/Foam_cell foam cell] formation, which can be important as an atherosclerosis-protective role for cathepsin B. Also, Cathepsin B has been involved in the degradation [http://en.wikipedia.org/wiki/Myofibril myofibrillar proteins] in [http://en.wikipedia.org/wiki/Myocardial_infarction myocardial infarction].

== References ==

Sandbox Reserved 484: Difference between revisions

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@@ Line 26: / Line 26: @@
 Another mechanism of action that Cathepsin B takes on is its function to regulate [http://en.wikipedia.org/wiki/Angiogenesis angiogenic] threshold of [http://en.wikipedia.org/wiki/Endothelium endothelial]  cells.  Cathepsin B has the ability to suppress the [http://en.wikipedia.org/wiki/Intrinsic_and_extrinsic_properties intrinsic] angiogenic switch.  When bovine retinal endothelial cells (BREC) are cultured between two layers of collagen, the BRECS can produce both proangiogenic factors ([http://en.wikipedia.org/wiki/Vascular_endothelial_growth_factor cascular endothelial growth factor]) and antioangiogenic factors ([http://en.wikipedia.org/wiki/Endostatin 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.  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 is shown.
+[[Image:Cathepsin B VEGF.gif ]]
 == Medical Implications  ==
-Cathepsin B has been very involved in the field of medicine.  It has been implicated in diseases such as invasive cancers, neurodegenerative diseases, and cardiovascular diseases.  In invasive cancers, the over-expression of cathepsin B messenger Ribonucleic acid (mRNA) has been seen in many human tumours such tumors in brain, colon, prostate, and thyroid.  Studies have found that the increased expression of Cathepsin B in premalignant lesions suggests that the enzyme has a significant role in the transformation of pre-malignant lesions to malignant tumours.  Also, Cathepsin B has been shown to be involved in the processes of tumour growth, vascularisation, invasion, and metastasis [http://en.wikipedia.org/wiki/Metastasis metastasis].  The tumour tissue extracts can provide useful clinical information to predict disease free and survival in breast, prostate, lung, colorectal and other cancer patients.  In neurodegenerative diseases, Cathepsin B can act as an inhibitor to the amyloid plaques which form in Alzheimer's disease.  Inhibitors of Cathepsin B can be used as therapeutic agents to reduce the dangerous beta-amyloid plaques in Alzheimer's patients.  Cathepsin B plays a major role in cardiovascular diseases such as [http://en.wikipedia.org/wiki/Restenosis], [http://en.wikipedia.org/wiki/Neointima neointima] formation,[http://en.wikipedia.org/wiki/Aneurysm aneurysm] formation, and atherosclerosis. Cathepsin B is expressed in macrophages, but it can also be expressed in smooth muscle cells and human umbilical venous endothelial cells.  Research has shown that the relocation of Cathepsin B from the lysosome into the cytosol, where it may act as cleavage enzymes in [http://en.wikipedia.org/wiki/Apoptosis apoptosis], can lead to the formation of the necrotic core and can be involved in an atherosclerosis-stimulating role. Inhibition of Cathepsin B reduces lysosomal degradation of modified LDL, therefore allowing [http://en.wikipedia.org/wiki/Foam_cell foam cell] formation, which can be important as an atherosclerosis-protective role for cathepsin B.  Also, Cathepsin B has been involved in the degradation [http://en.wikipedia.org/wiki/Myofibril myofibrillar proteins] in [http://en.wikipedia.org/wiki/Myocardial_infarction myocardial infarction].
+Cathepsin B has been very involved in the field of medicine.  It has been implicated in diseases such as invasive cancers, neurodegenerative diseases, and cardiovascular diseases.  In invasive cancers, the over-expression of cathepsin B messenger Ribonucleic acid (mRNA) has been seen in many human tumours such tumors in brain, colon, prostate, and thyroid.  Studies have found that the increased expression of Cathepsin B in premalignant lesions suggests that the enzyme has a significant role in the transformation of pre-malignant lesions to malignant tumours.  Also, Cathepsin B has been shown to be involved in the processes of tumour growth, vascularisation, invasion, and metastasis [http://en.wikipedia.org/wiki/Metastasis metastasis].  The tumour tissue extracts can provide useful clinical information to predict disease free and survival in breast, prostate, lung, colorectal and other cancer patients.  In neurodegenerative diseases, Cathepsin B can act as an inhibitor to the amyloid plaques which form in Alzheimer's disease.  Inhibitors of Cathepsin B can be used as therapeutic agents to reduce the dangerous beta-amyloid plaques in Alzheimer's patients.  Cathepsin B plays a major role in cardiovascular diseases such as [http://en.wikipedia.org/wiki/Restenosis restenosis], [http://en.wikipedia.org/wiki/Neointima neointima] formation,[http://en.wikipedia.org/wiki/Aneurysm aneurysm] formation, and atherosclerosis. Cathepsin B is expressed in macrophages, but it can also be expressed in smooth muscle cells and human umbilical venous endothelial cells.  Research has shown that the relocation of Cathepsin B from the lysosome into the cytosol, where it may act as cleavage enzymes in [http://en.wikipedia.org/wiki/Apoptosis apoptosis], can lead to the formation of the necrotic core and can be involved in an atherosclerosis-stimulating role. Inhibition of Cathepsin B reduces lysosomal degradation of modified LDL, therefore allowing [http://en.wikipedia.org/wiki/Foam_cell foam cell] formation, which can be important as an atherosclerosis-protective role for cathepsin B.  Also, Cathepsin B has been involved in the degradation [http://en.wikipedia.org/wiki/Myofibril myofibrillar proteins] in [http://en.wikipedia.org/wiki/Myocardial_infarction myocardial infarction].
 == References ==