Sandbox Reserved 508: Difference between revisions
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Heart diseases are the leading cause of death for Americans today. Mitochondria play a crucial role in recovery following ischemia (blood flow restriction) and reperfusion (blood flow return) injury, when a surge of reactive oxygen species (radicals) originating from the mitochondrial electron transport chain causes damage to proteins, lipids and DNA. Uncoupling protein 2 (UCP2), an inner mitochondrial membrane transport protein, is speculated to participate in this protection. The presumed function of UCP2 is carrying protons (H+) into the mitochondrial matrix along a concentration gradient generated by the electron transport chain. Normally, this proton (H+) gradient is used by ATP synthase to phosphorylate ADP to ATP. Under certain conditions, protons (H+) may preferentially be transported through UCP2, creating a detour past ATP synthase (“uncoupling”). Such uncoupling reduces damaging reactive oxygen species whose presence may actually activate UCP2 by residue modification. There are two proposed mechanisms for the transport of protons (H+) into the matrix. One is the direct transport of protons (H+) through UCP2. Alternatively, a fatty acid anion is transported out of the matrix through UCP2, while the protonated fatty acid permeates through the membrane into the matrix. UCP2 must be tightly regulated so it is only active when required, enabling the mitochondria to produce ATP. Understanding transport mechanism and regulation of UCP2 could lead to effective prevention of tissue injury due to heart attack. The Brookfield Central High School SMART Team created a physical model of UCP2 using 3-D modeling printing technology in order to better understand the structure-function relationship of UCP2. | Heart diseases are the leading cause of death for Americans today. Mitochondria play a crucial role in recovery following ischemia (blood flow restriction) and reperfusion (blood flow return) injury, when a surge of reactive oxygen species (radicals) originating from the mitochondrial electron transport chain causes damage to proteins, lipids and DNA. Uncoupling protein 2 (UCP2), an inner mitochondrial membrane transport protein, is speculated to participate in this protection. The presumed function of UCP2 is carrying protons (H+) into the mitochondrial matrix along a concentration gradient generated by the electron transport chain. Normally, this proton (H+) gradient is used by ATP synthase to phosphorylate ADP to ATP. Under certain conditions, protons (H+) may preferentially be transported through UCP2, creating a detour past ATP synthase (“uncoupling”). Such uncoupling reduces damaging reactive oxygen species whose presence may actually activate UCP2 by residue modification. There are two proposed mechanisms for the transport of protons (H+) into the matrix. One is the direct transport of protons (H+) through UCP2. Alternatively, a fatty acid anion is transported out of the matrix through UCP2, while the protonated fatty acid permeates through the membrane into the matrix. UCP2 must be tightly regulated so it is only active when required, enabling the mitochondria to produce ATP. Understanding transport mechanism and regulation of UCP2 could lead to effective prevention of tissue injury due to heart attack. The Brookfield Central High School SMART Team created a physical model of UCP2 using 3-D modeling printing technology in order to better understand the structure-function relationship of UCP2. | ||
[[Image:BCSMART_11-12_Figure_1.JPG|left|375px|thumb|FIGURE 1: Movement of Protons (H+) Across Inner Mitochondrial Membrane | [[Image:BCSMART_11-12_Figure_1.JPG|left|375px|thumb|'''FIGURE 1: Movement of Protons (H+) Across Inner Mitochondrial Membrane'''<br> | ||
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1. The electron transport chain pumps protons (H+) into the inter membrane space. | 1. The electron transport chain pumps protons (H+) into the inter membrane space. | ||
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of ADP to ATP. | of ADP to ATP. | ||
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[[Image:BCSMART_11-12_Figure_2.JPG|right|375px|thumb|FIGURE 2: ROS Production | [[Image:BCSMART_11-12_Figure_2.JPG|right|375px|thumb|'''FIGURE 2: ROS Production''' | ||
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1. During reperfusion (return of blood flow), the electron transport chain sends more protons (H+) into the inter membrane space, producing a high concentration. | 1. During reperfusion (return of blood flow), the electron transport chain sends more protons (H+) into the inter membrane space, producing a high concentration. | ||
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that carry a negative charge (O2 | that carry a negative charge (O2 | ||
-)]] | -)]] | ||
[[Image:BCSMART_11-12_Figure_3.JPG|left|375px|thumb|FIGURE 3: UCP2 Relieving the High Concentration Gradient | [[Image:BCSMART_11-12_Figure_3.JPG|left|375px|thumb|'''FIGURE 3: UCP2 Relieving the High Concentration Gradient''' | ||
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One way the mitochondria can alleviate the proton buildup in the inter membrane space is to transport the protons (H+) back into the matrix. One possible protein involved in this transportation is uncoupling protein 2 (UCP2). | One way the mitochondria can alleviate the proton buildup in the inter membrane space is to transport the protons (H+) back into the matrix. One possible protein involved in this transportation is uncoupling protein 2 (UCP2). | ||
1.UCP2 brings protons (H+) into the matrix, relieving the high concentration gradient. | 1.UCP2 brings protons (H+) into the matrix, relieving the high concentration gradient. | ||
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2.The “back up” of electrons and radical production is reduced, minimizing damage to cardiomyocytes. | 2.The “back up” of electrons and radical production is reduced, minimizing damage to cardiomyocytes. | ||
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