Gun, van der, Zoë (2019) The signaling pathways and cross communication between the three gasotransmitters Nitric Oxide, Carbon Monoxide and Hydrogen Sulfide in our vascular system. Bachelor's Thesis, Life Science and Technology.
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Abstract
The endothelial cells are of high importance to the regulation of our vascular resistance. This cell type is able to produce various signaling molecules to induce either vasorelaxation, or by inhibition of the relaxation, vasoconstriction. Among these are the gasotransmitters nitric oxide, carbon monoxide and hydrogen sulfide. All of these gasses have shown to induce vasorelaxation, but next to relaxation also posttranslational modification of proteins is mediated by these gasotransmitters. In this literature research I would like to identify the signaling mechanisms of the gasotransmitters to induce vasodilatation, including the possibility of cross communication between the gasotransmitters. Additionally, since the three gasotransmitters share the ability to induce vasorelaxation, I would like to debate if one gasotransmitter is able to compensate for the loss of another. The gasotransmitters have shown to induce vasorelaxation through overlapping pathways. All via cyclic guanosine monophosphate mediated pathways and via reducing intracellular calcium availability. Additionally, nitric oxide and hydrogen sulfide mediate posttranslational protein modification which regulates the activity of their target proteins. The three gasotransmitters have shown to influence production of each other by altering enzyme activity. Next to affecting enzyme activity, hydrogen sulfide influences gene transcription of the carbon monoxide producing enzyme heme oxygenase 1. Cross communication independent of the producing enzymes is mostly via competition. Nitric oxide and carbon monoxide share cofactors and signaling targets for the induction of vasorelaxation, alowing competition for those to take place. Cross communication between nitric oxide and hydrogen sulfide is mediated via competition for the same cysteine residues to mediate posttranslational protein modification. When the nitric oxide system is dysregulated carbon monoxide reveals to compensate some vasorelaxation, a protective mechanism to keep the resistance under control. Nitric oxide signaling is dependent on the endothelial cells, whereas hydrogen sulfide mediated relaxation is able to continue if the endothelial cells are damaged. However, the compensated vasorelaxation remains to be partial, in the absence of one gasotransmitter the others are unable to regenerate full activity which would be medated by the missing gas.
| Item Type: | Thesis (Bachelor's Thesis) |
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| Supervisor name: | Deelman, L.E. |
| Degree programme: | Life Science and Technology |
| Thesis type: | Bachelor's Thesis |
| Language: | English |
| Date Deposited: | 12 Aug 2019 |
| Last Modified: | 19 Aug 2019 08:20 |
| URI: | https://fse.studenttheses.ub.rug.nl/id/eprint/20646 |
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