000009690 001__ 9690
000009690 005__ 20231129124950.0
000009690 0247_ $$2DOI$$a10.6083/5425kb45p
000009690 037__ $$aETD
000009690 245__ $$aChondroitin sulfate proteoglycan sulfation patterns prevent sympathetic nerve regeneration after myocardial infarction
000009690 260__ $$bOregon Health and Science University
000009690 269__ $$a2022
000009690 336__ $$aDissertation
000009690 502__ $$bPh.D.
000009690 520__ $$aSympathetic nerves are lost in the damaged myocardium (infarct) after myocardial infarction (MI), and the relative area of denervation predicts risk of sudden cardiac arrest due to arrhythmias leading to the hypothesis that sympathetic reinnervation of the infarct could reduce arrhythmias. This dissertation also describes an attempt to use genetically encoded FRET-biosensors to understand signaling pathways downstream ofTrkA altered by CSPGs. Due to a number of technological challenges, we limited our assessment to Protein Kinase A (PKA) and Protein Kinase C (PKC) sensors in primary sympathetic neurons but we did not observe any significant responses to CSPGs.
000009690 542__ $$fIn copyright - single owner
000009690 650__ $$aHeart Failure$$019939
000009690 650__ $$aNeuronal Outgrowth$$011790
000009690 650__ $$aExtracellular Matrix$$018796
000009690 650__ $$aNerve Regeneration$$022803
000009690 650__ $$aMyocardial Infarction$$022601
000009690 691__ $$aSchool of Medicine$$041369
000009690 692__ $$aDepartment of Physiology and Pharmacology$$041442
000009690 7001_ $$aBlake, Matthew R.
000009690 8564_ $$9d5abe394-3c66-45f4-bde6-c308ecb75ec1$$s22304282$$uhttps://digitalcollections.ohsu.edu/record/9690/files/Blake.Matthew.2022.pdf
000009690 905__ $$a/rest/prod/54/25/kb/45/5425kb45p
000009690 909CO $$ooai:digitalcollections.ohsu.edu:9690$$pstudent-work
000009690 980__ $$aTheses and Dissertations