Open Access. Powered by Scholars. Published by Universities.®

Life Sciences Commons

Open Access. Powered by Scholars. Published by Universities.®

Physiology

Washington University in St. Louis

Theses/Dissertations

Inflammation

Articles 1 - 2 of 2

Full-Text Articles in Life Sciences

Norepinephrine Induces Macrophage Polarization Critical To Eliciting Renal Fibrogenesis, Hannah Manoj Jan 2019

Norepinephrine Induces Macrophage Polarization Critical To Eliciting Renal Fibrogenesis, Hannah Manoj

Undergraduate Research Symposium Posters

Renal denervation before ischemic injury has been shown to protect against fibrogenesis and the inflammatory response, which are two causes for the progression of chronic kidney disease. However, the administration of norepinephrine (NE) to denervated renal systems induced fibrogenesis and inflammation after ischemic injury. Our previous data indicates that NE-mediated stimulation of the α2-AR receptors is responsible for regulating several of the processes implicated in fibrogenesis and inflammation, including the accumulation, migration, and infiltration of macrophages to the site of injury; this is especially relevant as macrophages have been implicated as one potential cause for the inflammatory response.

Recent studies, …


The Role Of Membrane Excitability In Insulin Regulation, Christopher Howard Emfinger Aug 2018

The Role Of Membrane Excitability In Insulin Regulation, Christopher Howard Emfinger

Arts & Sciences Electronic Theses and Dissertations

In mammals, ATP-sensitive K+ (KATP) channels are essential regulators of insulin secretion from pancreatic islet [beta]-cells, illustrated by the finding that gain-of-function mutations in KATP channels (KATP-GOF) cause neonatal diabetes mellitus (NDM). However, variability in symptom severity and effectiveness of treatment is seen in NDM, even for those with the same mutation and in the same family. Short-term treatment of mice expressing KATP-GOF mutations in [beta]-cells (KATP-GOF mice) with the KATP blocker glibenclamide during disease onset results in two outcomes: one subset becomes severely diabetic (non-remitters), whereas the other subset remains below the glucose levels at which significant side effects …