Kaitlyn E. Werner's research while affiliated with St. Joseph's Healthcare Hamilton and other places
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Publications (3)
Objective:
Our purpose was to determine if endoplasmic reticulum stress inhibition lowers blood pressure (BP) in hypertension by correcting vascular dysfunction.
Methods:
The spontaneously hypertensive rat (SHR) was used as a model of human essential hypertension with its normotensive control, the Wistar Kyoto rat. Animals were subjected to endo...
Chronic kidney disease (CKD) is a major healthcare problem with increasing prevalence in the population. CKD leads to end stage renal disease and increases the risk of cardiovascular disease. As such, it is important to study the mechanisms underlying CKD progression. To this end, an animal model was developed to allow the testing of new treatment...
Different forms of acute kidney injury (AKI) have been associated with endoplasmic reticulum (ER) stress; these include AKI caused by acetaminophen, antibiotics, cisplatin, and radiocontrast. Tunicamycin (TM) is a nucleoside antibiotic known to induce ER stress and is a commonly used inducer of AKI. 4-phenylbutyrate (4-PBA) is an FDA approved subst...
Citations
... 8 ERS inhibitors play a protective role in the vasculature by restoring ER calcium homeostasis, reducing apoptosis, correcting vascular dysfunction, and ameliorating ERS-related inflammation and fibrosis, thus improving hypertensioninduced cardiac dysfunction. [172][173][174] Additionally, ERS inhibitors can ameliorate vascular dysfunction by enhancing Beclin-1-dependent autophagy. 175 Chemical chaperones offer a means to modulate ER stress effectively, thereby alleviating atherosclerosis. ...
... Furthermore, Debelle et al. [16] applied AAI at a single dose of 10 mg kg −1 body weight, a dose regimen that in our hands resulted in acute and rapidly progressive nephropathy (data not shown) with high mortality in contrast to the more chronic type of kidney disease as elicited with repeated applications of AAI in smaller doses (3 mg kg −1 body weight) in our study. Finally, species differences between rats and mice, with rats being more susceptible to kidney disease than mice [24,32,36,42,44,49], may have contributed to the divergent results between the two studies. ...
![[object Object]](https://i1.rgstatic.net/ii/profile.image/466465204772865-1488225379753_Q64/Zahraa-Mohammed-Ali-2.jpg)
... Pretreatment with tauroursodeoxycholic acid (250 mg/kg) 30 min before I/R was shown to attenuate tubular damage in ischemic AKI and to inhibit ER stress-induced activation of apoptotic molecules, including CHOP and caspase-12 [10]. Additionally, when mice were pretreated with another chemical chaperone 4-phenylbutyrate (4-PBA) (1 g/kg/day) for 7 days, followed by 3 days of co-treatment of 4-PBA and tunicamycin (TM), an ER stress inducer, 4-PBA can inhibit TMcaused AKI [11]. Moreover, 4-PBA significantly mitigated TM-induced CHOP upregulation and protected the ultrastructure of proximal tubules against TM-induced tubular damage [11]. ...
