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035 a| (OCoLC)1381679039;

096 a| QU 68;

049 a| EREE;

100 1 a| Theobald, Drew,e| author.?| UNAUTHORIZED;

245 10 a| Kinin b1 receptor mediates bidirectional interaction between neuroinflammation and oxidative stress /c| by Drew Theobald.;

264 1 a| [Greenville, N.C.] :b| [East Carolina University],c| 2023.;

300 a| 1 online resource (70 pages) :b| illustrations (some color);

336 a| textb| txt2| rdacontent;

337 a| computerb| c2| rdamedia;

338 a| online resourceb| cr2| rdacarrier;

347 a| text fileb| PDFc| 5.913 MB2| rda;

490 1 a| ECU Brody School of Medicine thesis;

538 a| System requirements: Adobe Reader.;

538 a| Mode of access: World Wide Web.;

502 b| M.S.c| East Carolina Universityd| 2023.;

500 a| Presented to the Faculty of the Department of Pharmacology and Toxicology;

500 a| Advisor: Srinivas Sriramula;

500 a| Title from PDF t.p. (viewed June 26, 2024).;

520 3 a| Hypertension is the leading risk factor for cardiovascular disease and affects nearly half the adults in the United States. It is well established that hypertension is a low-grade inflammatory condition and is associated with increased release of proinflammatory cytokines, elevated oxidative stress levels, and increased activity of the kallikrein-kinin system (KKS). The KKS is a family of vasoactive proinflammatory peptides that play a vital role in regulating blood pressure. Activation of kinin B1 receptor (B1R) results in increased inflammation and vasoconstrictive effects which can ultimately lead to hypertension. Previously, we showed that angiotensin II (Ang II) can upregulate B1R expression and can induce oxidative stress and neuroinflammation in primary neurons. However, the order at which this occurs has not yet been investigated. In this study, we aim to determine the relationships between neuroinflammation, oxidative stress, and activation of B1R in both primary hypothalamic neurons and primary hypothalamic microglia. Following stimulation with tumor necrosis factor (TNF), lipopolysaccharide (LPS), or hydrogen peroxide (H2O2), we were able to identify a significant increase in reactive oxygen species production, inflammation, and B1R expression. Furthermore, we showed that B1R blockade using a B1R specific antagonist can attenuate these effects in both neurons and microglia. Together, these data provide novel evidence that the interaction between neuroinflammation, oxidative stress, and B1R activation in the brain is bidirectional and that blocking B1R may serve as a potential therapeutic target for neuroinflammation and oxidative stress in various disease pathologies.;

504 a| Includes bibliographical references.;

650 0 a| Oxidative stress.=| ^A605862;

650 0 a| Bradykinin.=| ^A10618;

650 2 a| Receptor, Bradykinin B10| (DNLM)D043783=| ^A1470222;

650 2 a| Neuroinflammatory Diseases0| (DNLM)D000090862=| ^A1470203;

650 2 a| Oxidative Stress0| (DNLM)D018384=| ^A930446;

650 2 a| Bradykinin0| (DNLM)D001920=| ^A949236;

653 a| Hypertension;

653 a| Neurons;

653 a| Microglia;

700 1 a| Sriramula, Srinivas,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| East Carolina University.b| Department of Biomedical Science.?| UNAUTHORIZED;

830 0 a| ECU Brody School of Medicine thesis.=| ^A964744;

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/12872;

994 a| C0b| ERE;

596 a| 1 4;

998 a| 6143713;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 6143713-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 6/9/2023x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 6143713-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 6/9/2023x| ETDz| HERESOURCE;

Kinin b1 receptor mediates bidirectional interaction between neuroinflammation and oxidative stress / by Drew Theobald.

Author/creator	Theobald, Drew author.
Other author	Sriramula, Srinivas, degree supervisor.
Other author	East Carolina University. Department of Biomedical Science.
Format	Theses and dissertations
Publication	[Greenville, N.C.] : [East Carolina University], 2023.
Description	1 online resource (70 pages) : illustrations (some color)
Supplemental Content	Access via ScholarShip
Subjects	Oxidative stress. Bradykinin. Receptor, Bradykinin B1 Neuroinflammatory Diseases Oxidative Stress Bradykinin

Series	ECU Brody School of Medicine thesis ECU Brody School of Medicine thesis. ^A964744
Summary	Hypertension is the leading risk factor for cardiovascular disease and affects nearly half the adults in the United States. It is well established that hypertension is a low-grade inflammatory condition and is associated with increased release of proinflammatory cytokines, elevated oxidative stress levels, and increased activity of the kallikrein-kinin system (KKS). The KKS is a family of vasoactive proinflammatory peptides that play a vital role in regulating blood pressure. Activation of kinin B1 receptor (B1R) results in increased inflammation and vasoconstrictive effects which can ultimately lead to hypertension. Previously, we showed that angiotensin II (Ang II) can upregulate B1R expression and can induce oxidative stress and neuroinflammation in primary neurons. However, the order at which this occurs has not yet been investigated. In this study, we aim to determine the relationships between neuroinflammation, oxidative stress, and activation of B1R in both primary hypothalamic neurons and primary hypothalamic microglia. Following stimulation with tumor necrosis factor (TNF), lipopolysaccharide (LPS), or hydrogen peroxide (H2O2), we were able to identify a significant increase in reactive oxygen species production, inflammation, and B1R expression. Furthermore, we showed that B1R blockade using a B1R specific antagonist can attenuate these effects in both neurons and microglia. Together, these data provide novel evidence that the interaction between neuroinflammation, oxidative stress, and B1R activation in the brain is bidirectional and that blocking B1R may serve as a potential therapeutic target for neuroinflammation and oxidative stress in various disease pathologies.
General note	Presented to the Faculty of the Department of Pharmacology and Toxicology
General note	Advisor: Srinivas Sriramula
General note	Title from PDF t.p. (viewed June 26, 2024).
Dissertation note	M.S. East Carolina University 2023.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

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Kinin b1 receptor mediates bidirectional interaction between neuroinflammation and oxidative stress / by Drew Theobald.

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