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PGE2 Signaling Triggers PECAM-Independent Transendothelial Migration In Vitro and In Vivo
PGE2 Signaling Triggers PECAM-Independent Transendothelial Migration In Vitro and In Vivo
Detailed Information
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202103515
- ISBN
- 9798315797739
- DDC
- 616.07
- 서명/저자
- PGE2 Signaling Triggers PECAM-Independent Transendothelial Migration In Vitro and In Vivo
- 발행사항
- [Sl] : Northwestern University, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 137 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 86-12, Section: B.
- 주기사항
- Advisor: Muller, William A.;Green, Kathleen J.
- 학위논문주기
- Thesis (Ph.D.)--Northwestern University, 2025.
- 초록/해제
- 요약Genetic deletion or antibody blockade of platelet endothelial cell adhesion molecule-1 (PECAM, CD31) inhibits transendothelial migration (TEM) of leukocytes in all mouse strains studied except C57BL/6. Previously, we showed that this phenotype maps to a single 35.8 Mb locus on mouse chromosome 2, that contains the genes Ptgs1, Ptges, and Ptges2, which encode key enzymes involved in the Prostaglandin E2 (PGE2) synthesis pathway. PGE2 is a pro-inflammatory lipid mediator that binds four E prostanoid receptors (EP1-4). We hypothesized that PGE2 signaling supports TEM via a PECAM-independent mechanism. In vitro TEM assays demonstrate that PGE2 or 16,16-dimethyl PGE2 can restore transmigration of polymorphonuclear leukocytes (PMNs) and peripheral blood mononuclear cells (PBMCs) despite a TEM blockade with anti-PECAM antibody. This pro-transmigratory effect could be blocked with a combination of EP1 and EP3 antagonists, SC-51089 and DG-041, or with transient receptor potential canonical 6 (TRPC6) antagonist, BI-749327. 17-phenyl trinor PGE2, an agonist of EP1 and EP3, also restored transmigration of PMNs blocked with anti-PECAM antibody. In vivo, PGE2 overcame an anti-PECAM blockade when administered to FVB/n mice in thioglycolate peritonitis or croton oil dermatitis models, whereas blocking EP1 with SC-51089 decreased TEM in C57BL/6 PECAM-/- mice. Our findings demonstrate that PGE2 induces of PECAM-independent TEM, and pinpoint EP1 and EP3 as the receptors that relay said signal.
- 일반주제명
- Pathology
- 일반주제명
- Immunology
- 일반주제명
- Cellular biology
- 일반주제명
- Genetics
- 키워드
- Genetic deletion
- 키워드
- TRPC6 antagonist
- 키워드
- EP3 antagonists
- 기타저자
- Northwestern University Driskill Graduate Training Program in Life Sciences
- 기본자료저록
- Dissertations Abstracts International. 86-12B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■00520260202103515
■006m o d
■007cr#unu||||||||
■020 ▼a9798315797739
■035 ▼a(MiAaPQ)AAI32038002
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a616.07
■1001 ▼aHayashi, Vanessa Sayuri.▼0(orcid)0000-0001-6968-1463
■24510▼aPGE2 Signaling Triggers PECAM-Independent Transendothelial Migration In Vitro and In Vivo
■260 ▼a[Sl]▼bNorthwestern University▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a137 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 86-12, Section: B.
■500 ▼aAdvisor: Muller, William A.;Green, Kathleen J.
■5021 ▼aThesis (Ph.D.)--Northwestern University, 2025.
■520 ▼aGenetic deletion or antibody blockade of platelet endothelial cell adhesion molecule-1 (PECAM, CD31) inhibits transendothelial migration (TEM) of leukocytes in all mouse strains studied except C57BL/6. Previously, we showed that this phenotype maps to a single 35.8 Mb locus on mouse chromosome 2, that contains the genes Ptgs1, Ptges, and Ptges2, which encode key enzymes involved in the Prostaglandin E2 (PGE2) synthesis pathway. PGE2 is a pro-inflammatory lipid mediator that binds four E prostanoid receptors (EP1-4). We hypothesized that PGE2 signaling supports TEM via a PECAM-independent mechanism. In vitro TEM assays demonstrate that PGE2 or 16,16-dimethyl PGE2 can restore transmigration of polymorphonuclear leukocytes (PMNs) and peripheral blood mononuclear cells (PBMCs) despite a TEM blockade with anti-PECAM antibody. This pro-transmigratory effect could be blocked with a combination of EP1 and EP3 antagonists, SC-51089 and DG-041, or with transient receptor potential canonical 6 (TRPC6) antagonist, BI-749327. 17-phenyl trinor PGE2, an agonist of EP1 and EP3, also restored transmigration of PMNs blocked with anti-PECAM antibody. In vivo, PGE2 overcame an anti-PECAM blockade when administered to FVB/n mice in thioglycolate peritonitis or croton oil dermatitis models, whereas blocking EP1 with SC-51089 decreased TEM in C57BL/6 PECAM-/- mice. Our findings demonstrate that PGE2 induces of PECAM-independent TEM, and pinpoint EP1 and EP3 as the receptors that relay said signal.
■590 ▼aSchool code: 0163.
■650 4▼aPathology
■650 4▼aImmunology
■650 4▼aCellular biology
■650 4▼aGenetics
■653 ▼aGenetic deletion
■653 ▼aTransendothelial migration
■653 ▼aPECAM-independent mechanism
■653 ▼aTRPC6 antagonist
■653 ▼aEP3 antagonists
■690 ▼a0571
■690 ▼a0982
■690 ▼a0379
■690 ▼a0369
■71020▼aNorthwestern University▼bDriskill Graduate Training Program in Life Sciences.
■7730 ▼tDissertations Abstracts International▼g86-12B.
■790 ▼a0163
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17357457▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
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