B6.Rag1 Knockout Mice Generated at the Jackson Laboratory in 2009 Show a Robust Wild-Type Hypertensive Phenotype in Response to Ang II (Angiotensin II)

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B6.Rag1 Knockout Mice Generated at the Jackson Laboratory in 2009 Show a Robust Wild-Type Hypertensive Phenotype in Response to Ang II (Angiotensin II). / Seniuk, Anika; Thiele, Jonas L; Stubbe, Andra; Oser, Philipp; Rosendahl, Alva; Bode, Marlies; Meyer-Schwesinger, Catherine; Wenzel, Ulrich O; Ehmke, Heimo.

In: HYPERTENSION, Vol. 75, No. 4, 02.2020, p. 1110-1116.

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@article{a6f147726c0b4ef1a5dfcabd1919e520,
title = "B6.Rag1 Knockout Mice Generated at the Jackson Laboratory in 2009 Show a Robust Wild-Type Hypertensive Phenotype in Response to Ang II (Angiotensin II)",
abstract = "A key finding supporting a causal role of the immune system in the pathogenesis of hypertension is the observation that RAG1 knockout mice on a C57Bl/6J background (B6.Rag1-/-), which lack functional B and T cells, develop a much milder hypertensive response to Ang II (angiotensin II) than control C57Bl/6J mice. Here, we report that we never observed any Ang II resistance of B6.Rag1-/- mice purchased directly from the Jackson Laboratory as early as 2009. B6.Rag1-/- mice displayed nearly identical blood pressure increases monitored via radiotelemetry and hypertensive end-organ damage in response to different doses of Ang II and different levels of salt intake (0.02%, 0.3%, and 3% NaCl diet). Similarly, restoration of T-cell immunity by adoptive cell transfer did not affect the blood pressure response to Ang II in B6.Rag1-/- mice. Full development of the hypertension-resistant phenotype in B6.Rag1-/- mice appears to depend on the action of yet unidentified nongenetic modifiers in addition to the absence of functional T cells.",
author = "Anika Seniuk and Thiele, {Jonas L} and Andra Stubbe and Philipp Oser and Alva Rosendahl and Marlies Bode and Catherine Meyer-Schwesinger and Wenzel, {Ulrich O} and Heimo Ehmke",
year = "2020",
month = feb,
doi = "10.1161/HYPERTENSIONAHA.119.13773",
language = "English",
volume = "75",
pages = "1110--1116",
journal = "HYPERTENSION",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

RIS

TY - JOUR

T1 - B6.Rag1 Knockout Mice Generated at the Jackson Laboratory in 2009 Show a Robust Wild-Type Hypertensive Phenotype in Response to Ang II (Angiotensin II)

AU - Seniuk, Anika

AU - Thiele, Jonas L

AU - Stubbe, Andra

AU - Oser, Philipp

AU - Rosendahl, Alva

AU - Bode, Marlies

AU - Meyer-Schwesinger, Catherine

AU - Wenzel, Ulrich O

AU - Ehmke, Heimo

PY - 2020/2

Y1 - 2020/2

N2 - A key finding supporting a causal role of the immune system in the pathogenesis of hypertension is the observation that RAG1 knockout mice on a C57Bl/6J background (B6.Rag1-/-), which lack functional B and T cells, develop a much milder hypertensive response to Ang II (angiotensin II) than control C57Bl/6J mice. Here, we report that we never observed any Ang II resistance of B6.Rag1-/- mice purchased directly from the Jackson Laboratory as early as 2009. B6.Rag1-/- mice displayed nearly identical blood pressure increases monitored via radiotelemetry and hypertensive end-organ damage in response to different doses of Ang II and different levels of salt intake (0.02%, 0.3%, and 3% NaCl diet). Similarly, restoration of T-cell immunity by adoptive cell transfer did not affect the blood pressure response to Ang II in B6.Rag1-/- mice. Full development of the hypertension-resistant phenotype in B6.Rag1-/- mice appears to depend on the action of yet unidentified nongenetic modifiers in addition to the absence of functional T cells.

AB - A key finding supporting a causal role of the immune system in the pathogenesis of hypertension is the observation that RAG1 knockout mice on a C57Bl/6J background (B6.Rag1-/-), which lack functional B and T cells, develop a much milder hypertensive response to Ang II (angiotensin II) than control C57Bl/6J mice. Here, we report that we never observed any Ang II resistance of B6.Rag1-/- mice purchased directly from the Jackson Laboratory as early as 2009. B6.Rag1-/- mice displayed nearly identical blood pressure increases monitored via radiotelemetry and hypertensive end-organ damage in response to different doses of Ang II and different levels of salt intake (0.02%, 0.3%, and 3% NaCl diet). Similarly, restoration of T-cell immunity by adoptive cell transfer did not affect the blood pressure response to Ang II in B6.Rag1-/- mice. Full development of the hypertension-resistant phenotype in B6.Rag1-/- mice appears to depend on the action of yet unidentified nongenetic modifiers in addition to the absence of functional T cells.

U2 - 10.1161/HYPERTENSIONAHA.119.13773

DO - 10.1161/HYPERTENSIONAHA.119.13773

M3 - SCORING: Journal article

C2 - 32078412

VL - 75

SP - 1110

EP - 1116

JO - HYPERTENSION

JF - HYPERTENSION

SN - 0194-911X

IS - 4

ER -