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.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -