IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells
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IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells. / Song, Ning; Xu, Yang; Paust, Hans-Joachim; Panzer, Ulf; Noriega, Maria de las Mercedes; Guo, Linlin; Renne, Thomas; Huang, Jiabin; Meng, Xianglin; Zhao, Mingyan; Thaiss, Friedrich.
In: CELL MOL LIFE SCI, Vol. 80, No. 5, 19.04.2023, p. 125.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells
AU - Song, Ning
AU - Xu, Yang
AU - Paust, Hans-Joachim
AU - Panzer, Ulf
AU - Noriega, Maria de las Mercedes
AU - Guo, Linlin
AU - Renne, Thomas
AU - Huang, Jiabin
AU - Meng, Xianglin
AU - Zhao, Mingyan
AU - Thaiss, Friedrich
PY - 2023/4/19
Y1 - 2023/4/19
N2 - Ischemia–reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI), and experimental work has revealed detailed insight into the inflammatory response in the kidney. T cells and NFκB pathway play an important role in IRI. Therefore, we examined the regulatory role and mechanisms of IkappaB kinase 1 (IKK1) in CD4+T lymphocytes in an experimental model of IRI. IRI was induced in CD4cre and CD4IKK1Δ mice. Compared to control mice, conditional deficiency of IKK1 in CD4+T lymphocyte significantly decreased serum creatinine, blood urea nitrogen (BUN) level, and renal tubular injury score. Mechanistically, lack in IKK1 in CD4+T lymphocytes reduced the ability of CD4 lymphocytes to differentiate into Th1/Th17 cells. Similar to IKK1 gene ablation, pharmacological inhibition of IKK also protected mice from IRI. Together, lymphocyte IKK1 plays a pivotal role in IRI by promoting T cells differentiation into Th1/Th17 and targeting lymphocyte IKK1 may be a novel therapeutic strategy for IRI.
AB - Ischemia–reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI), and experimental work has revealed detailed insight into the inflammatory response in the kidney. T cells and NFκB pathway play an important role in IRI. Therefore, we examined the regulatory role and mechanisms of IkappaB kinase 1 (IKK1) in CD4+T lymphocytes in an experimental model of IRI. IRI was induced in CD4cre and CD4IKK1Δ mice. Compared to control mice, conditional deficiency of IKK1 in CD4+T lymphocyte significantly decreased serum creatinine, blood urea nitrogen (BUN) level, and renal tubular injury score. Mechanistically, lack in IKK1 in CD4+T lymphocytes reduced the ability of CD4 lymphocytes to differentiate into Th1/Th17 cells. Similar to IKK1 gene ablation, pharmacological inhibition of IKK also protected mice from IRI. Together, lymphocyte IKK1 plays a pivotal role in IRI by promoting T cells differentiation into Th1/Th17 and targeting lymphocyte IKK1 may be a novel therapeutic strategy for IRI.
U2 - 10.1007/s00018-023-04763-2
DO - 10.1007/s00018-023-04763-2
M3 - SCORING: Journal article
C2 - 37074502
VL - 80
SP - 125
JO - CELL MOL LIFE SCI
JF - CELL MOL LIFE SCI
SN - 1420-682X
IS - 5
ER -