Time Course of Gene Expression Profile in Renal Ischemia and Reperfusion Injury in Mice

Junho, Carolina Victória Cruz; Panico, Karine; Nakama, Karina Kaori; Trentin-Sonoda, Mayra; Christoffolete, Marcelo A.; Beserra, Samuel Santos; Roman‐Campos, Danilo; Carneiro‐Ramos, Marcela Sorelli

doi:10.1016/j.transproceed.2020.06.029

Cited by 3 publications

(2 citation statements)

References 29 publications

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“…The gene expression analysis was performed with slight modifications as described elsewhere [56]. Total RNA was extracted from 50-100 mg of heart tissue as described above.…”

Section: Gene Chip Analysismentioning

confidence: 99%

Protein Phosphatase 2A Improves Cardiac Functional Response to Ischemia and Sepsis

Gergs

Jahn

Schulz

et al. 2022

IJMS

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Reversible protein phosphorylation is a posttranslational modification of regulatory proteins involved in cardiac signaling pathways. Here, we focus on the role of protein phosphatase 2A (PP2A) for cardiac gene expression and stress response using a transgenic mouse model with cardiac myocyte-specific overexpression of the catalytic subunit of PP2A (PP2A-TG). Gene and protein expression were assessed under basal conditions by gene chip analysis and Western blotting. Some cardiac genes related to the cell metabolism and to protein phosphorylation such as kinases and phosphatases were altered in PP2A-TG compared to wild type mice (WT). As cardiac stressors, a lipopolysaccharide (LPS)-induced sepsis in vivo and a global cardiac ischemia in vitro (stop-flow isolated perfused heart model) were examined. Whereas the basal cardiac function was reduced in PP2A-TG as studied by echocardiography or as studied in the isolated work-performing heart, the acute LPS- or ischemia-induced cardiac dysfunction deteriorated less in PP2A-TG compared to WT. From the data, we conclude that increased PP2A activity may influence the acute stress tolerance of cardiac myocytes.

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“…The gene expression analysis was performed with slight modifications as described elsewhere [56]. Total RNA was extracted from 50-100 mg of heart tissue as described above.…”

Section: Gene Chip Analysismentioning

confidence: 99%

Protein Phosphatase 2A Improves Cardiac Functional Response to Ischemia and Sepsis

Gergs

Jahn

Schulz

et al. 2022

IJMS

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“…It is often followed by an inflammatory state, redox imbalance and changes to the structure and function of renal cells, including apoptosis [9]. These features are also evident in cardiac tissue [10][11][12][13]. Previous studies from the group have already evidenced the importance of the first two weeks of renal reperfusion in the development of cardiac outcomes.…”

Section: Introductionmentioning

confidence: 99%

Unilateral Acute Renal Ischemia-Reperfusion Injury Induces Cardiac Dysfunction through Intracellular Calcium Mishandling

Junho

González‐Lafuente²,

Navarro‐García³

et al. 2022

IJMS

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Background: Acute renal failure (ARF) following renal ischemia-reperfusion (I/R) injury is considered a relevant risk factor for cardiac damage, but the underlying mechanisms, particularly those triggered at cardiomyocyte level, are unknown. Methods: We examined intracellular Ca2+ dynamics in adult ventricular cardiomyocytes isolated from C57BL/6 mice 7 or 15 days following unilateral renal I/R. Results: After 7 days of I/R, the cell contraction was significantly lower in cardiomyocytes compared to sham-treated mice. It was accompanied by a significant decrease in both systolic Ca2+ transients and sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) activity measured as Ca2+ transients decay. Moreover, the incidence of pro-arrhythmic events, measured as the number of Ca2+ sparks, waves or automatic Ca2+ transients, was greater in cardiomyocytes from mice 7 days after I/R than from sham-treated mice. Ca2+ mishandling related to systolic Ca2+ transients and contraction were recovered to sham values 15 days after I/R, but Ca2+ sparks frequency and arrhythmic events remained elevated. Conclusions: Renal I/R injury causes a cardiomyocyte Ca2+ cycle dysfunction at medium (contraction-relaxation dysfunction) and long term (Ca2+ leak), after 7 and 15 days of renal reperfusion, respectively.

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The mmu_circ_003062, hsa_circ_0075663/miR-490-3p/CACNA1H axis mediates apoptosis in renal tubular cells in association with endoplasmic reticulum stress following ischemic acute kidney injury

Zheng,

Li,

et al. 2024

International Immunopharmacology

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Time Course of Gene Expression Profile in Renal Ischemia and Reperfusion Injury in Mice

Cited by 3 publications

References 29 publications

Protein Phosphatase 2A Improves Cardiac Functional Response to Ischemia and Sepsis

Protein Phosphatase 2A Improves Cardiac Functional Response to Ischemia and Sepsis

Unilateral Acute Renal Ischemia-Reperfusion Injury Induces Cardiac Dysfunction through Intracellular Calcium Mishandling

The mmu_circ_003062, hsa_circ_0075663/miR-490-3p/CACNA1H axis mediates apoptosis in renal tubular cells in association with endoplasmic reticulum stress following ischemic acute kidney injury

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