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Pulmonary endothelial cells endocytosis of HMGB1 promotes lung injury after renal ischemia-reperfusion injury

ABSTRACT: Pulmonary endothelial cells endocytosis of HMGB1 promotes lung injury after renal ischemia-reperfusion injury

PROVIDER: PRJNA1268538 | ENA |

REPOSITORIES: ENA

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	SRR33716942_1.fastq.gz	Fastqsanger.gz
	SRR33716942_2.fastq.gz	Fastqsanger.gz
	SRR33716944_1.fastq.gz	Fastqsanger.gz
	SRR33716944_2.fastq.gz	Fastqsanger.gz

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Pulmonary endothelial cells endocytosis of HMGB1 promotes lung injury after renal ischemia-reperfusion injury

Project description:Dysfunction of other organs is a significant contributor to the poor outcomes associated with acute kidney injury (AKI). HMGB1 is proposed to play a crucial role in the development of common extra-renal complications: acute lung injury (ALI). However, the mechanisms underlying these connections are not fully understood. Here, we established mice models of renal ischemia-reperfusion injury (IRI). HMGB1 was observed to be released from renal cell nucleus 1 hour after reperfusion. Based on mass spectrometry screening, clathrin was identified and the released HMGB1 entered pulmonary endothelial cells via clathrin-mediated endocytosis after binding to TLR4. Further investigations revealed that blocking HMGB1 with neutralizing antibodies or knocking down clathrin in lungs reversed pulmonary injury induced by renal IRI through inhibiting neutrophil recruitment and the formation and release of neutrophil extracellular traps (NETs) in lungs. Moreover, knocking down HMGB1 in TCMK-1 cells or clathrin in MPVECs in the co-culture systems in vitro obtained similar results. These findings demonstrate the effect of HMGB1 released from kidney in promoting ALI following renal IRI, disclose pulmonary endothelial cell endocytosis of HMGB1 mediated by clathrin as the potential mechanism, and identify neutralizing antibody to HMGB1 as a promising ALI mitigation strategy by inhibiting NETs formation in lungs.

2025-05-31 | GSE298223 | GEO

Identification of proteins interacting with cytoplasmic high-mobility group box 1 (HMGB1) during the hepatocellular response to ischemia reperfusion injury

Project description:Ischemia/reperfusion injury (IRI) occurs in liver transplantations and major resections and can lead to liver dysfunction. HMGB1 locates in nucleus of normal hepatocytes, but translocates to cytoplasm and the extracellular space during IRI. Although the functions of nuclear and extracellular HMGB1 are well explored, the role cytoplasmic HMGB1 plays in hepatic IRI is still unknown. We hypothesize cytoplasmic HMGB1 interacts with binding proteins involved in the hepatocellular response to IRI. In this study binding proteins of cytoplasmic HMGB1 during hepatic IRI were identified. Normal and warm ischemia reperfusion (WI/R) liver tissues were used for cytoplasmic protein extraction. The protein extracts were subjected to co-immunoprecipitation to enrich HMGB1-protein complexes. To identify the immunoprecipitated proteins in eluates, 2DE and subsequent MS detection were performed. Three identified proteins were verified using western blotting: betaine--homocysteine S-methyltransferase 1 (BHMT), cystathionine gamma-lyase (CTH) and ATP synthase beta subunit (ATP5B). All three identified proteins have a role in metabolic pathways and autophagy. Our results demonstrate cytoplasmic HMGB1 binds to BHMT, CTH and ATP5B during hepatic WI/R. Since both, cytoplasmic HMGB1 and binding proteins, are involved in autophagy, we speculate this protein complex may be involved in the hepatocellular response to IRI via the autophagy pathway.

2017-03-10 | PXD003538 | Pride

MicroRNA Profiling in Ischemia-Reperfusion Injury of the Gracilis Muscle in Rats

Project description:This SuperSeries is composed of the following subset Series: GSE21405: MicroRNA Profiling In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats GSE21406: Potential Target Genes of MicroRNA-21 In Ischemia-Reperfusion Injury Of The Gracilis Muscle In Rats Refer to individual Series

2010-04-22 | E-GEOD-21423 | biostudies-arrayexpress

Intralipid protects the heart in late pregnancy against ischemia/reperfusion injury

Project description:The heart of late pregnant (LP) rodents is more prone to ischemia/reperfusion (I/R) injury compared to non-pregnant rodents. We hypothesized that Intralipid (ITLD) protects the heart in LP rodents against I/R injury. We performed genome-wide expression profiling to identify the underlying mechanisms. Female LP rat hearts were subjected to ischemia followed by reperfusion with vehicle or ITLD (one bolus of 5mg/kg).

2016-02-09 | E-GEOD-77698 | biostudies-arrayexpress

small RNA-Seq of rat kidney in a model of ischemic preconditioning/ischemia-reperfusion injury

Project description:Ischemic preconditioning is effective in limiting subsequent ischemic acute kidney injury in experimental models. microRNAs are an important class of post-transcriptional regulator and show promise as biomarkers of kidney injury. An evaluation was performed of the time- and dose-dependent effects of ischemic preconditioning in a rat model of functional (bilateral) ischemia-reperfusion injury. A short, repetitive sequence of ischemic preconditioning resulted in optimal protection from subsequent ischemia-reperfusion injury. A detailed characterization of microRNA expression in ischemic preconditioning/ischemia-reperfusion injury was performed by small RNA-Seq.

2021-12-31 | E-MTAB-9896 | biostudies-arrayexpress

Exiqon miRCURY microRNA array of rat kidney in a model of ischemic preconditioning/ischemia-reperfusion injury

2021-12-31 | E-MTAB-9900 | biostudies-arrayexpress

Proteome analysis of membranes from renal ischemia-reperfusion injury mouse models.

Project description:Ischemia-reperfusion injury (IRI) is a well-known model for acute kidney injury (AKI). We applied proteomic analysis to detect membrane proteins from IRI mouse kidneys. The analysis set are composed of negative control (sham operation), samples of 4-hour after IRI, and samples of 8-hour IRI.

2021-09-30 | PXD020708 | JPOST Repository

iRhom2 regulates HMGB1 secretion to modulate inflammation and hepatocyte senescence in an in vitro model of ischemia/reperfusion injury

Project description:Background and Aims: Ischemia/reperfusion injury (IRI), considered one of the most important causes of liver organ rejection in acute and chronic phases, generates an inflammatory environment leading to compromised allograft functionality and rejection. In the last ten years, iRhom2 emerged as an essential regulator of tumor necrosis factor (TNFα) release by controlling the activity of TNFα converting enzyme (TACE), thus implying its involvement in several inflammatory diseases. Our goal was to investigate iRhom2 function in IRI since no data have been described yet on its potential role in the insurgence of the injury. Methods: We analyzed iRhom2 expression in a cohort of 48 patients undergoing liver transplants (OT). We then study iRhom2 function via siRNA and CRISPR/Cas9 technology in macrophages subjected to in vitro IRI model. We used proteomics and cell biology assays to determine iRhom2 function during in vitro IRI. Finally, we used a novel in vitro IRI protocol to study the effects of iRhom2-ablated macrophages co-culture with hepatocytes. Results: We demonstrated that iRhom2 is involved in liver IRI progression in transplanted patients, and its downregulation modulates the secretion of pro-inflammatory cytokines, including HMGB1, in M1-like primary macrophages. Our findings showed that HMGB1 is secreted in an iRhom2-dependent manner and in a TACE-independent fashion, thus inducing IRI-associated senescence phenotype on injured hepatocytes. Conclusions: Our results show that HMGB1 iRhom2-dependent secretion is required to induce IRI-associated senescence phenotype on IRI-cultured hepatocytes. Thus, iRhom2 inhibition during IRI might represent a promising target to improve recovery from the damage and may prevent the development of late-onset allograft rejection by tackling the damage from two different aspects: TNF-dependent inflammation and HMGB1-dependent hepatocyte senescence.

2025-07-21 | PXD046469 | Pride

Mouse kidney ischemia-reperfusion injury time course

Project description:Time course experiments involving bilateral renal ischemia reperfusion injury (IRI) in C57BL/6J mice (0 hr control, 20 min bilateral ischemia without reperfusion, 4, 16, 24, 36, 48, and 72 hrs post IRI). This dataset also includes IRI at 48 hrs and 72 hrs in Azin1 A-to-I locked and Azin1 A-to-I uneditable mice.

2024-09-30 | GSE267650 | GEO

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