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RNA-seq results in the kidney of male tubule-specific Apela knockout mice treated with renal I/R injury

ABSTRACT: RNA-seq results in the kidney of male tubule-specific Apela knockout mice treated with renal I/R injury

PROVIDER: PRJNA880350 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21554811_1.fastq.gz	Fastqsanger.gz
	SRR21554811_2.fastq.gz	Fastqsanger.gz
	SRR21554812_1.fastq.gz	Fastqsanger.gz
	SRR21554812_2.fastq.gz	Fastqsanger.gz
	SRR21554813_1.fastq.gz	Fastqsanger.gz

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RNA-seq results in the kidney of male tubule-specific Apela knockout mice treated with renal I/R injury

Project description:To understand key pathways and regulatory genes in male tubule-specific Apela knockout mice treated with renal I/R injury

2023-09-08 | GSE213299 | GEO

Injured tubule-derived CCN1 exacerbates renal congestion-mediated acute kidney injury and fibrosis

Project description:Epidemiological studies showed that patients with heart failure frequently develop kidney dysfunction, called cardio-renal syndrome (CRS). Elevated central venous pressure rather than low cardiac output strongly correlates with worsening renal function, and is being increasingly recognized as the pathophysiology responsible for CRS. However, due to the lack of appropriate animal models, the molecular mechanisms underlying the congestion-mediated acceleration of kidney injury, called renal congestion, remain unclear. In the present study, using a novel mouse renal congestion model, we detected injured tubule-specific cell-cell interactions in congestive kidneys and showed that Cellular Communication Network Factor 1 (CCN1) played an important role in this process. Transcriptomics of kidneys with ischemia-reperfusion injury (IRI) and renal congestion revealed the up-regulation of paracrine chemokine-related pathways. The up-regulation of CCN1 was observed in the acute phase after kidney injury with renal congestion. Positive staining for phosphorylated focal adhesion kinase (pFAK), a downstream signaling molecule of CCN1, was noted in fibroblasts at injury sites in congestion-IRI kidneys. CCN1 activated the phosphorylation of FAK and ERK in vitro, which accelerated the migration of fibroblasts and macrophages. We then examined the effects of CCN1 deletion in tubular epithelia on congestion-mediated kidney injury in vivo. pFAK expression in injury sites was down-regulated in CCN1-KO mice, and the congestion-mediated worsening of tissue fibrosis was significantly ameliorated. In conclusion, we herein demonstrated the important role of injured tubule-derived CCN1 on pFAK-mediated fibroblast migration in congestive kidneys. The inhibition of CCN1 has potential as a therapeutic candidate for preventing the transition of renal congestion-mediated kidney injury to fibrosis.

2025-07-09 | GSE283859 | GEO

Ptprz Signaling, Tubule and Macrophage-Mediated Renal Injury and Subsequent Chronic Kidney Disease [TECs]

Project description:Background: Macrophages and tubular epithelial cell interactions are integral in kidney ischemia-incited interstitial inflammation leading to acute kidney injury (AKI). Ischemia/reperfusion injury (I/R) triggers tubular epithelial cells to express IL-34, a macrophage growth factor, that promotes AKI and subsequent CKD. IL-34 engages the cognate receptor, c-FMS, expressed by macrophages, and the recently discovered Protein-Tyrosine Phosphatase Z (Ptprz). Ptprz, binds to multiple ligands other than IL-34 that progressively increase their expression in kidneys after I/R. Methods: We tested the hypothesis that signaling through Ptprz promotes macrophage-mediated AKI and subsequent CKD, by comparing Ptprz knockout (KO) with wild-type (WT) mice after I/R. Results: Ptprz was expressed by leukocytes and in tubular epithelial cells after I/R in mice. Using Ptprz KO mice we determined that during AKI and CKD renal pathology, and loss of renal function were ameliorated. Ptprz-dependent mechanisms mediated: (i) tubular epithelial cell expression of chemokines that fostered macrophage and T cell rich renal inflammation, and (ii) tubule injury and apoptosis, that resulted in the loss of tubules and interstitial fibrosis during CKD. As macrophages release mediators that induce tubular epithelial cell apoptosis, thus Ptprz-dependent mechanisms promote tubule damage. These findings are translational, as after I/R in human kidney transplants, PTPRZ and PTPRZ ligands were upregulated and expressed by the same cell populations as in mice. Moreover, PTPRZ levels in sera were elevated in kidney transplant patients. Conclusion: Intra-renal Ptprz-dependent macrophage and tubular epithelial cell mediated mechanisms promote AKI and subsequent CKD.

2025-07-02 | GSE284134 | GEO

Ptprz Signaling, Tubule and Macrophage-Mediated Renal Injury and Subsequent Chronic Kidney Disease [macrophages]

2025-07-02 | GSE284133 | GEO

RNA-seq profiling of microdissected rat renal tubule segments

Project description:We sequenced mRNAs from glomeruli and 14 different rat renal tubule segments collected by hand microdissection. Collagenase-digested rat renal tubule segments were collected by hand microdissection. Poly(A)-mRNAs were captured from cell lysate and sequenced using paired-end protocol.

2015-03-31 | E-GEOD-56743 | biostudies-arrayexpress

Dysfunction of the circadian clock in the renal tubule leads to enhanced renal gluconeogenesis and exacerbated hyperglycemia in diabetes

Project description:In diabetes, the kidney contributes to the development of diabetic hyperglycemia by increasing glucose reabsorption from the primary urine and by upregulating gluconeogenesis in the proximal tubule. However, these two processes are also controlled by the circadian clock, a mechanism that synchronizes a large number of specific renal functions with environmental daily cycles. Here, we investigated the (patho)physiological role of intrinsic renal tubule circadian clocks in the diabetic kidney. We demonstrate that diabetic mice devoid of the circadian transcriptional regulator BMAL1 in the renal tubule exhibit additional enhancement of renal gluconeogenesis, exacerbated hyperglycemia, increased glucosuria, polyuria and renal hypertrophy. Collectively, our results suggest that diabetic hyperglycemia can be worsened by dysfunction or misalignment of intrinsic renal circadian clocks.

2022-05-27 | GSE178319 | GEO

Histone tail modification profiles of human renal tubule epithelial cells

Project description:To annotate the regulatory elements in the renal tubule epithelial cells, we profiled 6 histone ChIP-seq in the human kidney epithelical cells (HKC8). We pulled down the DNA with specific antibodies of interests against histone tail modifications in the human rebal tubule epithelial cells. The result can be interpretated with ChromHMM for different states.

2013-08-09 | E-GEOD-49637 | biostudies-arrayexpress

Transcription profiling of adult drosophila renal tubule vs whole fly

Project description:The experiment was designed to identify genes abundant or enriched in adult Drosophila melanogaster Malpighian (renal) tubule as compared to the whole fly.

2004-06-23 | E-MEXP-127 | biostudies-arrayexpress

RNA-seq profiling of microdissected rat renal tubule segments

Project description:We sequenced mRNAs from glomeruli and 14 different rat renal tubule segments collected by hand microdissection.

2015-03-31 | GSE56743 | GEO

Ptprz Signaling, Tubule and Macrophage-Mediated Renal Injury and Subsequent Chronic Kidney Disease

Project description:Ptprz Signaling, Tubule and Macrophage-Mediated Renal Injury and Subsequent Chronic Kidney Disease

| PRJNA1197408 | ENA