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Injured tubular epithelia-derived CCN1 promotes the mobilization of fibroblasts toward the injury sites in acute kidney injury

ABSTRACT: Injured tubular epithelia-derived CCN1 promotes the mobilization of fibroblasts toward the injury sites in acute kidney injury

PROVIDER: PRJNA1042822 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26879429.fastq.gz	Fastqsanger.gz
	SRR26879430.fastq.gz	Fastqsanger.gz
	SRR26879431.fastq.gz	Fastqsanger.gz
	SRR26879432.fastq.gz	Fastqsanger.gz
	SRR26879433.fastq.gz	Fastqsanger.gz

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Injured tubular epithelia-derived CCN1 promotes the mobilization of fibroblasts toward the injury sites in acute kidney injury

Project description:Humoral factors that prompt fibroblasts to migrate to an injury site at an appropriate time point are deemed indispensable for repair after kidney injury. We herein demonstrated the pivotal roles for of injured tubule-derived Cellular Communication Network Factor 1 (CCN1) in the mobilization of fibroblasts to the injury site after kidney injury. Based on analyses of ligand-receptor interactions in vitro and tubular epithelial-specific transcriptomics in vivo, we identified the up-regulation of CCN1 during the early phases of kidney injury. CCN1 promotes fibroblast chemotaxis through focal adhesion kinase-ERK signaling. In vivo analyses utilizing tubular-specific CCN1 knockout mice demonstrated the sparse accumulation of fibroblasts around injured sites after injury, resulting that tissue fibrosis was ameliorated in CCN1-KO mice. These results reveal an epithelial - fibroblast CCN1 signaling axis that mobilizes fibroblasts to injured tubule early after acute injury but that promotes interstitial fibrosis at late timepoints.

2025-03-03 | GSE248209 | GEO

Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

Project description:Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

| PRJNA497279 | ENA

The extent of liver injury determines hepatocyte fate toward senescence or cancer

Project description:The extent of liver injury determines hepatocyte fate toward senescence or cancer

| PRJNA423180 | ENA

Identification of a New Cell Population Constitutively Circulating in Healthy Conditions and Endowed with a Homing Ability Toward Injured Sites

Project description:Stem and progenitor cells are the critical units for tissue maintenance, regeneration, and repair. The activation of regenerative events in response to tissue injury has been correlated with mobilization of tissue-resident progenitor cells, which is functional to the wound healing process. However, until now there has been no evidence for the presence of cells with a healing capacity circulating in healthy conditions. We identified a rare cell population present in the peripheral blood of healthy mice that actively participates in tissue repair. These Circulating cells, with a Homing ability and involved in the Healing process (CH cells), were identified by an innovative flowcytometry strategy as small cells not expressing CD45 and lineage markers. Their transcriptome profile revealed that CH cells are unique and present a high expression of key pluripotency- and epiblast-associated genes. More importantly, CH-labeled cells derived from healthy Red Fluorescent Protein (RFP)-transgenic mice and systemically injected into syngeneic fractured wild-type mice migrated and engrafted in wounded tissues, ultimately differentiating into tissue-specific cells. Accordingly, the number of CH cells in the peripheral blood rapidly decreased following femoral fracture. These findings uncover the existence of constitutively circulating cells that may represent novel, accessible, and versatile effectors of therapeutic tissue regeneration. Analysis of murine circulating PlCH cells, two biological replicates

2015-12-04 | E-GEOD-64835 | biostudies-arrayexpress

G-CSF plus AMD3100 mobilization in adult patients with beta-thalassemia results in effective mobilization of CD34+ cells with primitive signatures

Project description:Successful gene therapy for Î²-thalassemia requires optimal numbers of autologous gene-transduced hematopoietic progenitors stem cells (HPSC) with high repopulating capacity and mobilization is the optimal approach for achieving this goal. We performed a clinical study to investigate safety and efficacy of G-CSF+AMD3100 mobilization in four adult with Î²-thalassemia to reach a cell dose of â¥8x106 CD34+cells/Kg and to characterize the CD34+cell populations mobilized before and after plerixafor administration. The procedure resulted well-tolerated in all patients. Three of the four patients reached the target cell dose or more in single-apheresis collections, even one patient where a significant dose reduction of G-CSF was imposed due to early hyperleukocytosis. A significant increase in the number of circulating CD34+ cells/Âµl (12.1Â± 8.2 fold), and in the frequency of the more primitive CD34+/CD133+/CD38- cells (1.7Â±0.7 fold) was unanimously observed after AMD3100 addiction. Intraindividual comparison of gene expression profile of CD34+ cells mobilized with G-CSF versus G-CSF+ AMD3100 highlighted a different expression pattern of genes involved in the processes of HSC/stroma adhesion, homing, cell motility and transcription regulation. Overall, the safety profile, the yield, and the expression of genes that potentially promote superior engraftment depict G-CSF+AMD3100 mobilized HSC as optimal graft source for Î²-thalassemia gene therapy One experiment performed on purified CD34+ PBPC of the same patient 1 after mobilization with G-CSF + Plerixafor , and after mobilization with G-CSF alone. Universal Human Reference RNA (Stratagene, La Jolla, CA), was used as reference.

2017-04-28 | E-GEOD-70219 | biostudies-arrayexpress

Organosulfur mobilization

Project description:Bacterial mobilization of organically bound sulfur in the mycorrhizosphere to improve plant sulfur supply

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Gene expression profiles of normal and injured podocytes induced by immunotoxin.

Project description:Podocyte injury is a key event for progressive renal failure. We previously established a mouse model of inducible podocyte injury (NEP25) and demonstrated relentless progression of glomerular injury toward sclerosis. To further investigate molecular events, we performed polysome analysis of intact and injured podocytes utilizing the NEP25 and RiboTag transgenic mice. We show here the expression profiling of normal podocytes and podocytes injured by immunotoxin.

2018-11-06 | GSE108629 | GEO

Identification of a New Cell Population Constitutively Circulating in Healthy Conditions and Endowed with a Homing Ability Toward Injured Sites

2015-12-04 | GSE64835 | GEO

Bmi1 mutant vs. WT dental epithelia

Project description:Transcriptional profiling of Bmi1 mutant dental epithelia including the stem cell compartment to determine which genes are upregulated in response to loss of Bmi1. Two condition experiment: dental epithelia homozygous null for Bmi1 and WT dental epithelia. 4 replicates each

2013-04-12 | E-GEOD-45999 | biostudies-arrayexpress

The extent of liver injury determines hepatocyte fate toward senescence or cancer

Project description:Induction of hepatocyte senescence is known to inhibit hepatocellular carcinoma (HCC). Until now, it has not been clear how the degree of liver injury dictates hepatocyte senescence and carcinogenesis. In this study, we investigated whether the severity of injury determines cell fate decisions between hepatocyte senescence and carcinogenesis. After testing of different degrees of liver injury, we found that hepatocyte senescence is strongly induced in the setting of severe acute liver injury. Longer-term, moderate liver injury did not result into hepatocyte senescence, but instead led to a significant incidence of HCC. In addition, carcinogenesis was significantly reduced by the induction of severe acute injury after chronic moderate liver injury. We conclude that severe acute liver injury leads to hepatocyte senescence along with a low incidence of HCC, whereas chronic moderate injury allows hepatocytes to proliferate rather than to enter into senescence, and correlates with a high incidence of HCC. This study improves our understanding in hepatocyte cell fate decisions and suggests a potential clinical strategy to induce senescence to treat HCC.

2018-12-20 | GSE108328 | GEO

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