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Lin28A Overexpression Triggers Inflammatory Response in Mouse Kidneys

ABSTRACT: Lin28A Overexpression Triggers Inflammatory Response in Mouse Kidneys

PROVIDER: PRJNA1071984 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27829866.fastq.gz	Fastqsanger.gz
	SRR27829867.fastq.gz	Fastqsanger.gz
	SRR27829868.fastq.gz	Fastqsanger.gz
	SRR27829869.fastq.gz	Fastqsanger.gz
	SRR27829870.fastq.gz	Fastqsanger.gz

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Lin28A Overexpression Triggers Inflammatory Response in Mouse Kidneys

Project description:The RNA-binding proteins Lin28A and Lin28B play critical roles in regulating gene expression through distinct mechanisms, including the inhibition of Let-7 microRNA maturation and direct mRNA binding. Predominantly expressed in pluripotent and multipotent stem cells, Lin28A and Lin28B contribute to a variety of biological processes such as development, growth, and tissue regeneration. Dysregulation of Lin28A/B expression is associated with numerous types of tumors. In this study, we demonstrate that overexpression of Lin28A in the mouse nephrons leads to severe inflammation and kidney damage, rather than to tumorigenesis. To investigate the causal relationship between kidney damage and inflammation, we utilized steroid treatment to suppress inflammation. This treatment also ameliorated the kidney damage phenotype, indicating that Lin28A overexpression directly induces inflammation, which in turn leads to kidney damage. Notably, Lin28A overexpression causes inflammation only when expressed in nephrons, but not in the stromal cells of the kidneys, highlighting its cell context-dependent nature. The nephron-specific, Lin28A-induced inflammatory response is distinct from the previously described Lin28B-mediated inflammatory feedback loops, as it is not IL-6 dependent. Instead, it is associated with the rapid upregulation of cytokines such as CXCL1 and CCL2. Overall, this study reveals that the impact of abnormal Lin28A expression is broader than previously understood, demonstrating that Lin28A overexpression also plays a role in inflammatory responses. Furthermore, this transgenic mouse model offers a valuable tool for advancing our understanding of the pathophysiology of acute kidney injury (AKI), where inflammation is a key factor.

2024-07-16 | GSE254805 | GEO

Overexpression of Lin28A in neural progenitor cells in vivo does not lead to brain tumor formation but results in reduced spine density

Project description:The RNA binding protein LIN28A is a stem- and progenitor marker and one of the factors necessary to induce pluripotent stem cells in vitro. LIN28A has been shown to promote the proliferative capacity of neural progenitor cells but its specific role during embryonal and postnatal brain development still remains widely unknown. A high and characteristic overexpression of LIN28A has been identified in malignant brain tumors called embryonal tumors with multilayered rosettes (ETMR). Radial glia cells of the ventricular zone are proposed as a cell of origin for those tumors.

2022-02-15 | PXD028044 | Pride

Nephron-Specific <i>Lin28A</i> Overexpression Triggers Severe Inflammatory Response and Kidney Damage.

Project description:The RNA-binding proteins LIN28A and LIN28B contribute to a variety of developmental biological processes. Dysregulation of Lin28A and Lin28B expression is associated with numerous types of tumors. This study demonstrates that Lin28A overexpression in the mouse nephrons leads to severe inflammation and kidney damage rather than to tumorigenesis. Notably, Lin28A overexpression causes inflammation only when expressed in nephrons, but not in the stromal cells of the kidneys, highlighting its cell context-dependent nature. The nephron-specific Lin28A-induced inflammatory response differs from previously described Lin28B-mediated inflammatory feedback loops as it is IL-6 independent. Instead, it is associated with the rapid upregulation of cytokines like Cxcl1 and Ccl2. These findings suggest that the pathophysiological effects of Lin28A overexpression extend beyond cell transformation. Our transgenic mouse model offers a valuable tool for advancing our understanding of the pathophysiology of acute kidney injury, where inflammation is a key factor.

| S-EPMC11302891 | biostudies-literature

Effects of Lin28a overexpression on gene expression changes during culturing neural stem cells (NSCs) derived from mouse embryonic ventral midbrain (VM)

Project description:Purpose: we want to see gene expression changes during in vitro expansion of VM-derived NSCs (VM-NSCs) with cell passges in the absence or presence of Lin28a overexpression. changes upon Lin28 overexpression in P1 and P3 stages of Neural stem cells. RNA-seq, sRNA-seq, and Polysome-seq with/without Lin28 overexpression in P1 and P3 stages of Neural stem cells.

2016-08-11 | E-GEOD-77851 | biostudies-arrayexpress

Effects of Lin28a overexpression on gene expression changes during culturing neural stem cells (NSCs) derived from mouse embryonic ventral midbrain (VM)

2016-08-11 | GSE77851 | GEO

RNA-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

Project description:We report the upregulated genes by the expression of LIN28A or loss of function mutant of LIN28A for 293FTcells..

2023-01-11 | GSE174387 | GEO

CLIP-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

Project description:We report the direct target genes by LIN28A or loss of function mutant of LIN28A for 293FTcells using CLIP-Seq

2023-01-11 | GSE174388 | GEO

Genome-wide analysis of skeletal muscle gene expression in Lin28A Tg mice

Project description:To identify mechanisms involved in growth and glucose metabolism, we performed whole genome mRNA expression analysis in five week old quadraceps muscle from 2 CD-1 background male Lin28A Tg and 2 WT littermates (all male) in which there was 7 fold overexpression of Lin28A, a RNA binding protein that enhances Igf2 translation and suppresses the let-7 microRNA biogenesis. Total RNA was harvested and processed using RNeasy mini kits from Qiagen. All RNA samples were DNase treated. The Illumina Ref-8 microarray platform was used to generate data.

2010-04-07 | E-GEOD-21226 | biostudies-arrayexpress

Genome-wide analysis of skeletal muscle gene expression in Lin28A Tg mice

2010-04-07 | GSE21226 | GEO

Expression profiling in LIN28A, SET7/9, and TUT4 depleted H9 cells, or in the silent mutations (siR) of LIN28A and LIN28A-K135R overexpressed H9 cells

Project description:A developmentally regulated RNA binding protein, LIN28A and its homolog LIN28B may share a similar mechanism to regulate the processing of let-7 microRNAs (miRNAs) in embryonic stem cells (ESCs) or certain cancer cells, although their predominant localization is different in cells. However, little is known about the regulatory mechanism of LIN28A for miRNA processing in the nucleus. Here, we show that SET7/9, a known histone methyltransferase, associates with LIN28A in vivo and in vitro. SET7/9-mediated methylation significantly leads to the nuclear retention and protein stability of LIN28A, and remarkably regulated RNA binding ability of LIN28A to pri-let-7. Using RNAi knockdown approach, we find that the methylated nuclear form of LIN28A may function in the nucleoli by sequestering the primary let-7 miRNA to block their processing through a Tut4 (Zcchc11)-independent mechanism to regulate human ESC pluripotency. We propose a new insight toward the understanding of the molecular mechanism for post-translational methylation of nuclear LIN28A along modulating pluripotency by regulating pri-let-7 miRNAs in human ESCs.

2016-12-05 | GSE53038 | GEO

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