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Microarray analysis of defective cartilage in Hoxc8- and Hoxd4-transgenic mice

ABSTRACT: Microarray analysis of defective cartilage in Hoxc8- and Hoxd4-transgenic mice

PROVIDER: PRJNA120435 | ENA |

REPOSITORIES: ENA

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Microarray analysis of defective cartilage in Hoxc8- and Hoxd4-transgenic mice

Project description:This SuperSeries is composed of the following subset Series: GSE18991: Overexpression of Hoxd4 transcription factor alters transcriptional profiles in mouse chondrocytes at E18.5 GSE18992: Overexpression of Hoxc8 transcription factor alters transcriptional profiles in mouse chondrocytes at E18.5!Series_overall_design = Refer to individual Series Refer to individual Series

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Project description:Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxc8 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.

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Project description:Low-protein diets can mitigate renal fibrosis, yet the critical amino acid responsible for this benefit and its underlying mechanism remain unclear. By screening 15 amino acid–restricted diets in a unilateral ureteral obstruction (UUO) model, we identify methionine restriction (MetR) as the most effective intervention. Integrating transcriptomic and cistromic analyses further uncover Hoxc8 as a central pro-fibrotic transcription factor. Hoxc8 is induced by TGF-β–Smad3, amplifies its own expression, and drives fibrotic gene programs through recruitment of the P-TEFb transcriptional elongation complex. Clinically, HOXC8 is elevated in fibrotic human kidneys, and fibroblast-specific Hoxc8 deletion protects mice from fibrosis. MetR attenuates this pro-fibrotic circuit by reducing active histone marks (H3K4me3 and H3K36me3) at the Hoxc8 locus, thereby suppressing the Hoxc8-dependent fibrotic transcriptional program. Together, these findings establish the TGF-β–Smad3–Hoxc8/P-TEFb axis as a key driver of renal fibrosis and highlight MetR as a promising therapeutic strategy.

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Methionine Restriction Alleviates Kidney Fibrosis through Epigenetic Repression of the TGF-β/Smad3/Hoxc8/P-TEFb Axis

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