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Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE120778 | GEO | 2019/07/30

REPOSITORIES: GEO

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Aging of spermatogonial stem cells by Jnk-mediated glycolysis activation.

Project description:Because spermatogonial stem cells (SSCs) are immortal by serial transplantation, SSC aging in intact testes is considered to be caused by a deteriorated microenvironment. Here, we report a cell-intrinsic mode of SSC aging by glycolysis activation. Using cultured SSCs, we found that aged SSCs proliferated more actively than young SSCs and showed enhanced glycolytic activity. Moreover, they remained euploid and exhibited stable androgenetic imprinting patterns with robust SSC activity despite having shortened telomeres. Aged SSCs showed increased Wnt7b expression, which was associated with decreased Polycomb complex 2 activity. Our results suggest that aberrant Wnt7b expression activated c-jun N-terminal kinase (JNK), which down-regulated mitochondria numbers by suppressing Ppargc1a Down-regulation of Ppargc1a probably decreased reactive oxygen species and enhanced glycolysis. Analyses of the Klotho-deficient aging mouse model and 2-y-old aged rats confirmed JNK hyperactivation and increased glycolysis. Therefore, not only microenvironment but also intrinsic activation of JNK-mediated glycolysis contributes to SSC aging.

| S-EPMC6697785 | biostudies-literature

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

Project description:Because spermatogonial stem cells (SSCs) are virtually immortal by serial transplantation, SSC decrease in aged testes is considered to be caused by deteriorated microenvironment. Here we report cell-intrinsic mode of SSC aging. SSCs cultured for 5 years proliferate more actively than young SSCs and showed enhanced glycolytic activity but remain euploid and exhibited stable androgenetic imprinting patterns. Moreover, the aged SSCs kept constant SSC activity despite shortened telomeres. The increased proliferative activity of aged SSCs was caused by Wnt7b expression, which likely occurred due to decreased polycomb complex2 activity. Aberrant Wnt7b expression not only decreased reactive oxygen species levels and mitochondria activity but also stimulated glycolysis via c-jun N-terminal kinase (JNK) activation. Analysis of SSCs in Klotho aging mouse model also confirmed hyperactivation of JNK pathway and increased glycolysis. Therefore, not only SSC microenvironment but also intrinsic activation of Wnt7b-mediated glycolysis plays important roles in SSC aging.

2019-07-30 | GSE120777 | GEO

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [Bisulfite-seq]

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Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

Project description:Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

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Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

Project description:Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

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Project description:Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [Bisulfite-seq]

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