Cell-type specific and differential expression of LINC-RSAS long noncoding RNA declines in the testes during ageing of the rat.
Ajay Kumar DangaSukhleen KourAnita KumariPramod C RathPublished in: Biogerontology (2024)
Long noncoding RNAs (lncRNAs) have emerged as major regulators of gene expression, chromatin structure, epigenetic changes, post-transcriptional processing of RNAs, translation of mRNAs into proteins as well as contributing to the process of ageing. Ageing is a universal, slow, progressive change in almost all physiological processes of organisms after attaining reproductive maturity and often associated with age-related diseases. Mammalian testes contain various cell-types, vast reservoir of transcriptome complexity, produce haploid male gametes for reproduction and testosterone for development and maintenance of male sexual characters as well as contribute genetic variation to the species. We report age-related decline in expression and cellular localization of Long intergenic noncoding repeat-rich sense-antisense (LINC-RSAS) RNA in the testes and its major cell-types such as primary spermatocytes, Leydig cells and Sertoli cells during ageing of the rat. LINC-RSAS expression in testes increased from immature (4-weeks) to adult (16- and 44-weeks) and declined from adult (44-weeks) to nearly-old (70-weeks) rats. Genomic DNA methylation in the testes showed a similar pattern. Cell-type specific higher expression of LINC-RSAS was observed in primary spermatocytes (pachytene cells), Leydig cells and Sertoli cells of testes of adult rats. Over-expression of LINC-RSAS in cultured human cell lines revealed its possible role in cell-cycle control and apoptosis. We propose that LINC-RSAS expression is involved in molecular physiology of primary spermatocytes, Leydig cells and Sertoli cells of adult testes and its decline is associated with diminishing function of testes during ageing of the rat.
Keyphrases
- induced apoptosis
- cell cycle arrest
- gene expression
- long noncoding rna
- long non coding rna
- poor prognosis
- dna methylation
- cell proliferation
- oxidative stress
- cell cycle
- cell death
- endothelial cells
- stem cells
- multiple sclerosis
- mental health
- signaling pathway
- genome wide
- transcription factor
- dna damage
- pi k akt
- cell therapy
- binding protein
- mesenchymal stem cells
- heat shock protein
- preterm birth
- induced pluripotent stem cells