Single-cell analysis of adult mouse testis exposed to cigarette smoke

Smoking is a global public health issue, which can cause damage to testicular tissue and affect the entire process of spermatogenesis. We established a passive smoking model in mice exposed to cigarette smoke to investigate the single-cell transcriptome data of passively smoking mice, revealing a series of changes in the testicular damage and spermatogenesis process caused by smoking. Through measurements of mouse body weight and testicular weight, we found that, compared to the control group, both the testicular weight and body weight of the treatment group were significantly reduced, while the organ coefficient was significantly increased. The study on the impact of smoking on mouse sperm showed that smoking significantly damaged the spermatogenic process in mice. Pathological assessments of testicular damage and experimental results on cell apoptosis indicated that smoking significantly increased the proportion of apoptotic cells in mouse testicular tissue. Single-cell RNA sequencing (scRNA-seq) experiments using the 10x Genomics platform demonstrated that smoking had a time-dependent impact on the proportion of various cell types in mouse testes. Differentially expressed genes and Gene Ontology (GO) analysis results indicated that smoking affected the formation of the cytoskeleton and microtubules in various cells, as well as flagella formation during spermatogenesis; smoking induced apoptosis in multiple cell types within mouse testes; smoking affected the exocrine functions of various cells; and smoking influenced mitochondrial energy metabolism in multiple cell types within mouse testes. GSEA results also suggested that smoking could induce apoptosis in various cells of the mouse testes. The time-dependent changes in the proportion of reproductive cells we discovered may be due to the combined effects of multiple biological processes. Thus, we will continue to pay attention to and conduct more comprehensive research.