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应激导致生精标记基因和生精细胞群体表达的变化。

Changes in Expressions of Spermatogenic Marker Genes and Spermatogenic Cell Population Caused by Stress.

机构信息

Department of Reproductive Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, China.

出版信息

Front Endocrinol (Lausanne). 2021 Oct 11;12:584125. doi: 10.3389/fendo.2021.584125. eCollection 2021.

DOI:10.3389/fendo.2021.584125
PMID:34707565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8542882/
Abstract

Many young adults are in a state of stress due to social and psychological pressures, which may result in male reproductive dysfunction. To provide new insight into this phenomenon, we investigated the effect of stress on the regulation of key genes and biological events in specific stages of spermatogenesis. After establishing rat stress models of different time durations, we observed pathological changes in testis through haematoxylin and eosin staining, and analysed gene expression in testis by RNA-seq, bioinformatic analysis, and reverse transcription qPCR (RT-qPCR). Immunohistochemistry (IHC) with the TissueFAXS quantitative imaging system was used to verify changes of different population of spermatogenic cells marked by differentially expressed marker genes. Our results showed that prolonged stress can lead to pathological changes in the testes, such as thinning of the spermatogenic epithelium, a decreased number of spermatogenic epithelial cells, the disordered arrangement of spermatogenic cells, and a decreased number of mature sperms. RNA-seq revealed that key marker spermatogenesis-related genes such as , , , and had significantly decreased expression levels in chronic stress groups, and this was confirmed by RT-qPCR and IHC. Collectively, these findings suggest that chronic stress causes damaging pathological changes in testis and dysregulates the marker genes of specific stages of spermatogenesis and change the population of spermatogenic cells, which may be a critical responsible for male reproductive dysfunction.

摘要

许多年轻人由于社会和心理压力而处于压力状态，这可能导致男性生殖功能障碍。为了深入了解这一现象，我们研究了应激对特定精子发生阶段关键基因和生物事件调节的影响。在建立不同持续时间的大鼠应激模型后，我们通过苏木精和伊红染色观察睾丸的病理变化，并通过 RNA-seq、生物信息学分析和逆转录 qPCR（RT-qPCR）分析睾丸中的基因表达。免疫组织化学（IHC）与 TissueFAXS 定量成像系统结合使用，验证了由差异表达标记基因标记的不同生精细胞群体的变化。我们的结果表明，长期应激会导致睾丸发生病理变化，例如生精上皮变薄、生精上皮细胞数量减少、生精细胞排列紊乱以及成熟精子数量减少。RNA-seq 显示，关键标记生精相关基因如 、 、 、 在慢性应激组中的表达水平显著降低，这通过 RT-qPCR 和 IHC 得到了证实。综上所述，这些发现表明慢性应激会导致睾丸发生损伤性病理变化，并扰乱特定精子发生阶段的标记基因，改变生精细胞群体，这可能是导致男性生殖功能障碍的关键因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/169427ae9a6e/fendo-12-584125-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/1a900167289a/fendo-12-584125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/31c370afc0ec/fendo-12-584125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/65f7d43257eb/fendo-12-584125-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/ceaa094ca14d/fendo-12-584125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/50dfd4109efe/fendo-12-584125-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/eecf24491c6c/fendo-12-584125-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/169427ae9a6e/fendo-12-584125-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/1a900167289a/fendo-12-584125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/31c370afc0ec/fendo-12-584125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/65f7d43257eb/fendo-12-584125-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/ceaa094ca14d/fendo-12-584125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/50dfd4109efe/fendo-12-584125-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/eecf24491c6c/fendo-12-584125-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d20a/8542882/169427ae9a6e/fendo-12-584125-g007.jpg

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