The effect of secondary cholestasis on the CD68-positive and CD163-positive macrophage population, cellular proliferation, and apoptosis in rat testis

Shi, Shanshan; Jiang, Li; Xie, Haiyang; Xu, Jian; Youfa, Zhu; Zheng, Shusen

doi:10.1016/j.jri.2015.03.008

Cited by 7 publications

(2 citation statements)

References 52 publications

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“…One of the adverse effects of cholestasis on testes is infiltration by macrophages, subsequently leading to inflammation. Shi et al demonstrated that after bile duct ligation, the number of cells expressing proliferating cells nuclear antigen (PCNA+) significantly reduced while the expressions of apoptosis-related genes such as CASP-3 and Bcl-2associated X protein (BAX) elevated (24). Our finding also showed a higher expression of CASP-3, which could boost cellular death in testes of cholestasis rats.…”

Section: Discussionsupporting

confidence: 65%

Cholestasis Alters miR-34c-5p Expression in the Testes of Male Wistar Rats

2021

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Background: Cholestasis is a pathophysiological condition, significantly reducing spermatozoa production. MiR-34c is highly expressed in adult male testicles and controls different stages of spermatogenesis. Objectives: Here, we aimed to investigate miR-34c expression in the testes of rat models of cholestasis. The expressions of THY-1, FGF-2, and CASP-3 genes, that are targeted by mirR-34c were also investigated. Methods: Cholestasis was induced in six adult rats via bile duct ligation. Four weeks after cholestasis induction, sera and testicular tissues were collected for further examinations. The levels of liver enzymes were measured using the ELISA. The structure of the testes was evaluated by histological examination. Total RNA was extracted from testes using a special kit and converted to cDNA. The expressions of miR-34c-5p, THY-1, FGF-2, and CASP-3 genes were determined by Real-Time PCR. Results: The serum levels of ALP, AST, and ALT were significantly elevated in the rat models of cholestasis (P < 0.001). Real-Time PCR revealed that the expressions of miR-34c-5p, THY-1, and FGF-2 genes decreased while CASP-3 gene was upregulated in the testes of cholestatic animals (all differences were significant at P < 0.05). Conclusions: Our study indicated that cholestasis was associated with reduced expression of miR-34c and altered expression of its target genes in the testis. Our results highlight the potential effects of cholestasis, a hepatobiliary disease, on testicular tissue function and male fertility.

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Section: Discussionsupporting

confidence: 65%

Cholestasis Alters miR-34c-5p Expression in the Testes of Male Wistar Rats

2021

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“…The sequences of oligonucleotide primer pairs for claudin‐11, occludin, ZO‐1 and beta‐actin mRNA in rats were obtained from previous reports (Chung, Mruk, Mo, Lee, & Cheng, ; Lui, Lee, & Cheng, ; Sauer et al, ; Shi et al, ) and purchased from Europhinsgenomics. The sequences are shown in Table .…”

Section: Methodsmentioning

confidence: 99%

Effect of mirabegron on tight junction molecules in primary cultured rat Sertoli cells

et al. 2019

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Mirabegron is a selective beta3‐adrenoceptor (β3‐AR) agonist, which is commonly used for the treatment of overactive bladder. This medicine is associated with atrophy of reproductive organs in rats. However, no study has examined the detailed action and mechanism of its toxicity in reproductive cells. In this study, we examined the effect of mirabegron on primary cultured rat Sertoli cells. Firstly, RT‐PCR and immunocytochemistry revealed that β3‐AR was present in rat Sertoli cells. Then, primary cultured rat Sertoli cells were treated with mirabegron. Quantitative real‐time PCR revealed that mirabegron treatment induced a significant increase in claudin‐11 mRNA, which is crucial for spermatogenesis. Western blot analysis also showed that mirabegron treatment significantly activated p44/42 mitogen‐activated protein kinase (MAPK). After additional treatment with U0126, a specific noncompetitive inhibitor of mitogen‐activated protein kinase kinase (MAPKK), the upregulation of claudin‐11 mRNA induced by mirabegron was reduced. At the same time, immunocytochemistry showed mirabegron treatment disturbed claudin‐11 localisation to tight junction, which was recovered when treated with mirabegron in the presence of U0126. These results suggest that mirabegron treatment is associated with assembly of the blood–testis barrier through p44/42 MAPK pathway. These findings could explain one of the underlying mechanisms of reproductive toxicity induced by mirabegron.

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Microcircumstance for Induction and Prevention of Testicular Autoimmunity

Itoh

2017

Testicular Autoimmunity

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The effect of secondary cholestasis on the CD68-positive and CD163-positive macrophage population, cellular proliferation, and apoptosis in rat testis

Cited by 7 publications

References 52 publications

Cholestasis Alters miR-34c-5p Expression in the Testes of Male Wistar Rats

Cholestasis Alters miR-34c-5p Expression in the Testes of Male Wistar Rats

Effect of mirabegron on tight junction molecules in primary cultured rat Sertoli cells

Microcircumstance for Induction and Prevention of Testicular Autoimmunity

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