Hypoxia‐Induced Deacetylation Is Required for Tetraploid Differentiation in Response to Testicular Ischemia‐Reperfusion (IR) Injury

Hou, Wugang; Dong, Yushu; Zhang, Jinshan; Yin, Zhongmin; Hua, Wen; Xiong, Liang; Li, Wei

doi:10.2164/jandrol.112.016584

Cited by 12 publications

(6 citation statements)

References 33 publications

(42 reference statements)

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“…A plausible explanation is that sperm cells that were more susceptible to heat stress were eliminated in the first insulation. This mechanism would be similar to what occurs in the hypoxia-reperfusion syndrome [ 39 ] after organ transplantation. Oxidative damage may occur due to the increased oxygen supply during tissue reperfusion after hypoxia, generating a condition of oxidative stress due to the increased oxygen supply [ 40 – 42 ].…”

Section: Discussionsupporting

confidence: 56%

Effect of Heat Stress on Sperm DNA: Protamine Assessment in Ram Spermatozoa and Testicle

Hamilton

Siqueira

Castro

et al. 2018

Oxidative Medicine and Cellular Longevity

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Sperm DNA fragmentation is considered one of the main causes of male infertility. The most accepted causes of sperm DNA damage are deleterious actions of reactive oxygen species (ROS), defects in protamination, and apoptosis. Ram sperm are highly prone to those damages due to the high susceptibility to ROS and to oxidative stress caused by heat stress. We aimed to evaluate the effects of heat stress on the chromatin of ejaculated and epididymal sperm and the activation of apoptotic pathways in different cell types in ram testis. We observed higher percentages of ejaculated sperm with increased chromatin fragmentation in the heat stress group; a fact that was unexpectedly not observed in epididymal sperm. Heat stress group presented a higher percentage of spermatozoa with DNA fragmentation and increased number of mRNA copies of transitional protein 1. Epididymal sperm presented greater gene expression of protamine 1 on the 30th day of the spermatic cycle; however, no differences in protamine protein levels were observed in ejaculated sperm and testis. Localization of proapoptotic protein BAX or BCL2 in testis was not different. In conclusion, testicular heat stress increases ram sperm DNA fragmentation without changes in protamination and apoptotic patterns.

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Section: Discussionsupporting

confidence: 56%

Effect of Heat Stress on Sperm DNA: Protamine Assessment in Ram Spermatozoa and Testicle

Hamilton

Siqueira

Castro

et al. 2018

Oxidative Medicine and Cellular Longevity

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show abstract

“…14,19,23 Hypoxia During a testicular ischemic event resulting from testicular torsion, an imbalance between oxygen demand and supply develops, which results in profound tissue hypoxia. 24,25 Hypoxia plays an important role in lipid peroxidation, activation of inflammation pathways and germ cell-specific apoptosis in the testis. Hypoxia-inducible factor 1 is a key regulator of physiological responses to hypoxia.…”

Section: Inflammation and Apoptosismentioning

confidence: 99%

Testicular torsion–detorsion and potential therapeutic treatments: A possible role for ischemic postconditioning

et al. 2016

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Testicular torsion is a common urological emergency among adolescent boys and young men. Rotation of the testis and twisting of the spermatic cord rapidly leads to ischemia, resulting in a loss of germ cells. Thus, prompt diagnosis and urgent surgical intervention are required, but the subsequent release of the torsion induces reperfusion injury, which causes further damage to the ischemic testis. Testicular torsion -detorsion (ischemia-reperfusion) injury triggers the generation of reactive oxygen species, pro-inflammatory cytokines, neutrophil recruitment, lipid peroxidation, anoxia and apoptosis, which carry a significant risk of subsequent infertility. Previously, the effects of numerous pharmacological agents and treatments have been evaluated to prevent testicular ischemia-reperfusion injury in animal models. We propose a new treatment, especially postconditioning, to prevent adverse effects of ischemiareperfusion injury after testicular torsion-detorsion.

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“…Germ cells were released from seminiferous tubules in PBS as described elsewhere (Hou et al 2012). After germ cells were stained with 25 mg/l ethidium bromide (Sangon Biotech, Shanghai, China), samples were analyzed by flow cytometer with an excitation wavelength of 488 nm.…”

Section: Flow Cytometrymentioning

confidence: 99%

Endogenous EGF maintains Sertoli germ cell anchoring junction integrity and is required for early recovery from acute testicular ischemia/reperfusion injury

Zhang

Zeng

et al. 2013

Reproduction

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Administration of exogenous epidermal growth factor (EGF) improves testicular injury after acute ischemia-reperfusion (IR) stress, but the molecular basis is poorly understood. The role of endogenous EGF in testicular recovery and the underlying intracellular signaling pathways involved were herein investigated. In mice, testicular IR injury significantly enhanced the expression level of endogenous Egf at the very beginning of reperfusion. Expression of EGF receptor (Egfr (ErbB1)) was accordingly upregulated 3 h after reperfusion. Deprivation of majority of circulated EGF by sialoadenectomy aggravated testicular detriment (especially in pachytene spermatocytes), enhanced germ cell apoptosis, and thereafter resulted in impaired meiotic differentiation after IR insult. Mechanistically, endogenous EGF signaling appeared to be indispensable for the proper maintenance of Sertoli germ cells anchoring junction dynamics during the early testicular recovery. We also provided the in vitro evidences in a well-established rat Sertoli germ cell co-cultures model that the pro-survival effect of endogenous EGF on germ cells in response to testicular IR insult is mediated, at least in part, via the phosphatidylinositol 3-kinase/pAkt pathway. Collectively, our results suggest that the augment of endogenous EGF during the early testicular recovery may act on top of an endocrinous cascade orchestrating the intimate interactions between Sertoli cells and germ cells and may operate as indispensable defensive mechanism in response to testicular IR stress. Future studies in this field would shed light on this complicated pathogenesis.

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Hypoxia‐Induced Deacetylation Is Required for Tetraploid Differentiation in Response to Testicular Ischemia‐Reperfusion (IR) Injury

Cited by 12 publications

References 33 publications

Effect of Heat Stress on Sperm DNA: Protamine Assessment in Ram Spermatozoa and Testicle

Effect of Heat Stress on Sperm DNA: Protamine Assessment in Ram Spermatozoa and Testicle

Testicular torsion–detorsion and potential therapeutic treatments: A possible role for ischemic postconditioning

Endogenous EGF maintains Sertoli germ cell anchoring junction integrity and is required for early recovery from acute testicular ischemia/reperfusion injury

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