The role of ALOX15B in heat stress-induced apoptosis of porcine sertoli cells

Xue, Hongyan; Huo, Yuan-Nan; Hu, Yu; Zhang, Jinlong; Deng, Chengchen; Zhang, Jiaojiao; Wang, Xianzhong

doi:10.1016/j.theriogenology.2022.03.018

Cited by 10 publications

(5 citation statements)

References 66 publications

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“…However, some studies have proposed that several DiHETs, including 11,12-DiHET, may have some biological functions similar to their EET precursor, and therefore, 11,12-DiHET itself may be crucial in protecting the CNS against cellular damage. 29 However, these findings warrant further exploration.…”

Section: Discussionmentioning

confidence: 91%

“…27 However, additional experiments are required to substantiate this hypothesis and to uncover the cellular source and function of 15-HETE in the context of MS. Of note, both 8-HETE and 15-HETE are produced by the enzyme ALOX-15B, which could explain the similar trend observed in their relation with disability. 29 In addition, the backward selection procedure, which was used to create final linear regression models for disability, might have resulted in the removal of 8-HETE in these models because of the similar effect of 15-HETE and 8-HETE on the variance in EDSS.…”

Section: Discussionmentioning

confidence: 99%

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Association of Arachidonic Acid–Derived Lipid Mediators With Disease Severity in Patients With Relapsing and Progressive Multiple Sclerosis

Broos¹,

Loonstra²,

Ruiter³

et al. 2023

Neurology

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Background and objectives:Excessive activation of certain lipid mediator (LM) pathways play a role in the complex pathogenesis of multiple sclerosis (MS). However, the relation between bioactive LMs and different aspects of CNS-related pathophysiological processes remains largely unknown. Therefore, we here assessed the association of bioactive LMs belonging to the ω-3 / ω-6 lipid classes with clinical, biochemical (serum neurofilament light (sNfL) and serum glial fibrillary acidic protein (sGFAP)) parameters and MRI-based brain volumes in patients with MS (PwMS) and healthy controls (HC).Methods:A targeted high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) approach was used on plasma samples of PwMS and HC of the Project Y cohort, a cross-sectional population based cohort that contains PwMS all born in 1966 in the Netherlands and age-matched HCs. LMs were compared between PwMS and HC and were correlated with levels of sNfL, sGFAP, disability (EDSS) and brain volumes. Finally, significant correlates were included in a backward multivariate regression model to identify which LMs best related to disability.Results:The study sample consisted of 170 patients with relapsing remitting MS (RRMS), 115 patients with progressive MS (PMS) and 125 HC. LM profiles of patients with PMS significantly differed from RRMS and HC, in particular, patients with PMS showed elevated levels of several arachidonic acid (AA) derivatives. In particular 15-HETE (r = 0.24,p< 0.001), positively correlated (average r = 0.2,p< 0.05) with clinical and biochemical parameters such as EDSS and sNfL. In addition, higher 15-HETE levels were related to lower total brain (r = -0.24,p= 0.04) and deep gray matter volumes (r = -0.27,p= 0.02) in patients with PMS and higher lesion volume (r = 0.15,p =0.03) in all PwMS.Discussion:In PwMS of the same birth year, we show that ω-3 and -6 LMs are associated with disability, biochemical (sNfL, GFAP) and MRI measures. Furthermore, our findings indicate that particularly in patients with PMS, elevated levels of specific products of the AA pathway, such as 15-HETE, associate with neurodegenerative processes. Our findings highlight the potential relevance of ω-6 LMs in the pathogenesis of MS.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Association of Arachidonic Acid–Derived Lipid Mediators With Disease Severity in Patients With Relapsing and Progressive Multiple Sclerosis

Broos¹,

Loonstra²,

Ruiter³

et al. 2023

Neurology

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“…An important factor in the transmission of species from generation to generation is the selection of superior cellular traits and the rejection of cellular mechanisms that are detrimental to reproductive development. Various physical factors, toxins, radioactivity, etc., have the chance to stimulate the activation of this mechanism (Alam et al, 2010;Etemadi et al, 2020;Wang et al, 2017;Xue et al, 2022). If spermatogenesis is compromised in any way, germ cells often go into apoptosis by default (Lin et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Heat exposure promotes apoptosis and pyroptosis in Sertoli cells

WANG¹,

He²,

Gao³

et al. 2023

Biocell

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Heat stress is an important influence on the male reproductive organs. Therefore, the effects of heat stress on genes or pathways related to the reproductive system of male mice were experimentally explored in this paper to further determine the effects of heat stimulation on mammals. Herein, models of heat-exposed mouse testicular tissue and heatexcited cells were successfully established. Many scorched vesicles were found after heat excitation of testis supporting cells, testicular mesenchymal (TM4) cells. Western blot, in situ terminal deoxynucleotide transferase dUTP Nick end labeling (TUNEL) and transmission electron microscopy showed that membrane rupture, mitochondrial damage and autophagic vesicles occurred in TM4 cells after thermal excitation. The N-segment fragment of the associated protein shear was increased, and the TUNEL result was positive. In conclusion, thermal excitation induced apoptosis and scorch death in TM4 cells. Thus, the Hippo pathway and apoptosis-related pathway were significantly enriched after heat stimulation in mouse testis, and the scorch death effect in TM4 cells was induced by heat excitation.

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“…Molecular changes observed in boar Sertoli cells under heat stress involved the downregulation of the Kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway (associated with enhanced antioxidants) and low levels of heat shock protein 90 (HSP90) due to the suppression of melatonin receptor 1B (MTNR1B), resulting in abnormal regulation of stabilizing hypoxia-inducible factor-1α (HIF-1α) [ 104 ]. Another study by Xue H et al [ 105 ] found that HS primarily enhanced the lipid oxidation, oxidative stress, and apoptosis in Sertoli cells through the activation of arachidonate 15-lipoxygenase type B (ALOX15B) and the production of 8-hydroxyeicosatetraenoic acid (8-HETE) and 15-hydroxyeicosatetraenoic acid (15-HETE), with involvement of the P53-p38 pathway [ 105 ]. The disruption of arachidonic acid (AA) metabolism, a precursor to 20-carbon polyunsaturated fats, has been reported to be associated with poor spermatogenesis outcomes, as excessive AA levels altered cytomembrane structure and function and increased permeability and brittleness, potentially leading to mitochondrial changes, apoptosis, or necrosis.…”

Section: Impact Of Heat-stress-induced Oxidative Stress and Apoptosis...mentioning

confidence: 99%

Advancements in Genetic Biomarkers and Exogenous Antioxidant Supplementation for Safeguarding Mammalian Cells against Heat-Induced Oxidative Stress and Apoptosis

Khan,

Chen

et al. 2024

Antioxidants

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Heat stress represents a pervasive global concern with far-reaching implications for the reproductive efficiency of both animal and human populations. An extensive body of published research on heat stress effects utilizes controlled experimental environments to expose cells and tissues to heat stress and its disruptive influence on the physiological aspects of reproductive phenotypic traits, encompassing parameters such as sperm quality, sperm motility, viability, and overall competence. Beyond these immediate effects, heat stress has been linked to embryo losses, compromised oocyte development, and even infertility across diverse species. One of the primary mechanisms underlying these adverse reproductive outcomes is the elevation of reactive oxygen species (ROS) levels precipitating oxidative stress and apoptosis within mammalian reproductive cells. Oxidative stress and apoptosis are recognized as pivotal biological factors through which heat stress exerts its disruptive impact on both male and female reproductive cells. In a concerted effort to mitigate the detrimental consequences of heat stress, supplementation with antioxidants, both in natural and synthetic forms, has been explored as a potential intervention strategy. Furthermore, reproductive cells possess inherent self-protective mechanisms that come into play during episodes of heat stress, aiding in their survival. This comprehensive review delves into the multifaceted effects of heat stress on reproductive phenotypic traits and elucidates the intricate molecular mechanisms underpinning oxidative stress and apoptosis in reproductive cells, which compromise their normal function. Additionally, we provide a succinct overview of potential antioxidant interventions and highlight the genetic biomarkers within reproductive cells that possess self-protective capabilities, collectively offering promising avenues for ameliorating the negative impact of heat stress by restraining apoptosis and oxidative stress.

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The role of ALOX15B in heat stress-induced apoptosis of porcine sertoli cells

Cited by 10 publications

References 66 publications

Association of Arachidonic Acid–Derived Lipid Mediators With Disease Severity in Patients With Relapsing and Progressive Multiple Sclerosis

Association of Arachidonic Acid–Derived Lipid Mediators With Disease Severity in Patients With Relapsing and Progressive Multiple Sclerosis

Heat exposure promotes apoptosis and pyroptosis in Sertoli cells

Advancements in Genetic Biomarkers and Exogenous Antioxidant Supplementation for Safeguarding Mammalian Cells against Heat-Induced Oxidative Stress and Apoptosis

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