Biological Research最新文献

{"title":"Small extracellular vesicles enhance the survival of Sca-1+ cardiac stem cells against ROS-induced ischemic-reoxygenation injury in vitro.","authors":"Radwa A Mehanna, Hagar Elkafrawy, Marwa M Essawy, Samar S Ibrahim, Ashraf K Awaad, Nehal A Khalil, Marwa A Kholief, Abeer Sallam, Heba A Hamed, Mona A Barkat, Mohamed F ElKady, Eman H Thabet","doi":"10.1186/s40659-025-00593-7","DOIUrl":"10.1186/s40659-025-00593-7","url":null,"abstract":"<p><strong>Background: </strong>Ischemic reperfusion (IR) generates reactive oxygen species (ROS) that inevitably result in myocardial cell death and heart failure. The regenerative power of cardiac progenitor/stem pools (CSCs), especially the Sca1⁺ population, in response to IR injury remains unclear.</p><p><strong>Methods: </strong>Our work sought to investigate whether small extracellular vesicles (sEVs) isolated from bone marrow-mesenchymal stem cells (BMMSCs) could rescue CSCs, specifically Sca-1+/CSCs, from IR by increasing their proliferative capacity and limiting their apoptosis in vitro. The Sca-1+/CSCs-IR model was induced by the oxygen-glucose deprivation/reoxygenation method (OGD/R). The effects of treatment with BMMSCs-derived sEVs on oxidative stress, cell proliferation, apoptosis, and cell cycle were assessed. To further test the mechanistic action, we assessed the PTEN/pAkt/HIF-1α pathway.</p><p><strong>Results: </strong>Compared to hypoxic untreated CSCs, BMMSCs-derived sEVs-treated cells had shifted from their quiescent to proliferative phase (p > 0.05) and showed decreased apoptosis (p < 0.001). sEVs-treated CSCs were predominately in the S phase (11.8 ± 0.9%) (p < 0.01). We identified an abundance of miRNA-21-5P in BMMSCs. HIF-1α expression was highest in CSCs treated with sEVs (p < 0.05). Moreover, miRNA-21-5p-rich sEVs shifted the redox state, reducing oxidative stress and promoting balance (p > 0.05).</p><p><strong>Conclusion: </strong>Conditioning Sca-1+/CSCs, an essential population in the postnatal heart, with sEVs rich in miRNA-21 robustly enhanced the proliferation, and synthesis phase of the cell cycle, and stabilized HIF-1α while alleviating oxidative stress and apoptosis. Such sEVs rich in miRNA-21-5p can be further used as a preconditioning tool to enhance endogenous Sca-1+/CSCs regeneration in response to IR injury.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"12"},"PeriodicalIF":4.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serotonin regulates in a cell-type specific manner light-evoked response and synaptic activity in mouse retinal ganglion cells.","authors":"Claudia Di Berardino, Sebastián F Estay, Alejandro Alcaino, Andrés E Chávez","doi":"10.1186/s40659-025-00594-6","DOIUrl":"10.1186/s40659-025-00594-6","url":null,"abstract":"<p><strong>Background: </strong>Serotonin (5-HT) is known to be synthesized and accumulated in the vertebrate retina through the 5-HT transporter, SERT. While manipulation of the serotonergic system has been shown to impact visual processing, the role of 5-HT and SERT as modulators of retinal synaptic function remains poorly understood.</p><p><strong>Results: </strong>Using mouse retinal slices, we show that acute application of 5-HT produces a cell-type specific reduction in light-evoked excitatory responses (L-EPSC) in ON-OFF retinal ganglion cells (RGCs), but not in ON RGCs. Similarly, increasing 5-HT tone by acute application of citalopram, a selective 5-HT reuptake inhibitor, also reduces L-EPSC in ON-OFF RGCs while not affecting ON RGCs. Importantly, citalopram-mediated reduction of L-EPSC was absent in ON-OFF RGCs recorded from SERT null retina, highlighting the role of SERT in regulating light-evoked responses in RGCs. The effects of both exogenous and endogenous 5-HT on L-EPSC in ON-OFF RGCs are likely due to a presynaptic reduction in excitatory synaptic strength as 5-HT and citalopram reduced the frequency but not the amplitude of spontaneous excitatory currents (sEPSCs) in ON-OFF RGCs. Moreover, 5-HT and citalopram had no effect on currents elicited by the direct activation of postsynaptic receptors in RGCs by brief application of glutamate in the inner retina.</p><p><strong>Conclusions: </strong>Altogether these findings indicate that 5-HT modulates excitatory inputs onto RGCs in a cell-type specific manner and highlight that in the adult mouse retina, 5-HT-mediated effects onto RGCs are tightly controlled by the 5-HT transporter SERT.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"11"},"PeriodicalIF":4.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calcium electroporation induces stress response through upregulation of HSP27, HSP70, aspartate β-hydroxylase, and CD133 in human colon cancer cells.","authors":"Anna Szewczyk, Nina Rembiałkowska, Jolanta Saczko, Małgorzata Daczewska, Vitalij Novickij, Julita Kulbacka","doi":"10.1186/s40659-025-00591-9","DOIUrl":"10.1186/s40659-025-00591-9","url":null,"abstract":"<p><strong>Background: </strong>Electroporation (EP) leverages electric pulses to permeabilize cell membranes, enabling the delivery of therapeutic agents like calcium in cancer treatment. Calcium electroporation (CaEP) induces a rapid influx of calcium ions, disrupting cellular calcium homeostasis and triggering cell death pathways. This study aims to compare the cellular responses between microsecond (µsEP) and nanosecond (nsEP) electroporation, particularly in terms of oxidative stress, immune response activation, and cancer stem cell (CSC) viability in drug-resistant (LoVo Dx) and non-resistant (LoVo) colorectal cancer cell lines.</p><p><strong>Results: </strong>Both µsEP and nsEP, particularly when combined with Ca²⁺, significantly reduced the viability of cancer cells, with nsEP showing greater efficacy. Reactive oxygen species (ROS) levels increased 5-fold in malignant cells following nsEP, correlating with decreased ATP production and mitochondrial dysfunction. Nanosecond CaEP (nsCaEP) also induced significant expression of aspartate-β-hydroxylase (ASPH), a protein linked to calcium homeostasis and tumor progression. Moreover, nsEP led to heightened expression of heat shock proteins (HSP27/70), indicating potential immune activation. Interestingly, nsEP without calcium drastically reduced the expression of CD133, a marker for CSCs, while the addition of Ca²⁺ preserved CD133 expression. The expression of death effector domain-containing DNA binding protein (DEDD), associated with apoptosis, was significantly elevated in treated cancer cells, especially in the nucleus after nsCaEP.</p><p><strong>Conclusions: </strong>The study confirms that nsEP is more effective than µsEP in disrupting cancer cell viability, enhancing oxidative stress, and triggering immune responses, likely through HSP overexpression and ROS generation. nsEP also appears to reduce CSC viability, offering a promising therapeutic approach. However, preserving CD133 expression in the presence of calcium suggests complex interactions that require further investigation. These findings highlight the potential of nsCaEP as an innovative strategy for targeting both cancer cells and CSCs, potentially improving treatment outcomes in colorectal cancer. Further studies are needed to explore the exact cell death mechanisms and optimize protocols for clinical applications.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"10"},"PeriodicalIF":4.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: The periplasmic protein HslJ is the firstline of defense against oxidative stress in Acinetobacter baumannii.","authors":"Daniela Scribano, Martina Pasqua, Dolores Limongi, Lucia Nencioni, Anna Teresa Palamara, Cecilia Ambrosi","doi":"10.1186/s40659-025-00588-4","DOIUrl":"10.1186/s40659-025-00588-4","url":null,"abstract":"","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"9"},"PeriodicalIF":4.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11780828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"hUC-MSC preserves erectile function by restoring mitochondrial mass of penile smooth muscle cells in a rat model of cavernous nerve injury via SIRT1/PGC-1a/TFAM signaling.","authors":"Mengbo Yang, Xinda Chen, Ming Zhang, Xiaolin Zhang, Dongdong Xiao, Huiming Xu, Mujun Lu","doi":"10.1186/s40659-024-00578-y","DOIUrl":"10.1186/s40659-024-00578-y","url":null,"abstract":"<p><strong>Background: </strong>Cavernous nerve injury-induced erectile dysfunction (CNI-ED) is a common complication following radical prostatectomy and severely affects patients' quality of life. The mitochondrial impairment in corpus cavernosum smooth muscle cells (CCSMCs) may be an important pathological mechanism of CNI-ED. Previous studies have shown that transplantation of human adipose derived stem cells (ADSC) can alleviate CNI-ED in a rat model. However, little is known about the effect of human umbilical cord mesenchymal stem cells (hUC-MSC) on CNI-ED. It remains unclear whether hUC-MSC can ameliorate mitochondrial damage in CCSMCs. In this study, we aimed to investigate the impacts of hUC-MSC on the mitochondrial mass and function of CCSMCs, as well as elucidate its underlying molecular mechanism.</p><p><strong>Methods: </strong>The CNI-ED rat model was established by bilaterally crushing cavernous nerves. Subsequently, hUC-MSC were transplanted into the cavernosum and ADSC were injected as a positive control group. Erectile function evaluation and histological detection were performed 4 weeks after cell transplantation. In vitro, CCSMCs underwent hypoxia and were then co-cultured with ADSC or hUC-MSC using a transwell system. The mitochondrial mass and function, as well as signaling pathways, were investigated. To explore the role of the SIRT1/PGC-1α/TFAM pathway in regulating mitochondrial biogenesis of CCSMCs, we knocked down SIRT1 by siRNA.</p><p><strong>Results: </strong>The administration of hUC-MSC significantly improved erectile function of CNI-ED rats and reduced the ratio of collagen to smooth muscle. Specifically, hUC-MSC treatment restored mitochondrial mass and function in CCSMCs injured by CNI or hypoxia, and inhibited the apoptosis of CCSMCs. Mechanistically, the application of hUC-MSC activated SIRT1/PGC-1α/TFAM pathway both in rat penile tissues and CCSMCs. In addition, knockdown of SIRT1 in CCSMCs abolished the protective effects of hUC-MSC on mitochondrial mass and function, while leading to an increase in cellular apoptosis.</p><p><strong>Conclusions: </strong>hUC-MSC contribute to the recovery of erectile function in CNI-ED rats by restoring mitochondrial mass and function of CCSMCs through the SIRT1/PGC-1α/TFAM pathway. Our present study offers new insights into the role and molecular mechanisms of hUC-MSC in regulating mitochondrial homeostasis, thereby facilitating the restoration of the erectile function in CNI-ED.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"8"},"PeriodicalIF":4.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative stress and dysregulated long noncoding RNAs in the pathogenesis of Parkinson's disease.","authors":"Jialu Wang, Meitong Liu, Jiuhan Zhao, Pan Hu, Lianbo Gao, Shen Tian, Jin Zhang, Huayan Liu, Xiaoxue Xu, Zhenwei He","doi":"10.1186/s40659-025-00585-7","DOIUrl":"10.1186/s40659-025-00585-7","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive age-related neurodegenerative disease whose annual incidence is increasing as populations continue to age. Although its pathogenesis has not been fully elucidated, oxidative stress has been shown to play an important role in promoting the occurrence and development of the disease. Long noncoding RNAs (lncRNAs), which are more than 200 nucleotides in length, are also involved in the pathogenesis of PD at the transcriptional level via epigenetic regulation, or at the post-transcriptional level by participating in physiological processes, including aggregation of the α-synuclein, mitochondrial dysfunction, oxidative stress, calcium stabilization, and neuroinflammation. LncRNAs and oxidative stress are correlated during neurodegenerative processes: oxidative stress affects the expression of multiple lncRNAs, while lncRNAs regulate many genes involved in oxidative stress responses. Oxidative stress and lncRNAs also affect other processes associated with neurodegeneration, including mitochondrial dysfunction and increased neuroinflammation that lead to neuronal death. Therefore, modulating the levels of specific lncRNAs may alleviate pathological oxidative damage and have neuroprotective effects. This review discusses the general mechanisms of oxidative stress, pathological mechanism underlying the role of oxidative stress in the pathogenesis of PD, and teases out the mechanisms through which lncRNAs regulate oxidative stress during PD pathogenesis, as well as identifies the possible neuroprotective mechanisms of lncRNAs. Reviewing published studies will help us further understand the mechanisms underlying the role of lncRNAs in the oxidative stress process in PD and to identify potential therapeutic strategies for PD.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"7"},"PeriodicalIF":4.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11770960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluoride-induced testicular and ovarian toxicity: evidence from animal studies.","authors":"Seyedeh Fahimeh Talebi, Mohammad Seify, Ramji Kumar Bhandari, Hamed Shoorei, Shahram Dabiri Oskuei","doi":"10.1186/s40659-025-00586-6","DOIUrl":"10.1186/s40659-025-00586-6","url":null,"abstract":"<p><p>Fluoride (F), as a natural element found in a wide range of sources such as water and certain foods, has been proven to be beneficial in preventing dental caries, but concerns have been raised regarding its potential deleterious effects on overall health. Sodium fluoride (NaF), another form of F, has the ability to accumulate in reproductive organs and interfere with hormonal regulation and oxidative stress pathways, contributing to reproductive toxicity. While the exact mechanisms of F-induced reproductive toxicity are not fully understood, this review aims to elucidate the mechanisms involved in testicular and ovarian injury. In males, F exposure at different doses has been associated with reduced testis weight, reduced sperm quality in terms of count, motility, and viability, as well as abnormal sperm morphology and disruption of seminiferous tubules by altering hormone levels (especially testosterone), impairing spermatogenesis, and inducing oxidative stress and zinc deficiency. Similarly, administration of F can impact female reproductive health by affecting ovarian function, hormone levels, oocyte quality, and the regularity of the estrous cycle. However, the impact of F exposure on LH, FSH, and GnRH levels is controversial between males and females. In both males and females, F exerts its adverse effects by triggering apoptosis, autophagy, inflammation, mitochondrial dysfunction, reduction in ATP synthesis, and modulation of important genes involved in steroidogenesis. Furthermore, genetic susceptibility and individual variations in F metabolism may contribute to different responses to fluoride exposure.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"6"},"PeriodicalIF":4.3,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11762501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure of Apis mellifera (Hymenoptera: Apidae) colonies to imidacloprid impairs larval development, promotes oxidative stress in pupae, and induces changes in the midgut of adult bees.","authors":"Daiani Rodrigues Moreira, Tuan Henrique Smielevski de Souza, Douglas Galhardo, Cinthia Leão Figueira, Samara Calvi Baulli, Breno Gabriel da Silva, Francieli das Chagas, José Washington Santos Oliveira, Jean Samel Rocha, Angélica de Souza Khatlab, Eliane Gasparino, Vagner de Alencar Arnaut de Toledo, Adriana Aparecida Sinópolis Gigliolli, Maria Claudia Colla Ruvolo-Takasusuki","doi":"10.1186/s40659-024-00571-5","DOIUrl":"10.1186/s40659-024-00571-5","url":null,"abstract":"<p><p>Bees are essential pollinators that contribute to maintaining biodiversity and increasing agricultural production. However, by foraging on agricultural crops, bees may become contaminated with compounds used for pest control. In this study, we exposed bee (Apis mellifera L.) colonies to the insecticide imidacloprid (IMD) under field conditions to assess the occurrence of oxidative stress in larvae and pupae and investigate morphological changes in the fat body and midgut of larvae and midgut of adult bees. The apiary area was divided into three groups: control, commercial formulation containing IMD (Evidence^® 700WG) (IMD_CF), and IMD active ingredient (Sigma-Aldrich) (IMD_AI). Treatment groups were fed syrup containing 1 µg L^-1 IMD, whereas the control group was fed syrup only. Compared with the control, larvae exposed to IMD_CF or IMD_AI for 42 days exhibited morphological changes in the external body, midgut, and fat body. The midgut of adult bees contaminated with IMD_CF showed only structural remnants of the peritrophic membrane and absence of regenerative cell nests. Oxidative stress analyses revealed that IMD_CF-exposed larvae had higher nitrite and carbonylated protein contents and lower catalase and superoxide dismutase activity than control individuals. In pupae, IMD_AI decreased catalase activity while increasing superoxide dismutase activity. These findings indicate that IMD has the potential to significantly impact the development of bees and their colonies by disrupting vital organs responsible for normal physiological functioning and overall activities of individuals. Oxidative stress, which was detected at different stages of bee development, may induce lipid, protein, and DNA oxidation, leading to cell death.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"5"},"PeriodicalIF":4.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142999822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maraviroc/cisplatin combination inhibits gastric cancer tumoroid growth and improves mice survival.","authors":"Bárbara Mora-Lagos, María Elena Reyes, Lorena Lobos-Gonzalez, Matías Del Campo, Kurt Buchegger, Louise Zanella, Ismael Riquelme, Carmen Gloria Ili, Priscilla Brebi","doi":"10.1186/s40659-024-00581-3","DOIUrl":"10.1186/s40659-024-00581-3","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) is a significant cancer-related cause of death worldwide. GC's most used chemotherapeutic regimen is based on platinum drugs such as cisplatin (CDDP). However, CDDP chemoresistance reduces the survival rate of advanced GC. The immune C-C chemokine receptor type 5 (CCR5) have been proposed as a pivotal factor in cancer progression since its blockade has been linked with antineoplastic effects on tumor cell proliferation; nevertheless, its role in the chemoresistance of GC has not been elucidated. This study aimed to determine the effects induced by the CCR5 using Maraviroc (MVC), a highly selective CCR5 antagonist, on CDDP-resistant AGS cells (AGS R-CDDP), tumoroids (3D tumor spheroids), and animal models.</p><p><strong>Results: </strong>The combined CDDP and MVC treatment reduced cell viability and inhibited tumoroid formation in AGS R-CDDP cells. The effects of the MVC/CDDP combination on apoptosis and cell cycle progression were correlated with the increase in CDDP (dose-dependent). The mRNA levels of C-C Motif Chemokine Ligand 5 (CCL5), the main ligand for CCR5, decreased significantly in cells treated with the MVC/CDDP combination. MVC in the MVC/CDDP combination improved the survival rate and biochemical parameters of CDDP-treated mice by reducing the side effects of CDDP alone.</p><p><strong>Conclusions: </strong>This finding suggests that MVC/CDDP combination could be a potential complementary therapy for GC.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"4"},"PeriodicalIF":4.3,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142999837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein palmitoylation is involved in regulating mouse sperm motility via the signals of calcium, protein tyrosine phosphorylation and reactive oxygen species.","authors":"Yuping Xiong, Chenchen Yi, Haixia Zheng, Ya Ni, Yamei Xue, Kun Li","doi":"10.1186/s40659-024-00580-4","DOIUrl":"10.1186/s40659-024-00580-4","url":null,"abstract":"<p><strong>Background: </strong>Protein palmitoylation, a critical posttranslational modification, plays an indispensable role in various cellular processes, including the regulation of protein stability, mediation of membrane fusion, facilitation of intracellular protein trafficking, and participation in cellular signaling pathways. It is also implicated in the pathogenesis of diseases, such as cancer, neurological disorders, inflammation, metabolic disorders, infections, and neurodegenerative diseases. However, its regulatory effects on sperm physiology, particularly motility, remain unclear. This study aimed to elucidate the mechanism by which protein palmitoylation governs sperm motility.</p><p><strong>Methods: </strong>Protein palmitoylation in situ in mouse sperm was observed using innovative click chemistry. Sperm motility and motion parameters were evaluated using a computer-assisted sperm analyzer (CASA) after treatment with 2-bromopalmitic acid (2BP), a specific inhibitor of protein palmitoylation. Protein palmitoylation levels were confirmed by the acyl-biotin exchange (ABE) method. The interplay between protein palmitoylation, protein tyrosine phosphorylation, and intracellular calcium was investigated using Western blotting, ABE method, and fluorescent probes. The regulation of reactive oxygen species was also examined using fluorescent probes.</p><p><strong>Results: </strong>Localized patterns and dynamics of protein palmitoylation in distinct sperm regions were revealed, including the midpiece, post-acrosomal region, acrosome, and head. Alterations in protein palmitoylation in sperm were observed under in vitro physiological conditions. Treatment with 2BP significantly affected sperm motility and motion parameters. The study revealed interactions between protein palmitoylation, including heat shock protein 90, and protein kinase A/protein kinase C-associated protein tyrosine phosphorylation and intracellular calcium. Additionally, protein palmitoylation was found to be involved in reactive oxygen species regulation.</p><p><strong>Conclusions: </strong>Protein palmitoylation regulates sperm motility through calcium signaling, protein tyrosine phosphorylation, and reactive oxygen species. This study revealed the characteristics of protein palmitoylation in sperm and its role in regulating sperm motility, thereby providing novel insights into the causes of asthenozoospermia associated with sperm motility in humans.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"58 1","pages":"3"},"PeriodicalIF":4.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11734517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}