Pub Date : 2025-03-05DOI: 10.1016/j.bbrc.2025.151531
Lu Peng , Zilan Wang , Qing Sun , Chang Cao , Lianxin Li , Feiyang Zhang , Gang Chen , Jiyuan Bu , Zhong Wang , Haiying Li
Intracerebral hemorrhage (ICH) is a severe form of stroke with high rates of mortality and morbidity. Neuronal loss following ICH is a critical factor influencing patient outcomes. Emerging evidence suggests that microglial phagocytic activity is enhanced after ICH, yet its role in neuronal loss remains unclear. In this study, we observed microglia engulfing viable neurons, characterized by high NeuN signals or intact nuclear morphology, in the perihematomal region of a murine autologous blood injection ICH model. This phenomenon was also observed in an in vitro ICH model, where microglia engulfed neurons in a neuron-microglia co-culture system treated with oxyhemoglobin. Furthermore, we found that oxyhemoglobin exposure induced phosphatidylserine (PS) externalization in non-apoptotic (PI-) neurons and led to a downregulation of the PS flippase ATP11C. Notably, lentivirus-mediated overexpression of ATP11C in neurons specifically prevented the ICH-induced decline in ATP11C levels and inhibited microglial engulfment of neurons. Furthermore, ATP11C overexpression significantly improved neurological outcomes in the mouse ICH model. These findings offer new insights into the mechanisms of neuronal loss after ICH, positioning ATP11C as a promising therapeutic target for attenuating brain injury by regulating PS externalization in neurons.
{"title":"ATP11C as a key regulator of neuronal loss following intracerebral hemorrhage in mice","authors":"Lu Peng , Zilan Wang , Qing Sun , Chang Cao , Lianxin Li , Feiyang Zhang , Gang Chen , Jiyuan Bu , Zhong Wang , Haiying Li","doi":"10.1016/j.bbrc.2025.151531","DOIUrl":"10.1016/j.bbrc.2025.151531","url":null,"abstract":"<div><div>Intracerebral hemorrhage (ICH) is a severe form of stroke with high rates of mortality and morbidity. Neuronal loss following ICH is a critical factor influencing patient outcomes. Emerging evidence suggests that microglial phagocytic activity is enhanced after ICH, yet its role in neuronal loss remains unclear. In this study, we observed microglia engulfing viable neurons, characterized by high NeuN signals or intact nuclear morphology, in the perihematomal region of a murine autologous blood injection ICH model. This phenomenon was also observed in an in vitro ICH model, where microglia engulfed neurons in a neuron-microglia co-culture system treated with oxyhemoglobin. Furthermore, we found that oxyhemoglobin exposure induced phosphatidylserine (PS) externalization in non-apoptotic (PI-) neurons and led to a downregulation of the PS flippase ATP11C. Notably, lentivirus-mediated overexpression of ATP11C in neurons specifically prevented the ICH-induced decline in ATP11C levels and inhibited microglial engulfment of neurons. Furthermore, ATP11C overexpression significantly improved neurological outcomes in the mouse ICH model. These findings offer new insights into the mechanisms of neuronal loss after ICH, positioning ATP11C as a promising therapeutic target for attenuating brain injury by regulating PS externalization in neurons.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"756 ","pages":"Article 151531"},"PeriodicalIF":2.5,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143611465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-05DOI: 10.1016/j.bbrc.2025.151584
Jinyang Zhai , Runxi Fu , Shangjian Luo , Xiaoman Liu , Yang Xie , Kejing Cao , Wensong Ge , Yingwei Chen
Background
Ulcerative colitis (UC) is a chronic inflammatory disease linked to early-onset colorectal cancer and metabolic abnormalities. While intestinal lactate disturbances are observed in UC, the role of lactate and lactylation in its pathogenesis remains unclear. The lack of specific biomarkers reflecting these processes limits understanding of their biological significance.
Methods
UC subtypes were classified using ConsensusClusterPlus and NMF based on LRGs. Immune infiltration was assessed with ssGSEA, xCell, and CIBERSORT. WGCNA identified subtype-specific gene modules, and Lasso regression pinpointed hub genes. Single-cell analysis determined cellular localization, while WB and IHC validated findings in clinical, mouse, and cell models. Prognostic machine learning models evaluated the clinical significance of these results.
Results
LRGs distinguished UC patients from controls and stratified them into high and low immune infiltration groups. MSN and MAPRE1, strongly linked to UC, showed elevated expression in vitro and in vivo. They aid in diagnosing UC and UC-associated colorectal cancer and serve as predictors of UC severity and response to immunosuppressants.
Conclusion
Using high-throughput transcriptomic data, we identified hub LRGs and highlighted the role of lactate-mediated lactylation in UC. MSN and MAPRE1 were confirmed to be upregulated in an inflammatory environment, underscoring their potential for personalized UC diagnosis and treatment.
{"title":"Lactylation-related molecular subtyping reveals the immune heterogeneity and clinical characteristics in ulcerative colitis","authors":"Jinyang Zhai , Runxi Fu , Shangjian Luo , Xiaoman Liu , Yang Xie , Kejing Cao , Wensong Ge , Yingwei Chen","doi":"10.1016/j.bbrc.2025.151584","DOIUrl":"10.1016/j.bbrc.2025.151584","url":null,"abstract":"<div><h3>Background</h3><div>Ulcerative colitis (UC) is a chronic inflammatory disease linked to early-onset colorectal cancer and metabolic abnormalities. While intestinal lactate disturbances are observed in UC, the role of lactate and lactylation in its pathogenesis remains unclear. The lack of specific biomarkers reflecting these processes limits understanding of their biological significance.</div></div><div><h3>Methods</h3><div>UC subtypes were classified using ConsensusClusterPlus and NMF based on LRGs. Immune infiltration was assessed with ssGSEA, xCell, and CIBERSORT. WGCNA identified subtype-specific gene modules, and Lasso regression pinpointed hub genes. Single-cell analysis determined cellular localization, while WB and IHC validated findings in clinical, mouse, and cell models. Prognostic machine learning models evaluated the clinical significance of these results.</div></div><div><h3>Results</h3><div>LRGs distinguished UC patients from controls and stratified them into high and low immune infiltration groups. MSN and MAPRE1, strongly linked to UC, showed elevated expression <em>in vitro</em> and <em>in vivo</em>. They aid in diagnosing UC and UC-associated colorectal cancer and serve as predictors of UC severity and response to immunosuppressants.</div></div><div><h3>Conclusion</h3><div>Using high-throughput transcriptomic data, we identified hub LRGs and highlighted the role of lactate-mediated lactylation in UC. MSN and MAPRE1 were confirmed to be upregulated in an inflammatory environment, underscoring their potential for personalized UC diagnosis and treatment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"756 ","pages":"Article 151584"},"PeriodicalIF":2.5,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143611464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-04DOI: 10.1016/j.bbrc.2025.151585
Kaori Ito , Jahidul Islam , Kota Sakurai , Saeka Koyama , Ayumi Matsuo , Kunihiro Okano , Ryota Hirakawa , Mutsumi Furukawa , Tomonori Nochi
The development and maintenance of a balanced microbiota is crucial for human health. Milk contains immune factors that not only protect offspring from infectious diseases but also play an important role in promoting the development and maintenance of the microbiota. However, the persisting effects of milk-derived immune factors on the maintenance of the microbiota after weaning have not been carefully examined. In this study, a cross-fostering model was employed using immunocompetent (IC) and immunodeficient (ID) mice in which one-half of the pups born from two dams were replaced. As a result, breast milk from the IC dam (IC milk) affected the development of the microbiota during lactation and maintained it even after weaning in the large intestine of the ID pups. The large intestinal microbiota of ID pups raised on IC milk remained similar to that of normal IC pups. Under normal conditions, the genus Mucispirillum was closely associated with other bacteria, forming a diverse bacterial community in the large intestine. In the small intestine, there were no differences in the microbiota before weaning, regardless of whether IC or ID milk was consumed. By contrast, significant differences were observed in the small intestinal microbiota between IC and ID mice after weaning; however, this was dependent on the immune-related characteristics of offspring (rather than milk-derived immune factors). These results indicate that breast milk plays an important role in the large (not small) intestine of offspring to create and maintain a diverse microbiota with a balanced bacterial network even after weaning.
{"title":"Breast milk stabilizes bacterial communities in the large intestine even after weaning","authors":"Kaori Ito , Jahidul Islam , Kota Sakurai , Saeka Koyama , Ayumi Matsuo , Kunihiro Okano , Ryota Hirakawa , Mutsumi Furukawa , Tomonori Nochi","doi":"10.1016/j.bbrc.2025.151585","DOIUrl":"10.1016/j.bbrc.2025.151585","url":null,"abstract":"<div><div>The development and maintenance of a balanced microbiota is crucial for human health. Milk contains immune factors that not only protect offspring from infectious diseases but also play an important role in promoting the development and maintenance of the microbiota. However, the persisting effects of milk-derived immune factors on the maintenance of the microbiota after weaning have not been carefully examined. In this study, a cross-fostering model was employed using immunocompetent (IC) and immunodeficient (ID) mice in which one-half of the pups born from two dams were replaced. As a result, breast milk from the IC dam (IC milk) affected the development of the microbiota during lactation and maintained it even after weaning in the large intestine of the ID pups. The large intestinal microbiota of ID pups raised on IC milk remained similar to that of normal IC pups. Under normal conditions, the genus <em>Mucispirillum</em> was closely associated with other bacteria, forming a diverse bacterial community in the large intestine. In the small intestine, there were no differences in the microbiota before weaning, regardless of whether IC or ID milk was consumed. By contrast, significant differences were observed in the small intestinal microbiota between IC and ID mice after weaning; however, this was dependent on the immune-related characteristics of offspring (rather than milk-derived immune factors). These results indicate that breast milk plays an important role in the large (not small) intestine of offspring to create and maintain a diverse microbiota with a balanced bacterial network even after weaning.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"756 ","pages":"Article 151585"},"PeriodicalIF":2.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143579046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic stress is one of the potential causes of the progression of metabolic syndrome (MS). Chronic stress decreases the release of Sirtuin-6 (SIRT6), which regulates MS by controlling glucose, insulin, lipids, and hypertension. Vagus nerve stimulation (VNS) activates SIRT6 via the cholinergic anti-inflammatory pathway (CAP). However, the effectiveness of VNS therapy for treating MS induced by chronic stress has not yet been studied. In this study, we first validated a rat model of chronic unpredictable stress (CUS) and assessed the characteristic features of MS. The CUS rats were exposed to random stressors daily for 8 weeks. The stress response was then confirmed by behavioral alteration and elevated serum corticosterone levels in rats, as measured by various behavioral tests and an ELISA kit, respectively. The MS characteristics in CUS rats were assessed using measurements of fasting blood glucose (FBG), systolic blood pressure (SBP), lipid indices, insulin levels, and HOMA-IR. The stressed animals demonstrated a rise in FBG, SBP, and insulin along with altered lipid indices. After CUS, the rats were treated with VNS (6 Hz, 1.0 ms, 6 V, for 40 min × 14 days, alternatively), and their metabolic activity and vagal flow were assessed. Moreover, SIRT6 and AMP-activated protein kinase (AMPK) expression in rats was also assessed by immunohistochemistry and mRNA expression of liver and pancreatic tissue. SIRT6 and AMPK expression was decreased in CUS animals. Interestingly, VNS treatment attenuated CUS induced MS-associated parameters. These results indicate that VNS may be a beneficial complementary and non-pharmacological method for managing CUS-associated MS.
{"title":"Stimulation of auricular vagus nerve ameliorates chronic stress induced metabolic syndrome via activation of Sirtuin-6","authors":"Arjun Singh Kaushik , Vipul Agarwal , Neeraj Kumar , Mujeeba Rehman , Rishabh Chaudhary , Siddhi Srivastava , Sukriti Srivastava , Vikas Mishra","doi":"10.1016/j.bbrc.2025.151567","DOIUrl":"10.1016/j.bbrc.2025.151567","url":null,"abstract":"<div><div>Chronic stress is one of the potential causes of the progression of metabolic syndrome (MS). Chronic stress decreases the release of Sirtuin-6 (SIRT6), which regulates MS by controlling glucose, insulin, lipids, and hypertension. Vagus nerve stimulation (VNS) activates SIRT6 via the cholinergic anti-inflammatory pathway (CAP). However, the effectiveness of VNS therapy for treating MS induced by chronic stress has not yet been studied. In this study, we first validated a rat model of chronic unpredictable stress (CUS) and assessed the characteristic features of MS. The CUS rats were exposed to random stressors daily for 8 weeks. The stress response was then confirmed by behavioral alteration and elevated serum corticosterone levels in rats, as measured by various behavioral tests and an ELISA kit, respectively. The MS characteristics in CUS rats were assessed using measurements of fasting blood glucose (FBG), systolic blood pressure (SBP), lipid indices, insulin levels, and HOMA-IR. The stressed animals demonstrated a rise in FBG, SBP, and insulin along with altered lipid indices. After CUS, the rats were treated with VNS (6 Hz, 1.0 ms, 6 V, for 40 min × 14 days, alternatively), and their metabolic activity and vagal flow were assessed. Moreover, SIRT6 and AMP-activated protein kinase (AMPK) expression in rats was also assessed by immunohistochemistry and mRNA expression of liver and pancreatic tissue. SIRT6 and AMPK expression was decreased in CUS animals. Interestingly, VNS treatment attenuated CUS induced MS-associated parameters. These results indicate that VNS may be a beneficial complementary and non-pharmacological method for managing CUS-associated MS.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"756 ","pages":"Article 151567"},"PeriodicalIF":2.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143563404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-04DOI: 10.1016/j.bbrc.2025.151583
Lulu Wang , Tingting Hu , Ruxuan Zhang , Yingzhou Shi , Yan Wang , Qiuhui Xuan , Xinli Zhou
Obesity, a significant risk factor for cardiovascular diseases, induces cardiolipin (CL) remodeling. Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1), a key enzyme in CL metabolism, drives mitochondrial impairment and cardiac dysfunction in obesity. Although glucagon-like peptide-1 receptor agonists (GLP-1RAs) exhibit cardioprotective properties, their effects on ALCAT1-mediated CL remodeling in obesity-induced myocardial injury remain unclear. Male C57BL/6 mice fed a high-fat diet (HFD) or standard diet (STD) for 12 weeks received liraglutide (200 μg/kg/day) or saline during the last 4 weeks. Cardiac function was evaluated by echocardiography; CL content was quantified using LC-MS, and myocardial alterations were assessed through histological and protein analyses. In HFD-fed mice, cardiac lipid accumulation, left ventricular hypertrophy, and myocardial collagen deposition were observed. Additionally, these mice exhibited reduced CL content, altered CL aliphatic chain composition, and upregulated ALCAT1 expression. In contrast, liraglutide treatment significantly increased total CL content, modified CL acyl chain composition, and downregulated ALCAT1 expression. Mechanistically, liraglutide activated the PI3K/AKT pathway via GLP-1 receptor signaling, attenuated oxidative stress markers (3-nitrotyrosine, Rac1 activation), and improved mitochondrial dynamics by reducing DRP1-mediated fission. These results demonstrate that liraglutide mitigates obesity-induced cardiac dysfunction by suppressing ALCAT1-driven CL remodeling, enhancing mitochondrial homeostasis, and reducing oxidative stress. This study elucidates the cardioprotective mechanisms of liraglutide and highlights its therapeutic potential for obesity-related cardiomyopathy.
{"title":"Liraglutide modulates ALCAT1-Mediated cardiolipin remodeling to improve cardiac function in obese mice","authors":"Lulu Wang , Tingting Hu , Ruxuan Zhang , Yingzhou Shi , Yan Wang , Qiuhui Xuan , Xinli Zhou","doi":"10.1016/j.bbrc.2025.151583","DOIUrl":"10.1016/j.bbrc.2025.151583","url":null,"abstract":"<div><div>Obesity, a significant risk factor for cardiovascular diseases, induces cardiolipin (CL) remodeling. Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1), a key enzyme in CL metabolism, drives mitochondrial impairment and cardiac dysfunction in obesity. Although glucagon-like peptide-1 receptor agonists (GLP-1RAs) exhibit cardioprotective properties, their effects on ALCAT1-mediated CL remodeling in obesity-induced myocardial injury remain unclear. Male C57BL/6 mice fed a high-fat diet (HFD) or standard diet (STD) for 12 weeks received liraglutide (200 μg/kg/day) or saline during the last 4 weeks. Cardiac function was evaluated by echocardiography; CL content was quantified using LC-MS, and myocardial alterations were assessed through histological and protein analyses. In HFD-fed mice, cardiac lipid accumulation, left ventricular hypertrophy, and myocardial collagen deposition were observed. Additionally, these mice exhibited reduced CL content, altered CL aliphatic chain composition, and upregulated ALCAT1 expression. In contrast, liraglutide treatment significantly increased total CL content, modified CL acyl chain composition, and downregulated ALCAT1 expression. Mechanistically, liraglutide activated the PI3K/AKT pathway via GLP-1 receptor signaling, attenuated oxidative stress markers (3-nitrotyrosine, Rac1 activation), and improved mitochondrial dynamics by reducing DRP1-mediated fission. These results demonstrate that liraglutide mitigates obesity-induced cardiac dysfunction by suppressing ALCAT1-driven CL remodeling, enhancing mitochondrial homeostasis, and reducing oxidative stress. This study elucidates the cardioprotective mechanisms of liraglutide and highlights its therapeutic potential for obesity-related cardiomyopathy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"756 ","pages":"Article 151583"},"PeriodicalIF":2.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143563400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Reactive oxygen species (ROS) have been confirmed closely associated with the pathological process of periodontitis, but the specific roles played by different ROS types are still to be investigated. Catalase (CAT) and Superoxide dismutase (SOD) specifically eliminate hydrogen peroxide (H2O2) and superoxide anion (O2•-), respectively. We for the first time compare the effects and mechanisms of CAT and SOD in protecting periodontal ligament cells (PDLCs) against oxidative damage, reducing the expression of macrophage inflammatory factors, and preserving the osteogenic differentiation function of PDLCs by modulating the inflammatory environment.
Methods
CAT or SOD in combination with lipopolysaccharide (LPS) were added to the culture medium of RAW 264.7 and PDLCs. The intracellular ROS level, lipid peroxidation and DNA damage were observed by confocal microscope. Inflammation levels were assessed by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. A co-culture system of macrophages and PDLCs was established, and the osteogenic differentiation of PDLCs was evaluated by alkaline phosphatase staining, alizarin red S staining, RT-qPCR and Western blot. Finally, differentially expressed genes (DEGs) in CAT and SOD were detected by RNA sequencing and the biological functions and signaling pathways involved were analyzed.
Results
CAT or SOD can effectively inhibit intracellular ROS levels, lipid peroxidation and DNA damage, as well as increase the levels of antioxidative molecules and decrease the levels of inflammatory factors. SOD increased the levels of antioxidative molecules more strongly, while CAT reduced inflammatory factors more effectively. The RNA sequencing results indicate that CAT exhibits stronger inhibitory effects on inflammation-related signaling pathways, which could account for the observed differences.
Conclusions
In this study, we observed differential antioxidant and anti-inflammatory effects between CAT and SOD, which may be associated with CAT's better inhibition of the activation of inflammatory pathways. Our study will provide scientific references for the future development of highly selective ROS- scavenging antioxidant drugs.
{"title":"Comparison of the effects between catalase and superoxide dismutase on regulating macrophage inflammatory response and protecting osteogenic function of periodontal ligament cells","authors":"Bijun Zhu, Lutong Song, Mengchen Li, Mingyue Cheng, Wenyue Tang, Leiying Miao","doi":"10.1016/j.bbrc.2025.151523","DOIUrl":"10.1016/j.bbrc.2025.151523","url":null,"abstract":"<div><h3>Background</h3><div>Reactive oxygen species (ROS) have been confirmed closely associated with the pathological process of periodontitis, but the specific roles played by different ROS types are still to be investigated. Catalase (CAT) and Superoxide dismutase (SOD) specifically eliminate hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and superoxide anion (O<sub>2</sub><sup>•-</sup>), respectively. We for the first time compare the effects and mechanisms of CAT and SOD in protecting periodontal ligament cells (PDLCs) against oxidative damage, reducing the expression of macrophage inflammatory factors, and preserving the osteogenic differentiation function of PDLCs by modulating the inflammatory environment.</div></div><div><h3>Methods</h3><div>CAT or SOD in combination with lipopolysaccharide (LPS) were added to the culture medium of RAW 264.7 and PDLCs. The intracellular ROS level, lipid peroxidation and DNA damage were observed by confocal microscope. Inflammation levels were assessed by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. A co-culture system of macrophages and PDLCs was established, and the osteogenic differentiation of PDLCs was evaluated by alkaline phosphatase staining, alizarin red S staining, RT-qPCR and Western blot. Finally, differentially expressed genes (DEGs) in CAT and SOD were detected by RNA sequencing and the biological functions and signaling pathways involved were analyzed.</div></div><div><h3>Results</h3><div>CAT or SOD can effectively inhibit intracellular ROS levels, lipid peroxidation and DNA damage, as well as increase the levels of antioxidative molecules and decrease the levels of inflammatory factors. SOD increased the levels of antioxidative molecules more strongly, while CAT reduced inflammatory factors more effectively. The RNA sequencing results indicate that CAT exhibits stronger inhibitory effects on inflammation-related signaling pathways, which could account for the observed differences.</div></div><div><h3>Conclusions</h3><div>In this study, we observed differential antioxidant and anti-inflammatory effects between CAT and SOD, which may be associated with CAT's better inhibition of the activation of inflammatory pathways. Our study will provide scientific references for the future development of highly selective ROS- scavenging antioxidant drugs.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"756 ","pages":"Article 151523"},"PeriodicalIF":2.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143579044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-03DOI: 10.1016/j.bbrc.2025.151581
Takashi Furukawa , Yasunobu Miyake , Hiroshi Ito , Atsushi Ogata , Hajime Maeyama , Yukiko Nakahara , Fumitaka Yoshioka , Jun Masuoka , Hiroki Yoshida , Tatsuya Abe
Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. Cytokines such as interleukins 17 and 23 (IL-17, IL-23) have been involved in stroke. IL-27 is a member of the IL-12 family that consists of IL-27p28 and Epstein-Barr virus-induced gene 3 (EBI3), having anti-inflammatory properties and regulating T cell polarization and cytokine production. However, whether IL-27 plays an important role in the acute stage of brain ischemia remains unclear. In the acute stage, IL-27 was upregulated after intracerebral ischemia in wild-type mice while mice lacking IL-27 showed decreased infarction area and suppressed inflammatory cytokines. These findings suggest that IL-27 may be involved in cerebral ischemia and could be a potential therapeutic target for mitigating inflammation and avoiding increasing the initial damage in cerebral ischemia.
{"title":"Interleukin-27 deletion has neuroprotective effects in the acute ischemic stage of cerebral infarction","authors":"Takashi Furukawa , Yasunobu Miyake , Hiroshi Ito , Atsushi Ogata , Hajime Maeyama , Yukiko Nakahara , Fumitaka Yoshioka , Jun Masuoka , Hiroki Yoshida , Tatsuya Abe","doi":"10.1016/j.bbrc.2025.151581","DOIUrl":"10.1016/j.bbrc.2025.151581","url":null,"abstract":"<div><div>Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. Cytokines such as interleukins 17 and 23 (IL-17, IL-23) have been involved in stroke. IL-27 is a member of the IL-12 family that consists of IL-27p28 and Epstein-Barr virus-induced gene 3 (EBI3), having anti-inflammatory properties and regulating T cell polarization and cytokine production. However, whether IL-27 plays an important role in the acute stage of brain ischemia remains unclear. In the acute stage, IL-27 was upregulated after intracerebral ischemia in wild-type mice while mice lacking IL-27 showed decreased infarction area and suppressed inflammatory cytokines. These findings suggest that IL-27 may be involved in cerebral ischemia and could be a potential therapeutic target for mitigating inflammation and avoiding increasing the initial damage in cerebral ischemia.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"755 ","pages":"Article 151581"},"PeriodicalIF":2.5,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-03DOI: 10.1016/j.bbrc.2025.151582
Aisheng Zhan , Keke Zhong , Kejing Zhang
Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron degenerative disorder. Protein aggregates induce various forms of neuronal dysfunction and represent pathological hallmarks in ALS patients. Reducing protein aggregates could be a promising therapeutic strategy for ALS. While most studies have focused on cytoplasmic protein homeostasis, neurons adaptively reduce aggregates across subcellular compartments during stress through previously uncharacterized mechanisms. Here, we summarize novel compartment-specific proteostatic mechanisms: (1) the ERAD/RESET pathways, (2) HSPs-mediated nuclear sequestration, (3) mitochondrial aggregate import (MAGIC), (4) neurite-localized UPS/autophagosome and NMP, and (5) exopher-mediated extracellular disposal. These mechanisms collectively ensure cellular stress adaptation and provide novel therapeutic targets for ALS treatment.
{"title":"Novel subcellular regulatory mechanisms of protein homeostasis and its implications in amyotrophic lateral sclerosis","authors":"Aisheng Zhan , Keke Zhong , Kejing Zhang","doi":"10.1016/j.bbrc.2025.151582","DOIUrl":"10.1016/j.bbrc.2025.151582","url":null,"abstract":"<div><div>Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron degenerative disorder. Protein aggregates induce various forms of neuronal dysfunction and represent pathological hallmarks in ALS patients. Reducing protein aggregates could be a promising therapeutic strategy for ALS. While most studies have focused on cytoplasmic protein homeostasis, neurons adaptively reduce aggregates across subcellular compartments during stress through previously uncharacterized mechanisms. Here, we summarize novel compartment-specific proteostatic mechanisms: (1) the ERAD/RESET pathways, (2) HSPs-mediated nuclear sequestration, (3) mitochondrial aggregate import (MAGIC), (4) neurite-localized UPS/autophagosome and NMP, and (5) exopher-mediated extracellular disposal. These mechanisms collectively ensure cellular stress adaptation and provide novel therapeutic targets for ALS treatment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"756 ","pages":"Article 151582"},"PeriodicalIF":2.5,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143579047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-03DOI: 10.1016/j.bbrc.2025.151580
Yang Yu , Conglei Wang , Xiao Zhang , Jianhe Wang , Mengting Li , Tianqi Song , Dan Liang , Gang Feng
Drought stress severely affects wheat yield, and Whirly (WHY) transcription factors (TFs) are essential in modulating plant tolerance to abiotic stresses. In this study, we identified six WHY members in the wheat whole-genome database, categorized into Group I and Group II, with three homologous WHY genes in each group. From the four selected drought-responsive candidate genes with upregulated expression, we focused on TaWHY2-6A, which was significantly upregulated under drought stress. Under drought conditions, TaWHY2-6A transgenic Arabidopsis exhibited significantly higher chlorophyll content and better growth status compared to wild-type (WT) plants, indicating that TaWHY2-6A enhances drought resistance in transgenic Arabidopsis. In contrast, wheat lines with silenced-TaWHY2-6A exhibited a more severe wilting phenotype following drought treatment, accompanied by elevated levels of H2O2 and O2.-, and reduced antioxidant enzyme activity. These findings suggest that the wheat TaWHY2-6A gene positively regulates drought resistance under drought stress. This research provides a theoretical basis and valuable genetic resources for drought-resistance breeding in wheat.
{"title":"The transcription factor TaWHY2-6A acts as a positive regulator in response to drought tolerance in transgenic plants","authors":"Yang Yu , Conglei Wang , Xiao Zhang , Jianhe Wang , Mengting Li , Tianqi Song , Dan Liang , Gang Feng","doi":"10.1016/j.bbrc.2025.151580","DOIUrl":"10.1016/j.bbrc.2025.151580","url":null,"abstract":"<div><div>Drought stress severely affects wheat yield, and Whirly (WHY) transcription factors (TFs) are essential in modulating plant tolerance to abiotic stresses. In this study, we identified six WHY members in the wheat whole-genome database, categorized into Group I and Group II, with three homologous <em>WHY</em> genes in each group. From the four selected drought-responsive candidate genes with upregulated expression, we focused on <em>TaWHY2-6A</em>, which was significantly upregulated under drought stress. Under drought conditions, <em>TaWHY2-6A</em> transgenic <em>Arabidopsis</em> exhibited significantly higher chlorophyll content and better growth status compared to wild-type (WT) plants, indicating that TaWHY2-6A enhances drought resistance in transgenic <em>Arabidopsis</em>. In contrast, wheat lines with silenced-<em>TaWHY2-6A</em> exhibited a more severe wilting phenotype following drought treatment, accompanied by elevated levels of H<sub>2</sub>O<sub>2</sub> and O<sub>2</sub><sup>.-</sup>, and reduced antioxidant enzyme activity. These findings suggest that the wheat <em>TaWHY2-6A</em> gene positively regulates drought resistance under drought stress. This research provides a theoretical basis and valuable genetic resources for drought-resistance breeding in wheat.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"755 ","pages":"Article 151580"},"PeriodicalIF":2.5,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-03DOI: 10.1016/j.bbrc.2025.151549
Ben B. Wang , Pirjo M. Apaja
{"title":"Corrigendum to “ATG8 in single membranes: Fresh players of endocytosis and acidic organelle quality control in cancer, neurodegeneration, and inflammation” [Biochem. Biophys. Res. Commun. 749 (2025) 151384]","authors":"Ben B. Wang , Pirjo M. Apaja","doi":"10.1016/j.bbrc.2025.151549","DOIUrl":"10.1016/j.bbrc.2025.151549","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"755 ","pages":"Article 151549"},"PeriodicalIF":2.5,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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