Biochemical and biophysical research communications最新文献_第3页

Neutrophils suppress osteogenic differentiation of Gli1+ stem cells via neutrophil extracellular traps and contribute to bone loss in periodontitis 中性粒细胞通过中性粒细胞胞外捕获器抑制 Gli1+ 干细胞的成骨分化，导致牙周炎患者骨质流失。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150916

Xinyue Cai , Siyuan Fan , Bingdong Sui , Zilin Xuan , Xiaoyao Huang , Anqi Liu , Ji Chen , Hao Wang , Jiexi Liu , Haokun Xu , Chenxi Zheng , Hao Guo

{"title":"Neutrophils suppress osteogenic differentiation of Gli1+ stem cells via neutrophil extracellular traps and contribute to bone loss in periodontitis","authors":"Xinyue Cai , Siyuan Fan , Bingdong Sui , Zilin Xuan , Xiaoyao Huang , Anqi Liu , Ji Chen , Hao Wang , Jiexi Liu , Haokun Xu , Chenxi Zheng , Hao Guo","doi":"10.1016/j.bbrc.2024.150916","DOIUrl":"10.1016/j.bbrc.2024.150916","url":null,"abstract":"<div><div>Periodontitis is a severe and chronic oral inflammatory disease that leads to the progressive and irreversible destruction of periodontal tissues, ultimately resulting in tooth loss. Among the immune cell subtypes involved, neutrophils play a crucial role in the initiation and progression of periodontitis. Mesenchymal stem cells (MSCs) are essential components of periodontal tissue, contributing to tissue development, homeostasis, and regeneration. Recent studies have demonstrated that neutrophils significantly affect the function of MSCs by changing the inflammatory environment. However, the specific effects of neutrophils on periodontal MSCs during periodontitis remain unclear, highlighting a gap in our understanding of the disease mechanisms. In this study, we utilized the <em>Gli1-CreER</em><sup><em>T2</em></sup><em>;mT/mG</em> transgenic mouse model to specifically mark Gli1<sup>+</sup> cells, a critical and representative subset of MSCs in the periodontal tissues responsible for maintaining tissue homeostasis. We reveal that neutrophils inhibit the osteogenic differentiation of Gli1<sup>+</sup> cells and exacerbate alveolar bone destruction by secreting neutrophil extracellular traps (NETs), which induce endoplasmic reticulum stress in Gli1<sup>+</sup> cells. These findings highlight the pivotal impact of neutrophils on distinct subpopulations of periodontal MSCs in the pathogenesis of periodontitis, offering valuable insights into the underlying mechanisms of the disease and suggesting potential future therapeutic strategies aimed at modulating the interactions between neutrophils and MSCs.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567639","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}

引用次数: 0

Inhibition of ferroptosis attenuate lipopolysaccharide-induced early pregnancy loss by protecting against decidual damage of stromal cells 通过保护基质细胞免受蜕膜损伤，抑制铁变态反应可减轻脂多糖诱发的早期妊娠丢失。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150904

Yanmei Liu , Yaping Zhou , Binhe Hao , Zining Wu , Min Gao , Ling Liu , Qiang Xia , Kainan Zheng , Shuang Yang , Yaoting Tang , Ming Gong , Cun Feng , Honglu Diao , Yan Tan , Hongtao Zheng

{"title":"Inhibition of ferroptosis attenuate lipopolysaccharide-induced early pregnancy loss by protecting against decidual damage of stromal cells","authors":"Yanmei Liu , Yaping Zhou , Binhe Hao , Zining Wu , Min Gao , Ling Liu , Qiang Xia , Kainan Zheng , Shuang Yang , Yaoting Tang , Ming Gong , Cun Feng , Honglu Diao , Yan Tan , Hongtao Zheng","doi":"10.1016/j.bbrc.2024.150904","DOIUrl":"10.1016/j.bbrc.2024.150904","url":null,"abstract":"<div><div>Endometrial decidualization is critical for successful embryo implantation. Dysregulation of the immune microenvironment can disrupt normal decidualization processes, potentially resulting in early pregnancy loss. Ferroptosis, a form of cell death dependent on iron and lipid hydroperoxides, is closely associated with inflammation. In this study, we developed an inflammatory early pregnancy loss model to elucidate the mechanisms of decidual damage induced by lipopolysaccharide (LPS) and to assess whether ferroptosis contributes to LPS-induced early pregnancy loss. Through in vivo experiments, we observed that embryo implantation was significantly inhibited and endometrial decidualization was impaired during LPS-induced early pregnancy loss. LPS exposure resulted in abnormal mitochondrial morphology, reduced antioxidant capacity, accumulation of reactive oxygen species (ROS) and disruptions in iron metabolism during decidualization in mouse endometrial stromal cells (mESCs). The administration of ferroptosis inhibitors, specifically ferrostatin-1 (Fer-1) and deferoxamine (DFO), effectively reversed embryo loss and mitigated the decidual damage associated with LPS-induced early pregnancy loss. Fer-1 and DFO exhibited resistance to ferroptosis during decidualization by modulating the antioxidant system and iron metabolism in mESCs, respectively. Our findings indicate that the inhibition of ferroptosis can confer protective effects against decidual damage during LPS-induced early pregnancy loss in mice.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543396","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}

引用次数: 0

Empagliflozin reduces renal calcium oxalate deposition in hyperoxaluria rats induced with ethylene glycol-ammonium chloride Empagliflozin 可减少乙二醇氯化铵诱导的高草酸尿症大鼠肾脏草酸钙沉积。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150912

Yu Duan , Qing Wang , Xiaolong Chen , Guanyun Deng , Kunyuan Huang , Fa Sun , Jianguo Zhu , Kehua Jiang

{"title":"Empagliflozin reduces renal calcium oxalate deposition in hyperoxaluria rats induced with ethylene glycol-ammonium chloride","authors":"Yu Duan , Qing Wang , Xiaolong Chen , Guanyun Deng , Kunyuan Huang , Fa Sun , Jianguo Zhu , Kehua Jiang","doi":"10.1016/j.bbrc.2024.150912","DOIUrl":"10.1016/j.bbrc.2024.150912","url":null,"abstract":"<div><div>A retrospective study reported that empagliflozin reduced the risk of urinary stone events in patients with diabetes mellitus. To further investigate empagliflozin's potential, we conducted an animal experiment to determine whether empagliflozin can prevent renal stone formation in hyperoxaluria rats. Hyperoxaluria rat models were constructed by administrating 0.75 % ethylene glycol and 1 % ammonium chloride in water. The empagliflozin-treated rats were gauged with empagliflozin at different concentrations, and their body weight and blood sugar data were recorded. After 30 days of treatment, we obtained 24-h urine, kidney, and blood samples. The urine samples were subjected to component detection. Blood samples were prepared for component detection and cytokines detection. Renal samples were subjected to von Kossa staining, transmission electron microscopy, immunohistochemistry, and transcriptome sequencing analysis. Results showed that in empagliflozin-treated hyperoxaluria rats, renal crystal deposition and mitochondria injury, urinary concentration, and excretion of oxalate were significantly decreased. Additionally, plasma levels of VEGF, IL-2, IL-1β, and MCP-1 were decreased. Immunohistochemistry showed that renal expression of KIM-1, MCP-1 was significantly decreased in empagliflozin-treated hyperoxaluria rats. Transcriptome sequencing of renal tissue represented that 25 genes were down-regulated while 12 were up-regulated in empagliflozin-treated hyperoxaluria rats. These regulated genes were mainly enriched in fatty acid metabolism, insulin resistance, muscle contraction, bile secretion, and parathyroid metabolism. Our animal experiments found that empagliflozin could reduce urinary concentration and excretion of oxalate and inhibit renal inflammation, then abating renal calcium oxalate deposition in hyperoxaluria rats in a non-diabetic state.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567602","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}

引用次数: 0

Ovalbumin-induced food allergy suppression via regulatory T cell expansion mediated by a TNFR2 agonist in mice 在小鼠体内通过 TNFR2 激动剂介导的调节性 T 细胞扩增抑制卵清蛋白诱导的食物过敏。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150909

Masaki Inoue , Yuta Tsuji , Saya Shibata , Mei Okuda , Chihiro Najima , Honoka Yamasaki , Shin-ichi Tsunoda

{"title":"Ovalbumin-induced food allergy suppression via regulatory T cell expansion mediated by a TNFR2 agonist in mice","authors":"Masaki Inoue , Yuta Tsuji , Saya Shibata , Mei Okuda , Chihiro Najima , Honoka Yamasaki , Shin-ichi Tsunoda","doi":"10.1016/j.bbrc.2024.150909","DOIUrl":"10.1016/j.bbrc.2024.150909","url":null,"abstract":"<div><div>Food allergies represent a growing health concern worldwide, characterized by abnormal immune responses to specific dietary antigens. This condition is often associated with a dysregulation of immune tolerance, especially within the intestinal mucosa. Regulatory T cells (Tregs), a crucial subset of lymphocytes, play a central role in maintaining peripheral immune tolerance and are abundant in the intestinal lamina propria. Recent studies have highlighted Treg dysfunction in patients with food allergies, suggesting a potential connection between impaired Treg function and allergy onset. Therefore, strategies to adequately control and activate Tregs could offer new avenues for the prevention and treatment of food allergies. Our research focuses on targeting the regulatory molecule, tumor necrosis factor receptor type 2 (TNFR2), a key modulator of Treg function. We have developed a TNFR2 agonist, scR2agoTNF-Fc, characterized by high TNFR2-stimulating activity and enhanced blood retention <em>in vivo</em> for Treg expansion. In this study, we utilized an ovalbumin (OVA)-induced food allergy mouse model to verify the therapeutic potential of scR2agoTNF-Fc in modulating allergic responses and restoring immune balance. The results showed that scR2agoTNF-Fc promoted the expansion of Treg population <em>in vivo</em> in mice. In addition, scR2agoTNF-Fc reduced diarrhea caused by the food allergy. This was consistent with the molecular mechanisms of suppression of blood immunoglobulins and Th2 cells. Therefore, it was shown that quantitative and functional enhancement of Tregs by the TNFR2 agonist, scR2agoTNF-Fc, may be effective in treating food allergies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567640","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}

引用次数: 0

Flll32, a curcumin analog, improves adipose tissue thermogenesis 姜黄素类似物 Flll32 可改善脂肪组织的生热功能

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150919

Zeyu Guo , Enhui Chen , Xianghong Xie , Yanfang Guo , Minglong Zhang , Yinghan Zhu , Yiting Wang , Fude Fang , Li Yan , Xiaojun Liu

{"title":"Flll32, a curcumin analog, improves adipose tissue thermogenesis","authors":"Zeyu Guo , Enhui Chen , Xianghong Xie , Yanfang Guo , Minglong Zhang , Yinghan Zhu , Yiting Wang , Fude Fang , Li Yan , Xiaojun Liu","doi":"10.1016/j.bbrc.2024.150919","DOIUrl":"10.1016/j.bbrc.2024.150919","url":null,"abstract":"<div><div>Adipose tissue is a key regulator of systemic energy homeostasis and improving adipose tissue function provides a brand-new theoretical reference for the prevention and treatment of obesity. FLLL32, a curcumin analog, can hinder various carcinogenic processes, however, its role in adipose tissue has not been fully elucidated. In this study, we observed that FLLL32 treatment significantly improved cold intolerance and reduced white adipose tissue (WAT) adipocyte size in mice, but had no effect on body weight and adipose tissues weight. Furthermore, FLLL32 treatment upregulated the expression level of uncoupling protein 1 and downregulated the expression level of peroxisome proliferator-activated receptor gamma in adipose tissue. Additionally, FLLL32 promoted the mRNA level of transferrin receptor protein 1, a key iron transporter on the cell membrane, and the lipid peroxidation in inguinal WAT. Finally, FLLL32 significantly inhibited the differentiation and maturation of preadipocytes. In summary, our results demonstrated that FLLL32 plays a crucial role in regulating adipose tissue function.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560713","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}

引用次数: 0

Maternal immune activation induces neurodevelopmental impairments of adult offspring through alterations in tryptophane-kynurenine pathway in the placenta 母体免疫激活通过改变胎盘中的色氨酸-犬尿氨酸通路诱发成年后代的神经发育障碍

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150922

Masaya Hasegawa , Moe Niijima , Kazuo Kunisawa , Tomoaki Teshigawara , Hisayoshi Kubota , Suwako Fujigaki , Hidetsugu Fujigaki , Yasuko Yamamoto , Hyoung-Chun Kim , Kuniaki Saito , Toshitaka Nabeshima , Akihiro Mouri

{"title":"Maternal immune activation induces neurodevelopmental impairments of adult offspring through alterations in tryptophane-kynurenine pathway in the placenta","authors":"Masaya Hasegawa , Moe Niijima , Kazuo Kunisawa , Tomoaki Teshigawara , Hisayoshi Kubota , Suwako Fujigaki , Hidetsugu Fujigaki , Yasuko Yamamoto , Hyoung-Chun Kim , Kuniaki Saito , Toshitaka Nabeshima , Akihiro Mouri","doi":"10.1016/j.bbrc.2024.150922","DOIUrl":"10.1016/j.bbrc.2024.150922","url":null,"abstract":"<div><div>Maternal immune activation (MIA) is recognized as one of the significant environmental risk factors for neuropsychiatric disorders such as schizophrenia in adult offspring. However, the pathophysiological mechanisms remain unknown. The tryptophan (TRP)-kynurenine (KYN) pathway, influenced by inflammation, may be implicated in the pathophysiology of neuropsychiatric disorders. We investigated whether abnormal behaviors in adult offspring could be induced by MIA through alterations in the TRP-KYN pathway. MIA increased not only IL-6 expression in the placenta but also reactive oxygen species (ROS) levels in both the placenta and fetal brain and disrupted cortical layering in the fetal brain. We observed increased levels of 3-hydroxykynurenine (3-HK), a metabolite with oxidative stress properties, in both the placenta and fetal brain. In the knockout mice of kynurenine 3-monooxygenase (KMO), the enzyme responsible for 3-HK production, MIA failed to induce the abnormal behaviors in adult offspring. Notably, RO-618048, a KMO inhibitor that does not cross the blood-brain barrier (BBB), also blocked MIA-induced abnormal behaviors in adult offspring, reduced not only increased IL-6 expression in the placenta but also ROS levels in both the placenta and fetal brain, and prevented abnormal cortical development in the fetal brain. These findings suggest that MIA-induced abnormal behaviors in adult offspring may result from the increase in 3-HK levels through activation of KMO. Therefore, KMO is an attractive target for the prevention of neuropsychiatric disorders associated with MIA.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560714","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}

引用次数: 0

Unraveling the mechanism of the anticancer potential of emodin using 2D and spheroid models of A549 cells 利用 A549 细胞的二维和球形模型揭示大黄素的抗癌机制。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150908

Wannapa Sangseekew , Narittira Ornnork , Thiwaree Sornprachum , Jitnapa Sirirak , Kriengsak Lirdprapamongkol , Jutatip Boonsombat , Jisnuson Svasti , Siriporn Keeratichamroen

{"title":"Unraveling the mechanism of the anticancer potential of emodin using 2D and spheroid models of A549 cells","authors":"Wannapa Sangseekew , Narittira Ornnork , Thiwaree Sornprachum , Jitnapa Sirirak , Kriengsak Lirdprapamongkol , Jutatip Boonsombat , Jisnuson Svasti , Siriporn Keeratichamroen","doi":"10.1016/j.bbrc.2024.150908","DOIUrl":"10.1016/j.bbrc.2024.150908","url":null,"abstract":"<div><div>The increasing global cancer burden necessitates the development of new treatment options. Herbal medicine offers a viable alternative to conventional cancer treatments. Numerous studies have shown that 3-dimensional (3D) cell culture more accurately represents tumor characteristics <em>in vivo</em>. Therefore, this study utilized tumor spheroids to explore the therapeutic efficacy of emodin, a natural product-derived bioactive agent. We investigated differences in chemotherapeutic response between A549 cells cultured in 2D versus spheroids, assessing key factors influencing cancer progression, including apoptosis, cell proliferation, cell cycle, migration and invasion. The findings revealed that spheroid cells displayed increased resistance to emodin compared to cells cultured in 2D. Emodin exhibited a more pronounced cytostatic effect in 2D cells, while its cytotoxic effect was more prominent in spheroid cells. Moreover, emodin treatment diminished the migratory and invasive capabilities of the cells. Mechanistic investigations indicated that emodin triggered apoptosis in A549 cells <em>via</em> the mitochondrial apoptotic pathway. Emodin-treated cells exhibited a significant reduction in the phosphorylation of key cancer progression pathways, including JAK2, STAT3, FAK, and ERK, compared to untreated controls. Molecular docking analysis confirmed the interactions of emodin with JAK2 and FAK. These findings suggest that the JAK2/STAT3 and FAK/ERK signaling pathways may serve as critical drivers of the therapeutic effectiveness of emodin in A549 cells.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543400","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}

引用次数: 0

Urinary titin as an early biomarker of skeletal muscle proteolysis and atrophy in various catabolic conditions 尿液中的 titin 是在各种分解代谢条件下骨骼肌蛋白分解和萎缩的早期生物标志物。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150918

Mizusa Hyodo , Kazuhiro Nomura , Rie Tsutsumi , Yuna Izumi-Mishima , Hibiki Kawaguchi , Ayuka Kawakami , Kanako Hara , Yuki Suzuki , Taku Shirakawa , Kayo Osawa , Masafumi Matsuo , Hiroshi Sakaue

{"title":"Urinary titin as an early biomarker of skeletal muscle proteolysis and atrophy in various catabolic conditions","authors":"Mizusa Hyodo , Kazuhiro Nomura , Rie Tsutsumi , Yuna Izumi-Mishima , Hibiki Kawaguchi , Ayuka Kawakami , Kanako Hara , Yuki Suzuki , Taku Shirakawa , Kayo Osawa , Masafumi Matsuo , Hiroshi Sakaue","doi":"10.1016/j.bbrc.2024.150918","DOIUrl":"10.1016/j.bbrc.2024.150918","url":null,"abstract":"<div><div>Skeletal muscle atrophy impairs quality of life and increases the risk of disease, but current methods for assessment of muscle mass have several limitations. We here investigated the urinary concentration of a fragment of the muscle protein titin as a potential biomarker for the early detection of skeletal muscle atrophy. Four mouse models with different atrophy pathways were studied: those of cardiotoxin-induced acute muscle injury, cast-induced muscle immobilization, lipopolysaccharide-induced sepsis, and streptozotocin-induced diabetes. In all four models, urinary titin levels increased early, concurrent with or preceding upregulation of the atrophy-related genes for atrogin-1 and MuRF-1. The increase in the urinary titin concentration was thus associated with initial muscle damage and the onset of proteolysis, rather than with late-stage muscle wasting. Our findings suggest that urinary titin is a promising biomarker for detection of the onset of skeletal muscle catabolism and prediction of the subsequent development of atrophy in different catabolic states. Noninvasive measurement of urinary titin may therefore allow the earlier detection of skeletal muscle proteolysis compared with conventional techniques.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142563696","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}

引用次数: 0

Evaluation of the role of hepatic Gstm4 in diet-induced obesity and dyslipidemia 评估肝脏 Gstm4 在饮食诱发肥胖和血脂异常中的作用

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-28 DOI: 10.1016/j.bbrc.2024.150920

Liwei Hu, Delong Yuan, Qihan Zhu, Mengyue Wu, Meng Tie, Shaoxuan Song, Yali Chen, Yunzhi Yang, Anyuan He

{"title":"Evaluation of the role of hepatic Gstm4 in diet-induced obesity and dyslipidemia","authors":"Liwei Hu, Delong Yuan, Qihan Zhu, Mengyue Wu, Meng Tie, Shaoxuan Song, Yali Chen, Yunzhi Yang, Anyuan He","doi":"10.1016/j.bbrc.2024.150920","DOIUrl":"10.1016/j.bbrc.2024.150920","url":null,"abstract":"<div><div>Obesity and its related diseases continue to rise worldwide, necessitating further investigation to develop new therapeutic strategies. The dysregulation of redox homeostasis is tightly associated with metabolic diseases. Glutathione, an antioxidant, acts as a cofactor for antioxidant and detoxification enzymes such as glutathione S-transferases (GSTs)—a superfamily including Gstm4. So far, the physiological role of Gstm4 remains largely unknown. Human genetics is a powerful tool to discover novel therapeutic targets for metabolic diseases. The single nucleotide polymorphism rs650985, located within the sixth intron of the human gene Gstm4, was associated with plasma lipids, indicating that targeting Gstm4 might intervene in the progression of dyslipidemia. Furthermore, we found that Gstm4 is highly expressed in the liver and enriched in hepatocytes—the parenchymal cells of the liver. We established the mouse model with the hepatic deletion of Gstm4 and found that this mouse model did not present altered body weight, serum lipid profile, or liver fat content in the context of chow or high-fat high cholesterol diet feeding, indicating that hepatic Gstm4 is dispensable for diet-induced obesity and dyslipidemia. Further analysis revealed that hepatic deletion of Gstm4 upregulates the level of protein but not mRNA of Npc1l1—a critical protein mediating cholesterol uptake, suggesting that there might be a link between Gstm4 and lipid metabolic diseases in certain contexts.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142553928","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}

引用次数: 0

N-glycosylation negatively regulates the expression of tumor necrosis factor (TNF) in mouse macrophage N-糖基化负向调节小鼠巨噬细胞中肿瘤坏死因子（TNF）的表达。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-10-26 DOI: 10.1016/j.bbrc.2024.150897

Mai Murakami , Michio Onizawa , Naoto Abe , Tomoaki Mochimaru , Chikako Saito , Rie Hikichi , Takefumi Uemura , Masayuki Sekimata , Hiromasa Ohira

{"title":"N-glycosylation negatively regulates the expression of tumor necrosis factor (TNF) in mouse macrophage","authors":"Mai Murakami , Michio Onizawa , Naoto Abe , Tomoaki Mochimaru , Chikako Saito , Rie Hikichi , Takefumi Uemura , Masayuki Sekimata , Hiromasa Ohira","doi":"10.1016/j.bbrc.2024.150897","DOIUrl":"10.1016/j.bbrc.2024.150897","url":null,"abstract":"<div><div>Tumor necrosis factor alpha (TNF) is a potent inflammatory cytokine and is also involved in the pathogenesis of various diseases such as inflammatory bowel disease and rheumatoid arthritis. While the intracellular signal cascades of TNF stimulation have been extensively studied, the regulatory mechanism of TNF production is still largely unknown. In this study, we investigated the role of N-glycosylation of TNF in its production. First, an inducible-TNF expression model was established based on the newly created TNF-knockout cells where TNF expression is induced only by doxycycline. We further analyzed the effect of N-glycosylation by testing mutant TNF proteins in which a single amino acid of the putative glycosylation site was substituted with alanine. The resulting mutant TNF (N86A) exhibited enhanced protein expressions both in the cells and in cell culture supernatants while the level of TNF mRNA remained constant. Our results indicate that N-glycosylation suppresses the production of TNF.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142563616","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}

引用次数: 0