Biochemical and biophysical research communications最新文献_第5页

PINK1 link mitochondria-ER contacts controls deposition of intramuscular fat in pigs

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-21 DOI: 10.1016/j.bbrc.2025.151672

Jiaxin Cao , Nana Li , Ruolan Huang, Fengjuan Jia, Ziyi He, Wenlong Han, Wenzhang Liu, Songqiao Li, Weiye Wang, Weiyuan Ren, Bo Xia

{"title":"PINK1 link mitochondria-ER contacts controls deposition of intramuscular fat in pigs","authors":"Jiaxin Cao , Nana Li , Ruolan Huang, Fengjuan Jia, Ziyi He, Wenlong Han, Wenzhang Liu, Songqiao Li, Weiye Wang, Weiyuan Ren, Bo Xia","doi":"10.1016/j.bbrc.2025.151672","DOIUrl":"10.1016/j.bbrc.2025.151672","url":null,"abstract":"<div><div>Intramuscular fat (IMF) is a key determinant of meat quality in pigs, influencing characteristics such as tenderness, flavor, and marbling. The regulation of IMF deposition involves complex metabolic processes, with mitochondrial function playing a central role. PTEN-induced kinase 1 (PINK1), a protein involved in mitophagy and mitochondrial quality control, has recently been implicated in regulating fat deposition, although its role in IMF deposition in pigs remains unclear. This study investigates how PINK1 regulates IMF deposition by modulating mitochondrial-endoplasmic reticulum (ER) interactions. We utilized single-cell RNA sequencing to demonstrate that PINK1 is predominantly expressed in fibro-adipogenic progenitors (FAPs) and adipocytes, and its expression is negatively correlated with IMF content in multiple pig breeds. Knockdown of PINK1 in vivo led to increased intramuscular triglyceride content and enhanced adipogenic differentiation in primary porcine IMF cells. Additionally, PINK1 depletion resulted in impaired mitochondrial respiration, increased mitochondrial biogenesis, and disruption of mitochondria-ER contacts, further suggesting that PINK1 mediated of mitochondrial function and communication between mitochondria and ER is essential for controlling lipid deposition. These findings provide novel insights into the molecular mechanisms governing IMF accumulation and highlight PINK1 as a potential target for manipulating fat deposition in both agricultural and biomedical contexts.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151672"},"PeriodicalIF":2.5,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143698087","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

Antibody-induced TREM2 ectodomain shedding inhibits TREM2 signaling in macrophage

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-21 DOI: 10.1016/j.bbrc.2025.151674

Wenxing Li , Hui Jin , Yating Xu

引用次数: 0

Liquiritigenin protects against cadmium-induced testis damage in mice by inhibiting apoptosis and activating androgen receptor

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-21 DOI: 10.1016/j.bbrc.2025.151642

Siyu Yuan , Jun Guo , Bijun Yang , Aolin Xiao Huang , Shuqi Hu , Yingcan Li , Jingxuan Chen , Bin Yuan , Jing Yang

{"title":"Liquiritigenin protects against cadmium-induced testis damage in mice by inhibiting apoptosis and activating androgen receptor","authors":"Siyu Yuan , Jun Guo , Bijun Yang , Aolin Xiao Huang , Shuqi Hu , Yingcan Li , Jingxuan Chen , Bin Yuan , Jing Yang","doi":"10.1016/j.bbrc.2025.151642","DOIUrl":"10.1016/j.bbrc.2025.151642","url":null,"abstract":"<div><div>Cadmium (Cd) is a prevalent contaminant in both dietary and drinking water sources, posing harm to multiple tissues and disrupting reproductive function. Recent evidence indicates that natural products derived from plants may offer a mitigating Cd-induced tissue damage. However, the protective role of Liquiritigenin (LQ) and its underlying mechanism remain unclear. The present study was to investigate the protective effect of LQ against short-term, low-dose Cd-induced multi-organ damage. Notably, Cd exposure had no significant impact on body or tissue weight but did induce damage to the heart, liver, lungs, kidneys and testes of mice, while also reducing sperm quality. These adverse effects were reversed by LQ treatment, suggesting that LQ alleviates Cd toxicity. Mechanistically, LQ inhibited testicular apoptosis by modulating the protein levels of Bad, Caspase-3, Bax, Bcl-2, and NF-κB. Furthermore, molecular docking and molecular dynamics simulations provided insights into the interaction between LQ and the androgen receptor (AR). Further studies indicate that LQ increases AR level and further prevent testicular damage. Collectively, these findings support the potential of LQ in preventing Cd-induced tissue damage, particularly in the context of reproductive toxicity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151642"},"PeriodicalIF":2.5,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679415","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

In silico maturation of DNA aptamer against the prostate-specific antigen (PSA) and kinetic analysis

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-20 DOI: 10.1016/j.bbrc.2025.151638

Chi-Ping Huang , Wen-Pin Hu , Wei Yang , Zheng-Jie Lee , Wen-Yih Chen

{"title":"In silico maturation of DNA aptamer against the prostate-specific antigen (PSA) and kinetic analysis","authors":"Chi-Ping Huang , Wen-Pin Hu , Wei Yang , Zheng-Jie Lee , Wen-Yih Chen","doi":"10.1016/j.bbrc.2025.151638","DOIUrl":"10.1016/j.bbrc.2025.151638","url":null,"abstract":"<div><div>The detection of the prostate-specific antigen (PSA) serves as a critical marker for the diagnosis and follow-up of prostate cancer. DNA aptamers targeting PSA have been successfully screened using the systematic evolution of ligands by exponential enrichment (SELEX) technique, complemented by in silico maturation processes. In this study, we aim to optimize a truncated aptamer, denoted as TA87, through computational methods and to analyze potential aptamer candidates in the aptamer-PSA interactions. The PSA antibody, aptamer ΔPSap4#5, and an identified but unpublished aptamer, PSAG221, were evaluated in quartz crystal microbalance (QCM) experiments alongside aptamers derived from TA87. The Tanimoto similarity score and the ZDOCK program, coupled with the ZRANK scoring function, were adopted to assess the secondary structure of single-point mutants of TA87 and their binding interactions with PSA, respectively. Detailed analyses of the aptamer-protein complexes were conducted using molecular dynamics (MD) simulations. Mutations TA87M24 and TA87M49, along with PSAG221 and TA87, showed superior ZDOCK scores compared to ΔPSap4#5. MD simulations further suggested that PSAG221 aptamer might offer enhanced binding to PSA over ΔPSap4#5. The affinity constant (<em>K</em><sub><em>D</em></sub>) values for the antibody, ΔPSap4#5, PSAG221, TA87, TA87M24, and TA87M49 with PSA were determined through QCM measurements to be 0.35, 0.33, 0.35, 0.56, 0.45, and 0.51 μM<sup>−1</sup>, respectively. The experimental results showed that the truncated aptamers, TA87, and the two mutations, TA87M24 and TA87M49, did not demonstrate superior PSA binding affinity. Aptamer PSAG221 demonstrated performance comparable to that of the antibody, although slightly inferior to ΔPSap4#5. The aptamer PSAG221 reported in this study could be an alternative probe for developing future PSA aptasensor platforms.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151638"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679414","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

Role of bile acid-dependent Takeda G-coupled protein receptor 5 (TGR5) in regulating AMPK expression in human podocytes

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-20 DOI: 10.1016/j.bbrc.2025.151671

Patrycja Rachubik, Klaudia Grochowalska, Irena Audzeyenka, Dorota Rogacka, Agnieszka Piwkowska

{"title":"Role of bile acid-dependent Takeda G-coupled protein receptor 5 (TGR5) in regulating AMPK expression in human podocytes","authors":"Patrycja Rachubik, Klaudia Grochowalska, Irena Audzeyenka, Dorota Rogacka, Agnieszka Piwkowska","doi":"10.1016/j.bbrc.2025.151671","DOIUrl":"10.1016/j.bbrc.2025.151671","url":null,"abstract":"<div><div>Bile acids affect podocyte function by stimulating membrane-bound Takeda G protein-coupled receptor 5 (TGR5), the activity of which is linked to the regulation of glucose and lipid metabolism. In podocytes, adenosine monophosphate-dependent protein kinase (AMPK) is critical for maintaining energy balance, suggesting that the bile acid-dependent stimulation of TGR5 may impact AMPK activity to regulate metabolic processes in podocytes. Despite the beneficial effect of TGR5 activation on AMPK activity in podocytes that are exposed to hyperglycemic conditions, the effect of TGR5 signaling on AMPKα expression and phosphorylation state under control conditions have not been studied in podocytes. Our studies confirmed TGR5 expression in podocytes at both the mRNA and protein levels. Moreover, TGR5 inhibition decreased the protein expression of both AMPKα1 and AMPKα2 isoforms, which correlated with significantly lower levels of AMPKα phosphorylation at Thr172 in podocytes. Additionally, the immunofluorescent staining of podocytes with pharmacologically inhibited TGR5 activity were characterized by a lower mean intensity of the AMPKα fluorescence signal. TGR5 stimulation decreased the mRNA expression of AMPKα1 and AMPKα2 but did not change the degree of AMPKα phosphorylation at Thr172. These data suggest that TGR5 inactivation significantly downregulates AMPK activity. This may shed new light on the bile acid-dependent regulation of glucose and lipid metabolism in podocytes, especially under pathological conditions.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151671"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704397","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

The dilemma of nuclear mechanical forces in DNA damage and repair

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-20 DOI: 10.1016/j.bbrc.2025.151639

Iqra Ali , Fangning Xu , Qin Peng , Juhui Qiu

{"title":"The dilemma of nuclear mechanical forces in DNA damage and repair","authors":"Iqra Ali , Fangning Xu , Qin Peng , Juhui Qiu","doi":"10.1016/j.bbrc.2025.151639","DOIUrl":"10.1016/j.bbrc.2025.151639","url":null,"abstract":"<div><div>Genomic stability, encompassing DNA damage and repair mechanisms, plays a pivotal role in the onset of diseases and the aging process. The stability of DNA is intricately linked to the chemical and mechanical forces exerted on chromatin, particularly within lamina-associated domains (LADs). Mechanical stress can induce DNA damage through the deformation and rupture of the nuclear envelope, leading to DNA bending and cleavage. However, DNA can evade such mechanical stress-induced damage by relocating away from the nuclear membrane, a process facilitated by the depletion of H3K9me3-marked heterochromatin and its cleavage from the lamina. When DNA double-stranded breaks occur, they prompt the rapid recruitment of Lamin B1 and the deposition of H3K9me3. Despite these insights, the precise mechanisms underlying DNA damage and repair under mechanical stress remain unclear. In this review, we explore the interplay between mechanical forces and the nuclear envelope in the context of DNA damage, elucidate the molecular pathways through which DNA escapes force-induced damage, and discuss the corresponding repair strategies involving the nuclear cytoskeleton. By summarizing the mechanisms of force-induced DNA damage and repair, we aim to underscore the potential for developing targeted therapeutic strategies to bolster genomic stability and alleviate the impacts of aging and disease.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"758 ","pages":"Article 151639"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143683850","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

Long-term aerobic exercise enhances liver health: miRNA regulation and oxidative stress alleviation 长期有氧运动增强肝脏健康：miRNA调控与氧化应激缓解

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-20 DOI: 10.1016/j.bbrc.2025.151677

Chen-Kai Zhang , Zhuang-Zhi Wang , Fang-Hui Li

{"title":"Long-term aerobic exercise enhances liver health: miRNA regulation and oxidative stress alleviation","authors":"Chen-Kai Zhang , Zhuang-Zhi Wang , Fang-Hui Li","doi":"10.1016/j.bbrc.2025.151677","DOIUrl":"10.1016/j.bbrc.2025.151677","url":null,"abstract":"<div><div>This study aims to investigate the effects of long-term aerobic exercise on liver health in aging rats. As age increases, the continuous accumulation of endogenous reactive oxygen species (ROS) damages hepatocytes, leading to liver function decline and the development of diseases such as cirrhosis and liver cancer. Using an 18-month-old rat model, we implemented an eight-month aerobic exercise regimen to systematically evaluate its hepatoprotective effects. The results showed that aerobic exercise effectively reduced oxidative stress and inflammation levels in liver tissue, decreased the expression of cell cycle regulator P53 and inflammatory regulator NF-κB protein, upregulated NRF2 protein expression, improved mitochondrial function, and inhibited the progression of ferroptosis. These beneficial effects were achieved through the upregulation of miR-21 and miR-224 expression induced by exercise. These microRNAs inhibit the translation of MAP2K3 and MAPK14, thereby suppressing the activation of the P38 MAPK pathway. We further found that inhibiting P38 MAPK can enhance cellular antioxidant and anti-inflammatory capabilities, reversing hepatocyte damage caused by hydrogen peroxide. These results demonstrate that long-term aerobic exercise can reprogram aging-related oxidative stress and metabolic pathology by regulating miRNAs and the P38 MAPK pathway, thereby helping to prevent age-related liver diseases.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151677"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143696120","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

Net charge driven recruitment of supercharged GFP mutants into FUS droplets

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-20 DOI: 10.1016/j.bbrc.2025.151661

Kiyoto Kamagata , Yuxing Hong , Trishit Banerjee , Hiroto Takahashi , Eriko Mano

引用次数: 0

A liver-specific mouse model for MYO5B-associated cholestasis reveals a toxic gain-of-function as underlying disease mechanism

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-20 DOI: 10.1016/j.bbrc.2025.151669

Hui-Yu She , Yi-Ling Qiu , Jia-Yan Feng , Ye Cheng , Hao Chi , Sven C.D. van IJzendoorn , Qing-He Xing , Jian-She Wang

{"title":"A liver-specific mouse model for MYO5B-associated cholestasis reveals a toxic gain-of-function as underlying disease mechanism","authors":"Hui-Yu She , Yi-Ling Qiu , Jia-Yan Feng , Ye Cheng , Hao Chi , Sven C.D. van IJzendoorn , Qing-He Xing , Jian-She Wang","doi":"10.1016/j.bbrc.2025.151669","DOIUrl":"10.1016/j.bbrc.2025.151669","url":null,"abstract":"<div><div>Myosin Vb (MYO5B) deficiency, referring to the loss of protein expression or function, causes microvillus inclusion disease (MVID) and/or progressive familial intrahepatic cholestasis-type 10 (PFIC10) in humans. MYO5B plays a role in intracellular trafficking, but the mechanisms by which it contributes to cholestasis are not understood. The aim of this study was to generate a liver-specific mouse model and investigate the mechanism of MYO5B-associated cholestasis. In this study, we generated a liver-specific <em>Myo5b</em> cKO mice via CRISPR/Cas9 genome editing in conjunction with albumin-cre recombinase. Cholestatic stress was induced by dietary-administration of cholic acid (CA) or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). To investigate the frequently recurring <em>MYO5B</em> variant (c.2470C > T/p.(Arg824Cys)), adenoviral vectors encoding either the missense variant or blank control sequence were delivered to wild-type and <em>Myo5b</em> cKO mice through tail-vein injection. Serum and liver tissues were harvested from all mice for biochemical and histological analysis. Our findings indicated that loss of Myo5b expression did not cause cholestatic liver disease and did not augment CA or DDC feeding-induced cholestatic stress. By contrast, expression of the <em>MYO5B</em> c.2470C > T/p. (Arg824Cys) variant induced cholestasis, evidenced by elevated levels of serum alanine aminotransferase, alkaline phosphatase and bilirubin, mild hepatocellular injury, and altered bile salt export pump (Bsep) localization, resembling that observed in human PFIC10. In summary, we have developed a mouse model of MYO5B-associated cholestasis. The expression of the MYO5B-p. (Arg824Cys) variant but not the loss of Myo5b expression caused cholestasis, indicating a toxic gain-of-function as underlying disease mechanism.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"758 ","pages":"Article 151669"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143684429","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

Formononetin prevents intestinal injury caused by radiotherapy in colorectal cancer mice via the Keap1-Nrf2 signaling pathway

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-03-20 DOI: 10.1016/j.bbrc.2025.151676

Rongjun Tang , Lidan Zhang , Jun Lou , Weixing Mo , Linfang Zhao , Lingdi Li , Ke Zhang , Qingqing Yu

{"title":"Formononetin prevents intestinal injury caused by radiotherapy in colorectal cancer mice via the Keap1-Nrf2 signaling pathway","authors":"Rongjun Tang , Lidan Zhang , Jun Lou , Weixing Mo , Linfang Zhao , Lingdi Li , Ke Zhang , Qingqing Yu","doi":"10.1016/j.bbrc.2025.151676","DOIUrl":"10.1016/j.bbrc.2025.151676","url":null,"abstract":"<div><div>Radiation-induced intestinal injury (RIII) is a serious complication of radiation therapy. Formononetin (FT) is a methoxy isoflavone with anti-tumor and anti-oxidant properties. This study explored whether FT reduces ROS by activating the Keap1/Nrf2 pathway and thereby protecting against RIII. 30 BABL/C mice were used to construct a colorectal cancer model with CT26 cells and validated the model on day 7. Then, the cancer model mice were divided into 3 groups on day 14 (model control, model, and model + FT) with administration of FT or saline and radiated them on day 21. All samples were collected on day 28. Mechanical intestinal barrier assessed via intestinal absorption function, HE staining, and Claudin-1, Occludin, ZO-1 expression. Apoptosis was measured by TUNEL and cleaved-caspase 3, angiogenesis by CD31, and oxidative stress by NO and ROS levels. Keap1, Nrf2 (cytoplasm) and Nrf2 (nucleus) expression were measured by Western blot. FT treatment enhanced absorption and reduced damage and apoptosis in intestinal tissue. During FT treatment, inhibition of NO and ROS leads to suppression of oxidative stress and promotion of CD31 expression promotes angiogenesis. FT upregulated the expression of nuclear Nrf2 and reduced cytoplasmic Keap1 and Nrf2. FT strengthens mechanical barrier and decreases oxidative stress in intestinal tissue, providing radiation injury protection. Its anti-radiation effect may be through Keap1/Nrf2 pathway activation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"761 ","pages":"Article 151676"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143760956","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