Acta biochimica et biophysica Sinica最新文献_第6页

Validation of six commercially available angiotensin II type 1 receptor antibodies. 六种市售血管紧张素II型1受体抗体的验证。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-01-08 DOI: 10.3724/abbs.2024199

Bingjie Li, Xi Zhang, Fei Sun, Xingzhong Zhang, Huirong Liu, Suli Zhang

引用次数: 0

MYB represses ζ-globin expression through upregulating ETO2. MYB通过上调ETO2抑制ζ-珠蛋白的表达。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-01-06 DOI: 10.3724/abbs.2024239

Zejun Dong, Yuhua Ye, Wei Zhang, Hualei Luo, Jialong Li, Qianqian Zhang, Xinhua Zhang, Xiang Guo, Xiangmin Xu

{"title":"MYB represses ζ-globin expression through upregulating ETO2.","authors":"Zejun Dong, Yuhua Ye, Wei Zhang, Hualei Luo, Jialong Li, Qianqian Zhang, Xinhua Zhang, Xiang Guo, Xiangmin Xu","doi":"10.3724/abbs.2024239","DOIUrl":"https://doi.org/10.3724/abbs.2024239","url":null,"abstract":"Reactivating the embryonic ζ-globin gene represents a potential therapeutic approach to ameliorate the severe clinical phenotype of α-thalassemia and sickle cell disease. The transcription factor MYB has been extensively proven to be a master regulator of the γ-globin gene, but its role in the regulation of ζ-globin remains incompletely understood. Here, we report a mechanistic study on the derepression of ζ-globin both in vivo and in vitro. We show that MYB depletion in mouse models and human hematopoietic stem cells leads to consistent and remarkable reactivation of ζ-globin. Furthermore, multiomics analysis and functional validation of MYB-knockout and wild-type cell lines reveal that ETO2 functions as a novel repressor of ζ-globin through coordination with NuRD nucleosome remodeling and the deacetylation complex to modulate histone deacetylation of ζ-globin. Additionally, we evaluate the clinical significance of these findings by knocking out ETO2 in primary CD34 + cells from nondeletional hemoglobin H patients, which results in a significant increase in ζ-globin expression. The RNA-seq data reveal that key erythroid genes are more co-regulated by Myb and Eto2 than by Myb and Klf1, highlighting a distinctly enhanced erythroid-specific transcriptional impact within the MYB-ETO2 regulatory axis. Compared with ETO2 knockout alone, codepletion of ETO2 and BCL11A did not significantly activate ζ-globin, suggesting that the MYB-ETO2 pathway primarily silences ζ-globin. Our study reveals a linear MYB-ETO2 signaling pathway crucial for ζ-globin repression and offers new targets for treating α-thalassemia and sickle cell disease.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Macrophage NLRP3-dependent IL-1β production contributes to aortic fibrosis in heart failure with preserved ejection fraction. 巨噬细胞nlrp3依赖性IL-1β的产生有助于保留射血分数的心力衰竭的主动脉纤维化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-27 DOI: 10.3724/abbs.2024238

Sheng Chen, Zhiqiang Lu

{"title":"Macrophage NLRP3-dependent IL-1β production contributes to aortic fibrosis in heart failure with preserved ejection fraction.","authors":"Sheng Chen, Zhiqiang Lu","doi":"10.3724/abbs.2024238","DOIUrl":"https://doi.org/10.3724/abbs.2024238","url":null,"abstract":"Fibrosis is the main pathological feature of aortic stiffness, which is a common extracardiac comorbidity of heart failure with preserved ejection fraction (HFpEF) and a contributor to left ventricular (LV) diastolic dysfunction. Systemic low-grade inflammation plays a crucial role in the pathogenesis of HFpEF and the development of vascular fibrosis. In this study, we investigate the inflammatory mechanism of aortic fibrosis in HFpEF using a novel mouse model. LV diastolic dysfunction with preserved ejection fraction and aortic fibrosis induced by a high-fat diet (HFD) combined with subcutaneous aldosterone infusion are utilized. The constructed model exhibits augmented macrophage recruitment and NLR family pyrin domain containing 3 (NLRP3)-dependent interleukin (IL)-1β production in fibrotic aortas. In addition, a bone marrow transplant is employed to induce macrophage-specific NLRP3 deficiency in the HFpEF mouse model. These mice show almost completely suppressed cleaved-caspase-1 and mature IL-1β protein expression in the aortas, indicating that macrophage NLRP3 inflammasome activation enhances the IL-1β overproduction in fibrotic aortas. Furthermore, we show that macrophage NLRP3 inflammasome inhibition improves aortic fibrosis and LV diastolic dysfunction. In conclusion, this study demonstrates the pivotal effect of macrophage NLRP3-dependent IL-1β production on aortic fibrosis and cardiac function in HFpEF, suggesting a potential target for HFpEF therapy.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Undaria pinnatifida extract attenuates combined allergic rhinitis and asthma syndrome by the modulation of epithelial cell dysfunction and oxidative stress. 裙带菜提取物通过调节上皮细胞功能障碍和氧化应激减轻合并变应性鼻炎和哮喘综合征。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-25 DOI: 10.3724/abbs.2024190

Zhen Nan Yu, Yan Jing Fan, Thi Van Nguyen, Chun Hua Piao, Byung-Hoo Lee, So-Young Lee, Hee Soon Shin, Tae-Geum Kim, Chang Ho Song, Ok Hee Chai

{"title":"Undaria pinnatifida extract attenuates combined allergic rhinitis and asthma syndrome by the modulation of epithelial cell dysfunction and oxidative stress.","authors":"Zhen Nan Yu, Yan Jing Fan, Thi Van Nguyen, Chun Hua Piao, Byung-Hoo Lee, So-Young Lee, Hee Soon Shin, Tae-Geum Kim, Chang Ho Song, Ok Hee Chai","doi":"10.3724/abbs.2024190","DOIUrl":"https://doi.org/10.3724/abbs.2024190","url":null,"abstract":"Undaria pinnatifida ( U. pinnatifida) has long been a part of the human diet and medicine. Although U. pinnatifida has been reported to have immunomodulatory, anti-inflammatory, anti-diabetic and antibacterial activities, its specific effect on patients with combined allergic rhinitis and asthma syndrome (CARAS) has not been clarified. In this study, the anti-allergic and anti-inflammatory effects of U. pinnatifida extract (UPE) are investigated in a mouse model of ovalbumin (OVA)-induced CARAS. The oral administration of UPE inhibits allergic responses by reducing OVA-specific immunoglobulin levels. As a result, the symptoms of early reactions are also improved. UPE inhibits the accumulation of inflammatory cells and attenuates the expression of Th2 cytokines in both nasal and bronchoalveolar lavage fluid. Furthermore, UPE treatment inhibits the NF-κB/MAPK signaling pathway in lung homogenates. Additionally, UPE prevents shedding of the nasal mucosal epithelium, protects the integrity of the epithelium, enhances the expression of E-cadherin at the junction of epithelial cells, and inhibits the degradation of ZO-1 and occludin in the airway epithelium. In addition, UPE ameliorates dysfunction of the nasal epithelial barrier by enhancing antioxidant properties and downregulating the expression of the inflammatory factor IL-33. These results suggest that UPE may treat CARAS by modulating epithelial cell dysfunction and oxidative stress.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Corrigendum to: TIPE1 suppresses the invasion and migration of breast cancer cells and inhibits epithelial-to-mesenchymal transition primarily via the ERK signaling pathway. 更正：TIPE1TIPE1 主要通过 ERK 信号通路抑制乳腺癌细胞的侵袭和迁移，并抑制上皮细胞向间质转化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-25 DOI: 10.3724/abbs.2024177

Shusheng Qiu, Wei Hu, Qiuhong Ma, Yi Zhao, Liang Li, Yu Ding

引用次数: 0

Novel FGF21 analogues through structure-based optimization for therapeutic development. 基于结构优化的新型FGF21类似物用于治疗开发。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-25 DOI: 10.3724/abbs.2024227

Yiqing Guo, Yuxuan Bao, Zhichao Chen, Zhiheng Rao, Yongde Luo, Sheng Ye, Si Liu

引用次数: 0

Types of cell death in diabetic cardiomyopathy: insights from animal models. 糖尿病性心肌病的细胞死亡类型：来自动物模型的见解

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-25 DOI: 10.3724/abbs.2024213

Hongjiao Xu, Zhuang Yu, Jun Zhu, Haoran Liu, Xiangyuan Chen, Jihong Jiang, Minmin Zhu, Jinbao Li

{"title":"Types of cell death in diabetic cardiomyopathy: insights from animal models.","authors":"Hongjiao Xu, Zhuang Yu, Jun Zhu, Haoran Liu, Xiangyuan Chen, Jihong Jiang, Minmin Zhu, Jinbao Li","doi":"10.3724/abbs.2024213","DOIUrl":"https://doi.org/10.3724/abbs.2024213","url":null,"abstract":"Approximately one-tenth of the global population is affected by diabetes mellitus, and its incidence continues to rise each year. In China, 1.4 million patients die from diabetes-related complications every year. Additionally, approximately 26% of patients with diabetes develop diabetic cardiomyopathy, with heart failure being one of the main causes of death in these patients. However, early detection of diabetic cardiomyopathy has proven to be difficult in a clinical setting; furthermore, there are limited guidelines and targeted means of prevention and treatment for this disease. In recent years, several studies have provided evidence for the occurrence of various forms of regulated cell death in diabetic myocardial cells, including apoptosis, necroptosis, ferroptosis, and cuproptosis, which are closely linked to the pathological progression of diabetic cardiomyopathy. Although most research on diabetic cardiomyopathy is currently in the animal trial phase, the inhibition of these regulatory cell death processes can limit or slow down the progression of diabetic cardiomyopathy. Therefore, this review discusses the appropriate animal experimental models currently available for diabetic cardiomyopathy and evaluates the roles of apoptosis, necroptosis, ferroptosis, and cuproptosis in diabetic cardiomyopathy. We hope to provide new methods and ideas for future research in diabetic cardiomyopathy.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Structure-based design of covalent nanobody binders for a thermostable green fluorescence protein. 耐热绿色荧光蛋白共价纳米体结合物的结构设计。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-24 DOI: 10.3724/abbs.2024233

Zhihao Yue, Yanfang Li, Hongmin Cai, Hebang Yao, Dianfan Li, Aimin Ni, Tingting Li

引用次数: 0

YTHDF2 influences hepatic fibrosis by regulating ferroptosis in hepatic stellate cells by mediating the expression of ACSL4 in an m ⁶A-dependent manner. YTHDF2通过介导ACSL4的表达，以m6a依赖的方式调节肝星状细胞的铁下垂，从而影响肝纤维化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-24 DOI: 10.3724/abbs.2024162

Wentao Liu, Yuan He, Kunlun Chen, Jianwen Ye, Long Yu, Chuang Zhou, Wenlong Zhai

{"title":"YTHDF2 influences hepatic fibrosis by regulating ferroptosis in hepatic stellate cells by mediating the expression of ACSL4 in an m 6A-dependent manner.","authors":"Wentao Liu, Yuan He, Kunlun Chen, Jianwen Ye, Long Yu, Chuang Zhou, Wenlong Zhai","doi":"10.3724/abbs.2024162","DOIUrl":"https://doi.org/10.3724/abbs.2024162","url":null,"abstract":"Hepatic fibrosis (HF) is an abnormal reparative response of the liver to chronic injury and is histologically reversible. In recent years, increasing interest has been given to changes in m 6A in liver disease. In this study, we explore the role of the m 6A-modified reading protein YTHDF2 in HF and its regulatory mechanism. The HF mouse model is generated through CCl 4 injection, and the cell model is via TGF-β stimulation. The liver tissues are subjected to hematoxylin-eosin, Masson, and α-SMA immunohistochemical staining. Reactive oxygen species (ROS) and iron levels are examined via relevant kits. Quantitative real-time PCR, immunofluorescence staining, and western blot analysis were conducted to measure the YTHDF2 and ACSL4 levels. RNA immunoprecipitation, methylated RNA immunoprecipitation, RNA pull-down, and polysome fractionation were performed to understand the regulatory mechanism by which YTHDF2 affects ACSL4. The results show that YTHDF2 is highly expressed after HF induction, and the inhibition of YTHDF2 reduces fibrosis as well as ROS and iron levels. In vitro, overexpression of YTHDF2 increases hepatic stellate cell activation, as well as ROS and iron levels, and this effect is blocked by the silencing of ACSL4. YTHDF2 acts as a regulator of ACSL4 expression and is involved in m 6A modification. In addition, in vivo experiments indicate that overexpression of ACSL4 reverses the attenuating effect of YTHDF2 interference on HFs. Therefore, YTHDF2 mediates the expression of the ferroptosis marker protein ACSL4 in an m 6A-dependent manner, thereby affecting HF.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Human umbilical cord mesenchymal stem cells enhance liver regeneration and decrease collagen content in fibrosis mice after partial hepatectomy by activating Wnt/β-catenin signaling. 人脐带间充质干细胞通过激活Wnt/β-catenin信号通路，促进肝部分切除后纤维化小鼠肝脏再生，降低胶原含量。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-12-24 DOI: 10.3724/abbs.2024207

Xuewei Li, Jinghui Feng, Haiqin Cheng, Ning Jin, Shanshan Jin, Zhizhen Liu, Jun Xu, Jun Xie

{"title":"Human umbilical cord mesenchymal stem cells enhance liver regeneration and decrease collagen content in fibrosis mice after partial hepatectomy by activating Wnt/β-catenin signaling.","authors":"Xuewei Li, Jinghui Feng, Haiqin Cheng, Ning Jin, Shanshan Jin, Zhizhen Liu, Jun Xu, Jun Xie","doi":"10.3724/abbs.2024207","DOIUrl":"https://doi.org/10.3724/abbs.2024207","url":null,"abstract":"Liver fibrosis is a critical stage in the progression of various chronic liver diseases to cirrhosis and liver cancer. Early inhibition of liver fibrosis is crucial for the treatment of liver disease. Hepatectomy, a common treatment for liver-related diseases, promotes liver regeneration. However, in the context of liver fibrosis, liver regeneration is hindered. Many studies have shown that mesenchymal stem cells (MSCs) can promote liver regeneration after partial hepatectomy (PH). However, there are few reports on the impact of MSC therapy on liver regeneration post-PH in the context of hepatic fibrosis. The objective of this study is to examine the impact of MSCs on liver regeneration following PH in the fibrotic liver and uncover the related molecular mechanisms. This study reveals that MSC therapy significantly enhances liver function and mitigates liver inflammation after PH in the context of hepatic fibrosis. MSCs also significantly promote liver regeneration and alleviate liver fibrosis. In addition, this study identifies the role of MSCs in promoting liver regeneration and alleviating liver fibrosis via the activation of Wnt/β-catenin signaling. The combination of MSCs with hepatectomy may offer a novel approach for the treatment of liver fibrotic diseases.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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