Acta histochemica最新文献

英文中文

Corrigendum to “Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model” [Acta Histochem. 127 (2025) 152280] “在肝脏特异性斑马鱼模型中诱导gankyrin过表达驱动肝癌发生”的更正[组织化学学报，127(2025)152280]。

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-19 DOI: 10.1016/j.acthis.2025.152281

Yuxi Sun , Zhiyuan Gong , Yueh-Min Lin , Jeng-Wei Lu

引用次数: 0

Advancing triple-negative breast cancer therapy: 3D in vitro models to unravel drug resistance mechanisms and tumor microenvironment interactions 推进三阴性乳腺癌治疗：3D体外模型揭示耐药机制和肿瘤微环境相互作用

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-16 DOI: 10.1016/j.acthis.2025.152282

Gomathy Baskar , Thirunavukkarasu Palaniyandi

Triple-negative breast cancer (TNBC) poses considerable clinical challenges due to its aggressive nature, early metastasis, and limited treatment options. The simplified 2D models and the physiological differences in animal models often result in inconsistent responses to anticancer drugs. To tackle these challenges, three-dimensional (3D) in vitro bioengineered models that accurately replicate the in vivo tumor microenvironment (TME) have been developed, offering a more reliable platform for preclinical drug testing. Recent advancements in cell culture techniques have facilitated the creation of 3D models derived from patient tissues and tumors, which effectively mimic the native tissue environment and exhibit drug sensitivity and cytotoxicity behaviors similar to those observed in vivo. It is increasingly acknowledged that the extracellular matrix and cellular diversity within the TME significantly influence the fate of cancer cells. Consequently, strategies to explore drug resistance mechanisms must account for both microenvironmental factors and genetic mutations. This review examines 3D in vitro model systems that integrate microenvironmental influences to investigate drug resistance mechanisms in breast cancer. We discussed various bioengineered models, including spheroid-based, biomaterial-based (such as polymeric scaffolds and hydrogels), patient-derived xenograft (PDX), 3D bioprinting, and microfluidic chip-based models. Additionally, we discuss the relevance of these 3D models in understanding the effects of TME signals on drug response and resistance, as well as their potential for developing strategies to overcome drug resistance and optimize treatment regimens.

三阴性乳腺癌（TNBC）由于其侵袭性、早期转移和有限的治疗选择，给临床带来了相当大的挑战。二维模型的简化和动物模型的生理差异往往导致对抗癌药物的反应不一致。为了应对这些挑战，三维（3D）体外生物工程模型已经被开发出来，可以准确地复制体内肿瘤微环境（TME），为临床前药物测试提供更可靠的平台。细胞培养技术的最新进展促进了来自患者组织和肿瘤的3D模型的创建，这些模型有效地模拟了天然组织环境，并表现出与体内观察到的相似的药物敏感性和细胞毒性行为。越来越多的人认识到，TME内的细胞外基质和细胞多样性显著影响癌细胞的命运。因此，探索耐药机制的策略必须同时考虑微环境因素和基因突变。本文综述了整合微环境影响的3D体外模型系统，以研究乳腺癌的耐药机制。我们讨论了各种生物工程模型，包括基于球体的、基于生物材料的（如聚合物支架和水凝胶）、患者来源的异种移植物（PDX）、3D生物打印和基于微流控芯片的模型。此外，我们讨论了这些3D模型在理解TME信号对药物反应和耐药性的影响方面的相关性，以及它们在制定克服耐药性和优化治疗方案的策略方面的潜力。

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引用次数: 0

Detection assays of mitochondrial permeability transition pore: Current status and future prospects 线粒体通透性过渡孔的检测方法：现状与展望

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-04 DOI: 10.1016/j.acthis.2025.152278

Dongyang Hong , Jiawei Huang , Sicheng Hu , Yawen Zheng , Yuhuan Wu , Ziyang Cao , Zijun Yan , Hongyang Zhang , Huanhuan Feng , Jinxia Wang , Lin Zou

The mitochondrial permeability transition pore (mPTP) is a supramolecular entity in the inner mitochondrial membrane composed of various protein complexes, which is a critical component in maintaining mitochondrial function and cellular homeostasis. In this review, we provide a comprehensive summary of the current detection techniques for mPTP, including spectrophotometry, patch clamping, fluorescent probes, and flow cytometry, which have the potential to reveal the status of mPTP and its roles in degenerative diseases, inflammation, tumors and other diseases. Additionally, we discuss promising new methods to detect mPTP including enhancement in precision, high sensitivity, multi-parameter analysis, and technological integration. These advances highlight new possibilities of clinical diagnosis and treatment for mitochondria-related diseases.

线粒体通透性过渡孔（mitochondrial permeability transition pore, mPTP）是线粒体内膜上由多种蛋白复合物组成的超分子实体，是维持线粒体功能和细胞稳态的关键成分。本文综述了目前mPTP的检测技术，包括分光光度法、膜片夹紧法、荧光探针法和流式细胞术等，这些技术有望揭示mPTP的状态及其在退行性疾病、炎症、肿瘤等疾病中的作用。此外，我们还讨论了有前途的检测mPTP的新方法，包括提高精度，高灵敏度，多参数分析和技术集成。这些进展突出了线粒体相关疾病的临床诊断和治疗的新可能性。

引用次数: 0

Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model 在肝脏特异性斑马鱼模型中诱导gankyrin过表达驱动肝癌发生

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-01 DOI: 10.1016/j.acthis.2025.152280

Zhiyuan Gong , Yuxi Sun , Yueh-Min Lin , Jeng-Wei Lu

Background

Hepatocarcinogenesis is a complex, multistep process that begins with fatty liver, progresses to fibrosis, and ultimately leads to cancer. Numerous etiological factors contribute to this progression, highlighting the importance of developing animal models to facilitate both basic and translational research aimed at discovering new therapeutic strategies. Gankyrin is a key oncoprotein involved in the genetic regulation of liver pathology.

Material and method

To investigate its oncogenic role without the need for cancer cell inoculation or drug treatment, we employed a Tet-On system to drive zebrafish gankyrin overexpression in hepatocytes under the control of the fabp10a promoter. Results: After eight weeks of induction, fabp10a:eGFP-gankyrin transgenic zebrafish spontaneously developed persistent hyperplasia, bile duct hyperplasia, and hepatocellular carcinoma (HCC), demonstrating the oncogenic potential of gankyrin in liver tumorigenesis. In this study, we demonstrate that gankyrin activation drives the progressive development of HCC in zebrafish. Liver-specific overexpression of gankyrin in wild-type zebrafish led to hyperplasia, bile duct hyperplasia, and HCC, establishing a robust zebrafish model for studying liver cancer. Our findings highlight the utility of this model for investigating the molecular mechanisms underlying tumorigenesis.

Conclusion

This study establishes a robust zebrafish model in which liver-specific overexpression of gankyrin induces spontaneous progression from hyperplasia to hepatocellular carcinoma. The model provides a valuable platform for investigating the molecular mechanisms of hepatocarcinogenesis and exploring potential therapeutic strategies.

肝癌的发生是一个复杂的多步骤过程，从脂肪肝开始，发展到纤维化，最终导致癌症。许多病因因素促成了这一进展，强调了开发动物模型以促进旨在发现新的治疗策略的基础和转化研究的重要性。Gankyrin是参与肝脏病理遗传调控的关键癌蛋白。材料和方法为了研究其在不需要癌细胞接种或药物治疗的情况下的致癌作用，我们采用Tet-On系统在fabp10a启动子的控制下驱动斑马鱼肝细胞中gankyrin的过表达。结果：诱导8周后，转基因fabp10a:eGFP-gankyrin斑马鱼自发发生持续性增生、胆管增生和肝细胞癌（HCC），显示了gankyrin在肝脏肿瘤发生中的致癌潜力。在这项研究中，我们证明了gankyrin激活推动了斑马鱼HCC的进行性发展。野生型斑马鱼肝脏特异性过表达gankyrin导致增生、胆管增生和HCC，为研究肝癌建立了稳健的斑马鱼模型。我们的研究结果强调了该模型在研究肿瘤发生的分子机制方面的实用性。结论本研究建立了一个稳健的斑马鱼模型，在该模型中肝脏特异性过表达gankyrin可诱导从增生到肝细胞癌的自发进展。该模型为研究肝癌发生的分子机制和探索潜在的治疗策略提供了一个有价值的平台。

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引用次数: 0

HSPB1 promotes gastric cancer progression by suppressing PANoptosis HSPB1通过抑制PANoptosis促进胃癌进展

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-07-24 DOI: 10.1016/j.acthis.2025.152277

Lei Yang , Miaomiao Zeng , Binsheng Wang , Ze Yang , Bo Li , Xiaoliang Zhu

Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, driven by molecular mechanisms that promote tumor progression and therapeutic resistance. PANoptosis, an integrated programmed cell death pathway involving apoptosis, necroptosis, and pyroptosis, has emerged as a key regulator of tumorigenesis, yet its modulation in GC is poorly understood. This study aimed to investigate the role of heat shock protein beta-1 (HSPB1) in regulating PANoptosis and its impact on GC progression, hypothesizing that HSPB1 overexpression suppresses PANoptosis to enhance tumor malignancy. We employed an integrative approach combining bioinformatics analysis of GEO (GSE54129), TCGA, and GSE15460 datasets with experimental validations. HSPB1 expression was assessed in 40 paired GC and normal tissues and multiple GC cell lines (AGS, MKN-45, NCI-N87, HGC-27, SNU-1) via qPCR, Western blot, and immunohistochemistry. Functional roles were explored by overexpressing or silencing HSPB1 in NCI-N87 and AGS cells, followed by proliferation, colony formation, migration, and apoptosis assays. In vivo effects were evaluated using a nude mouse xenograft model with shHSPB1-transfected cells, analyzing tumor growth and PANoptosis markers (P-MLKL, RIPK3, Cleaved Caspase-1, NLRP3, Cleaved Caspase-3) via Western blot, IHC, and TUNEL assays. Bioinformatics revealed HSPB1 as a PANoptosis-related prognostic biomarker, with elevated expression in GC tissues correlating with poor survival. Experimental validation confirmed HSPB1 overexpression in GC tissues and cell lines. HSPB1 overexpression enhanced proliferation, invasion, and migration while suppressing apoptosis by downregulating PANoptosis markers. Conversely, HSPB1 silencing inhibited these oncogenic traits and activated PANoptosis, significantly reducing tumor growth in vivo, accompanied by upregulated PANoptosis-related proteins and increased apoptosis.HSPB1 promotes GC progression by inhibiting PANoptosis, thereby enhancing tumor survival and aggressiveness, whereas its silencing activates these cell death pathways to suppress tumorigenesis. These findings establish HSPB1 as a critical regulator of PANoptosis in GC and a potential therapeutic target, offering new avenues for overcoming resistance and improving patient outcomes.

胃癌（GC）仍然是全球癌症相关死亡的主要原因，由促进肿瘤进展和治疗耐药的分子机制驱动。PANoptosis是一种包括凋亡、坏死和焦亡在内的综合性程序性细胞死亡途径，已成为肿瘤发生的关键调节因子，但其在GC中的调节作用尚不清楚。本研究旨在探讨热休克蛋白β -1 （HSPB1）在调节PANoptosis中的作用及其对GC进展的影响，并假设HSPB1过表达抑制PANoptosis从而增强肿瘤恶性。我们采用了一种综合方法，将GEO （GSE54129）、TCGA和GSE15460数据集的生物信息学分析与实验验证相结合。通过qPCR、Western blot和免疫组化检测40对GC和正常组织以及多个GC细胞系（AGS、MKN-45、NCI-N87、HGC-27、SNU-1）中HSPB1的表达。通过在NCI-N87和AGS细胞中过表达或沉默HSPB1，然后进行增殖、集落形成、迁移和凋亡实验，探索其功能作用。利用转染shhspb1细胞的裸鼠异种移植模型评估体内效应，通过Western blot、IHC和TUNEL分析肿瘤生长和PANoptosis标志物（P-MLKL、RIPK3、Cleaved Caspase-1、NLRP3、Cleaved Caspase-3）。生物信息学显示HSPB1是panopsis相关的预后生物标志物，在GC组织中表达升高与生存不良相关。实验证实HSPB1在GC组织和细胞系中过表达。HSPB1过表达增强细胞增殖、侵袭和迁移，同时通过下调PANoptosis标志物抑制细胞凋亡。相反，HSPB1沉默抑制这些致癌性状并激活PANoptosis，显著降低肿瘤在体内的生长，并伴有PANoptosis相关蛋白上调和细胞凋亡增加。HSPB1通过抑制PANoptosis促进GC进展，从而提高肿瘤存活和侵袭性，而其沉默激活这些细胞死亡途径以抑制肿瘤发生。这些发现表明HSPB1是胃癌PANoptosis的关键调节因子和潜在的治疗靶点，为克服耐药性和改善患者预后提供了新的途径。

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引用次数: 0

Dihydroartemisinin inhibited tongue squamous cell carcinoma progression and tongue-to-lymph node metastasis through inhibiting RalB expression 双氢青蒿素通过抑制RalB表达抑制舌鳞癌的进展和舌向淋巴结转移

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-06-30 DOI: 10.1016/j.acthis.2025.152276

Yuman Zhang , Yuting Gao , Yanli Gong , Yanguang Yang , Yi Gong , Xiaoyong Song , Yajun Xiong , Dan Wang , Zhihan Liu , Xinli Shi

Background

Lymph node metastasis is a key determinant of the poor survival rate in patients with tongue squamous cell carcinoma (TSCC). Therefore, inhibiting lymph node metastasis is a primary strategy for TSCC treatment. Our previous research found that dihydroartemisinin (DHA) inhibited the migration in human tongue squamous carcinoma Cal-27 cells. However, the effect and mechanism of DHA on lymph node metastasis are unknown in TSCC.

Methods

The expression level of Ras related GTP binding protein B (RalB) was measured in TSCC samples by immunohistochemical staining. Wound healing, invasion, and cell adhesion assays were used to investigate cell motility. Western blot was used to investigate RalB expression level. An orthotopic nude mouse model of TSCC was established to investigate the effect and mechanism of DHA on lymph node metastasis.

Results

First, DHA inhibited the progression of tongue tumor and tongue-to-lymph node metastasis of TSCC. Secondly, DHA inhibited RalB expression level in vitro and in vivo. Finally, DHA inhibited tongue-to-lymph node metastasis through RALB.

Conclusions

DHA inhibited tongue-to-lymph node metastasis through RALB, providing a novel therapeutic strategy for TSCC metastasis.

背景：淋巴结转移是舌鳞状细胞癌（TSCC）患者生存率低的关键决定因素。因此，抑制淋巴结转移是治疗TSCC的主要策略。我们前期研究发现，双氢青蒿素（DHA）对人舌鳞癌Cal-27细胞的迁移具有抑制作用。然而，DHA对TSCC淋巴结转移的影响和机制尚不清楚。方法采用免疫组化染色法检测TSCC组织中Ras相关GTP结合蛋白B （RalB）的表达水平。伤口愈合、侵袭和细胞粘附试验用于研究细胞运动。Western blot检测RalB表达水平。建立原位裸鼠TSCC模型，探讨DHA对TSCC淋巴结转移的影响及其机制。结果首先，DHA抑制舌癌的进展和舌向淋巴结转移；其次，DHA抑制体外和体内RalB表达水平。最后，DHA通过RALB抑制舌向淋巴结转移。结论dha通过RALB抑制舌向淋巴结转移，为TSCC转移提供了新的治疗策略。

{"title":"Dihydroartemisinin inhibited tongue squamous cell carcinoma progression and tongue-to-lymph node metastasis through inhibiting RalB expression","authors":"Yuman Zhang , Yuting Gao , Yanli Gong , Yanguang Yang , Yi Gong , Xiaoyong Song , Yajun Xiong , Dan Wang , Zhihan Liu , Xinli Shi","doi":"10.1016/j.acthis.2025.152276","DOIUrl":"10.1016/j.acthis.2025.152276","url":null,"abstract":"<div><h3>Background</h3><div>Lymph node metastasis is a key determinant of the poor survival rate in patients with tongue squamous cell carcinoma (TSCC). Therefore, inhibiting lymph node metastasis is a primary strategy for TSCC treatment. Our previous research found that dihydroartemisinin (DHA) inhibited the migration in human tongue squamous carcinoma Cal-27 cells. However, the effect and mechanism of DHA on lymph node metastasis are unknown in TSCC.</div></div><div><h3>Methods</h3><div>The expression level of Ras related GTP binding protein B (RalB) was measured in TSCC samples by immunohistochemical staining. Wound healing, invasion, and cell adhesion assays were used to investigate cell motility. Western blot was used to investigate RalB expression level. An orthotopic nude mouse model of TSCC was established to investigate the effect and mechanism of DHA on lymph node metastasis.</div></div><div><h3>Results</h3><div>First, DHA inhibited the progression of tongue tumor and tongue-to-lymph node metastasis of TSCC. Secondly, DHA inhibited RalB expression level <em>in vitro</em> and <em>in vivo</em>. Finally, DHA inhibited tongue-to-lymph node metastasis through <em>RALB</em>.</div></div><div><h3>Conclusions</h3><div>DHA inhibited tongue-to-lymph node metastasis through <em>RALB</em>, providing a novel therapeutic strategy for TSCC metastasis.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"Article 152276"},"PeriodicalIF":2.3,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144522216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 “AARS1-mediated Osterix lactylation promotes its transcriptional activity during osteoblast differentiation” [Acta Histochem. 127 (2025) 152273] “aars1介导的Osterix乳酸化促进成骨细胞分化过程中的转录活性”的更正[Acta Histochem. 127(2025) 152273]。

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-06-23 DOI: 10.1016/j.acthis.2025.152275

Feige Nian , Linfeng Guo , Zhangli Fei , Mingfeng Yang , Lihong Chen , Ye Zhang , Zhufeng Zhang , Yezhou Qian , Bin Zhang

引用次数: 0

Calcipotriol inhibits the proliferation of psoriasis HaCaT cells by activating the ferroptosis pathway 钙化三醇通过激活铁下垂途径抑制银屑病HaCaT细胞的增殖

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-06-23 DOI: 10.1016/j.acthis.2025.152274

Lei Yang , Yue Zhang , Jiansong Wu , Lei Wang , Shan Liu , Li Zhou , Jigang Zhang , Chengxin Li

Calcipotriol is a well-established treatment for psoriasis and other dermatological conditions. This study aimed to investigate whether calcipotriol exerts its therapeutic effects through ferroptosis and to elucidate its underlying molecular mechanisms using bioinformatics and cellular experiments. Differentially expressed genes (DEGs) and their functional enrichment were analyzed in psoriatic skin lesions using bioinformatics. A lipopolysaccharide (LPS)-induced HaCaT cell model was established to simulate psoriatic inflammation. The effects of calcipotriol at various concentrations and time points on HaCaT cell proliferation, apoptosis, and expression of key markers were assessed. Additionally, ferrostatin-1 (a ferroptosis inhibitor) and RSL3 (a ferroptosis inducer) were used to evaluate ferroptosis-related changes, including cell proliferation, apoptosis, reactive oxygen species (ROS) levels, glutathione (GSH) content (via ELISA), and protein expression of GPX4 and Ki-67 (via Western blot). Bioinformatics analysis revealed significant differential expression of ferroptosis-related genes, such as GPX4 and SLC7A11, in psoriatic lesions. Calcipotriol treatment inhibited HaCaT cell proliferation in a dose- and time-dependent manner, elevated ROS levels, and reduced GSH, GPX4, and Ki-67 expression. These effects were reversed by ferrostatin-1, which restored antioxidant defenses and cell viability. Conversely, RSL3 increased ROS levels and partially negated the protective effects of ferrostatin-1. These findings suggest that calcipotriol regulates ferroptosis-related gene expression and inhibits keratinocyte proliferation through induction of oxidative stress and ferroptosis, offering new insights into its mechanism of action in psoriasis treatment.

钙化三醇是治疗牛皮癣和其他皮肤病的有效方法。本研究旨在通过生物信息学和细胞实验研究钙化三醇是否通过铁下垂发挥其治疗作用，并阐明其潜在的分子机制。应用生物信息学方法对银屑病皮损中的差异表达基因（DEGs）及其功能富集进行了分析。建立脂多糖（LPS）诱导HaCaT细胞模型，模拟银屑病炎症。观察不同浓度、不同时间点钙三醇对HaCaT细胞增殖、凋亡及关键标志物表达的影响。此外，利用铁抑素-1（一种铁下垂抑制剂）和RSL3（一种铁下垂诱诱剂）评估铁下垂相关的变化，包括细胞增殖、凋亡、活性氧（ROS）水平、谷胱甘肽（GSH）含量（通过ELISA）以及GPX4和Ki-67的蛋白表达（通过Western blot）。生物信息学分析显示，银屑病皮损中与铁中毒相关的基因GPX4和SLC7A11的表达存在显著差异。钙化三醇以剂量和时间依赖性的方式抑制HaCaT细胞增殖，升高ROS水平，降低GSH、GPX4和Ki-67的表达。这些作用被铁他汀-1逆转，恢复抗氧化防御和细胞活力。相反，RSL3增加ROS水平，部分抵消了铁stat -1的保护作用。这些发现提示钙化三醇通过诱导氧化应激和铁下垂调节铁中毒相关基因表达，抑制角化细胞增殖，为其治疗银屑病的作用机制提供了新的见解。

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引用次数: 0

AARS1-mediated Osterix lactylation promotes its transcriptional activity during osteoblast differentiation aars1介导的Osterix乳酸化在成骨细胞分化过程中促进其转录活性

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-06-11 DOI: 10.1016/j.acthis.2025.152273

Feige Nian , Linfeng Guo , Zhangli Fei , Mingfeng Yang , Lihong Chen , Ye Zhang , Bin Zhang , Yezhou Qian , Zhufeng Zhang

AARS1 is a newly reported lactyl-transferase that plays vital roles in tumorigenesis and innate immune response. However, the function of AARS1-mediated lactylation in osteoblast differentiation is still unclear. Here, we found that silencing of AARS1 impaired the ALP activity and formation of mineralized nodules during osteoblast differentiation. Additionally, our findings demonstrated that AARS1 catalyzed lactylation of Osterix (Osx), a crucial transcription factor involved in the differentiation process of osteoblast cells. Lactylation of Osx increased its binding to target genes and promoted the interaction between Osx and WDR5, facilitating H3K4 tri-methylation on downstream target genes. This in turn enhanced the expression of Osx target genes and osteoblast differentiation. In summary, our study revealed a novel role of AARS1-mediated Osx lactylation during osteoblast differentiation.

AARS1是一种新报道的乙酰转移酶，在肿瘤发生和先天免疫反应中起重要作用。然而，aars1介导的乳酸化在成骨细胞分化中的作用尚不清楚。我们发现，在成骨细胞分化过程中，AARS1的沉默会损害ALP活性和矿化结节的形成。此外，我们的研究结果表明，AARS1催化Osterix （Osx）的乳酸化，Osterix是参与成骨细胞分化过程的关键转录因子。Osx的乳酸化增加了其与靶基因的结合，促进了Osx与WDR5的相互作用，促进了下游靶基因上H3K4的三甲基化。这反过来又增强了Osx靶基因的表达和成骨细胞的分化。总之，我们的研究揭示了aars1介导的Osx乳酸化在成骨细胞分化中的新作用。

引用次数: 0

Retraction notice to “Targeting TEAD would be a potential strategy for scarless wound repair: A preliminary study" [ Acta Histochem. 127 (2025), 152223] “靶向TEAD可能是无疤痕伤口修复的潜在策略：一项初步研究”[Acta Histochem. 127(2025), 152223]。

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-06-10 DOI: 10.1016/j.acthis.2025.152271

Ming-Yan Yang , Hong-Yuan Quan , Da-Lei Li , Jian Ruan , Hua-Ying Fan

引用次数: 0

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