European Journal of Histochemistry最新文献

Tanshinone IIA attenuates hepatic stellate cell activation, oxidative stress, and liver fibrosis by inhibiting YAP signaling. 丹参酮IIA通过抑制YAP信号通路减弱肝星状细胞活化、氧化应激和肝纤维化。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 DOI: 10.4081/ejh.2025.4176

Dan Wang, Qingquan Tan, Qing Zheng, Yanling Ma, Li Feng

{"title":"Tanshinone IIA attenuates hepatic stellate cell activation, oxidative stress, and liver fibrosis by inhibiting YAP signaling.","authors":"Dan Wang, Qingquan Tan, Qing Zheng, Yanling Ma, Li Feng","doi":"10.4081/ejh.2025.4176","DOIUrl":"https://doi.org/10.4081/ejh.2025.4176","url":null,"abstract":"Tanshinone IIA is derived from Salvia miltiorrhiza and has multiple therapeutic targets and functions. The exact therapeutic effects on liver fibrosis as well as the underlying hepatoprotective mechanisms are still lacking. A liver fibrosis model was established via ligation of the common bile duct ligation (BDL). The mice were intraperitoneally administered different concentrations of tanshinone IIA (4 mg/kg, 8 mg/kg) for 2 weeks. Liver function was assessed through hematoxylin and eosin and Sirus red staining. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutathione (GSH) and malondialdehyde (MDA) were quantified by enzyme-linked immunosorbent assay (ELISA), via microplate reader. The total iron content of the liver was quantified via Triple Quad-ICP-MS. TGFβ-induced hepatic stellate cells (HSCs), a cell model of liver fibrosis, were treated with tanshinone IIA at different concentrations (10 mM, 20 mM, 30 mM, 40 mM). The combination of tanshinone IIA with YAP agonists was applied in activated HSCs and animal models. Tanshinone IIA treatment relieved BDL-induced liver fibrosis; mitigated histological liver damage; lowered the serum ALT and AST levels; reduced macrophage infiltration and the MDA and iron contents; and increased the GSH and GPX4 levels by inhibiting YAP signaling. tanshinone IIA also suppressed the activation of HSCs and collagen production through blocking the YAP signaling pathway. The YAP agonist reversed the therapeutic effect of tanshinone IIA on activated HSCs and BDL-induced liver fibrosis. Tanshinone IIA inhibited HSC activation and oxidative stress and alleviated liver fibrosis by inhibiting the YAP signaling pathway.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144318568","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

Targeting EphA2 suppresses the proliferation, migration and invasion of endometriosis via the AMPK signaling pathway. 靶向EphA2通过AMPK信号通路抑制子宫内膜异位症的增殖、迁移和侵袭。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 DOI: 10.4081/ejh.2025.4176

Chaoyi Yang, Shujun Wang, Mengru Li, Xiangli Pang, Aili Tan

引用次数: 0

Proceedings of the 70th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC). 意大利胚胎学组-意大利发育与细胞生物学学会（GEI-SIBSC）第70届大会论文集。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-09 DOI: 10.4081/ejh.2025.4245

The Scientific Committee

引用次数: 0

Cancer cell-derived exosomal miR-34a inhibits the malignant progression of pancreatic adenocarcinoma cells by restraining the M2 polarization of macrophages. 癌细胞来源的外泌体miR-34a通过抑制巨噬细胞的M2极化抑制胰腺腺癌细胞的恶性进展。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-04-17 DOI: 10.4081/ejh.2025.4176

Kui Long, Xiang Kui, Qingbin Zeng, Wenzhi Dong

{"title":"Cancer cell-derived exosomal miR-34a inhibits the malignant progression of pancreatic adenocarcinoma cells by restraining the M2 polarization of macrophages.","authors":"Kui Long, Xiang Kui, Qingbin Zeng, Wenzhi Dong","doi":"10.4081/ejh.2025.4176","DOIUrl":"https://doi.org/10.4081/ejh.2025.4176","url":null,"abstract":"This study aimed to investigate the crosstalk mechanism between pancreatic cancer (PAC) cells and M2 tumor-associated macrophages induced by tumor-derived exosomal miR-34a. MicroRNA and mRNA expression levels were detected using RT-qPCR. Cell Counting Kit-8, wound-healing, transwell assays and flow cytometry were respectively employed to assess cell proliferation, migration, invasion and apoptosis. Enzyme-linked immunosorbent assay was utilized to determine cytokine secretion. Transmission electron microscopy and nanoparticle tracking analyses were performed to detect the exosome morphology and particle size. Phagocytosis of exosomes by macrophages was verified by PKH26 labeling. The effects of exosome-treated macrophages on the epithelial-mesenchymal transition, invasion, and migration of PANC-1 cells were investigated using coculture experiments. The identification of miR-34a's potential targets were determined with TargetScan and validated by a dual-luciferase reporter assay. miR-34a was expressed at low levels in PAC tissues, cells, and exosomes. The overexpression of miR-34a restrains the malignant progression of PANC-1 cells. After miR-34a-overexpressed PANC-1-derived exosomes were phagocytosed by macrophages, the process of M2 polarization in macrophages was obstructed, leading to the suppression of epithelial-mesenchymal transition, migration, and invasion of the cocultured PANC-1 cells. Suppressor of cytokine signaling 3 is a direct target of miR-34a. MiR-34a negatively modulates the suppressor of cytokine signaling 3 to prevent the M2 polarization of macrophages by engaging the Janus kinase/signal transducers and activators of the transcription pathway and influencing the malignancy of PAC cells. miR-34a in cancer cell-derived exosomes inhibits the malignant progression of pancreatic cancer cells by restraining M2 polarization of macrophages.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144056556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Downregulation of S100 calcium-binding A4 (S100A4) ameliorates hepatic fibrosis via regulating Wnt/β-catenin signaling pathway. 下调S100钙结合A4 （S100A4）通过调节Wnt/β-catenin信号通路改善肝纤维化。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-04-14 DOI: 10.4081/ejh.2025.4186

Chixian Zhang, Kai Bai, Dexu Li

{"title":"Downregulation of S100 calcium-binding A4 (S100A4) ameliorates hepatic fibrosis via regulating Wnt/β-catenin signaling pathway.","authors":"Chixian Zhang, Kai Bai, Dexu Li","doi":"10.4081/ejh.2025.4186","DOIUrl":"https://doi.org/10.4081/ejh.2025.4186","url":null,"abstract":"S100 calcium-binding protein A4 (S100A4), a fibrosis-associated calcium-binding protein, has been implicated in fibrotic progression across multiple organs. Activation of the Wnt/β-catenin signaling pathway is a critical driver of hepatic fibrosis, yet the mechanistic role of S100A4 in this context remains poorly defined. This study investigated the regulatory role of S100A4 in hepatic fibrosis in vitro and in vivo. Hepatic stellate cells (HSCs) were treated with TGF-β to induce fibrotic activation, and S100A4 expression was silenced using shRNA. A carbon tetrachloride (CCl₄)-induced murine hepatic fibrosis model was employed for in vivo validation. Fibrotic markers, including collagen I, fibronectin, and α-smooth muscle actin (α-SMA), were assessed via qRT-PCR, Western blotting, immunofluorescence, and immunohistochemistry. Liver histopathology and function were evaluated using Masson trichrome staining, hematoxylin-eosin staining, and serum ALT/AST assays. In vitro experiments demonstrated that TGF-β treatment upregulated S100A4 expression in HSCs, while S100A4 silencing suppressed HSC activation, extracellular matrix (ECM) deposition, and Wnt/β-catenin signaling. In vivo, S100A4 downregulation attenuated CCl₄-induced hepatic fibrosis, reduced collagen accumulation, improved liver histology, and normalized serum ALT/AST levels. These findings indicate that S100A4 promotes hepatic fibrosis by activating the Wnt/β-catenin pathway, highlighting its potential as a therapeutic target.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Knockdown of miR-411-3p induces M2 macrophage polarization and promotes colorectal cancer progression by regulation of MMP7. 敲低miR-411-3p可诱导M2巨噬细胞极化，通过调控MMP7促进结直肠癌进展。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-05 DOI: 10.4081/ejh.2025.4178

Tianliang Bai, Ping Li, Yabin Liu, Bindan Cai, Gang Li, Wenbin Wang, Rui Yan, Xiangkui Zheng, Shangkun Du

{"title":"Knockdown of miR-411-3p induces M2 macrophage polarization and promotes colorectal cancer progression by regulation of MMP7.","authors":"Tianliang Bai, Ping Li, Yabin Liu, Bindan Cai, Gang Li, Wenbin Wang, Rui Yan, Xiangkui Zheng, Shangkun Du","doi":"10.4081/ejh.2025.4178","DOIUrl":"10.4081/ejh.2025.4178","url":null,"abstract":"Colorectal cancer (CRC) is prone to metastasis, leading to a poor prognosis. miR-411-3p exhibits a tumor-suppressive function in CRC, but its exact mechanism is unclear. The malignant biological properties of CRC cells were detected by Carboxyfluorescein diacetate succinimidyl ester (CFSE) staining, scratch-wound and transwell assay. Levels of markers associated with macrophage polarization were evaluated by flow cytometry and ELISA kits. Bioinformatics analysis to screen whether the downstream target mRNA of miR-411-3p is matrix metalloproteinase 7 (MMP7), and Dual-Luciferase reporter assay verified the targeting relationship between the two. qRT-PCR tested miR-411-3p and MMP7 levels. MMP7 level was quantified by Western blot. Additionally, a nude mouse subcutaneous graft tumor model was constructed, Ki-67 expression was detected by immunohistochemistry, and the impact of miR-411-3p/MMP7 on the polarization of M2 macrophages was explored. miR-411-3p expression is downregulated in CRC. Knockdown of miR-411-3p elevated the amount of CFSE-positive, migrating, and invading cells, decreased apoptosis, and elevated the levels of M2 macrophage polarization markers. After overexpression of miR-411-3p, all of the above metrics were reversed in CRC cells. miR-411-3p targeted negative regulation of MMP7 expression, and MMP7 overexpression further enhanced the promotional effect of knockdown of miR-411-3p on the malignant progression of CRC and M2 macrophage polarization. Furthermore, knockdown of miR-411-3p upregulated the MMP7 level, elevated Ki-67-positive cells count, and induced M2 macrophage polarization in vivo. Knockdown of miR-411-3p upregulates MMP7 and induces M2 macrophage polarization, which in turn promotes malignant biological progression of CRC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

MiR-122-5p inhibits the epithelial mesenchymal transition of liver cancer cells by inducing hiPSCs to differentiate into hepatocyte-like cells. MiR-122-5p通过诱导hiPSCs向肝细胞样细胞分化，抑制肝癌细胞上皮间充质转化。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-06 DOI: 10.4081/ejh.2025.4190

Qianzhe Xing, Yanjie Xu, Ying Luo, Chenglong Li, Peng Wang, Bin Kang, Chengjun Lu

{"title":"MiR-122-5p inhibits the epithelial mesenchymal transition of liver cancer cells by inducing hiPSCs to differentiate into hepatocyte-like cells.","authors":"Qianzhe Xing, Yanjie Xu, Ying Luo, Chenglong Li, Peng Wang, Bin Kang, Chengjun Lu","doi":"10.4081/ejh.2025.4190","DOIUrl":"10.4081/ejh.2025.4190","url":null,"abstract":"Epithelial-mesenchymal transition (EMT) is closely linked to liver cancer prognosis, invasiveness, and aggressiveness. One promising treatment for liver cancer is cell therapy, where stem cells are stimulated to develop into functional liver cells. This study aimed to investigate the effect of miR-122-5p on the differentiation of human induced pluripotent stem cells (hiPSCs) into hepatocyte-like cells and its impact on the EMT process in liver cancer cells. MiR-122-5p was overexpressed or silenced in hiPSCs to analyze the expression of liver-specific markers, including AFP, ALB and ASGPR, to confirm hepatocyte-like differentiation. A co-culture system with HepG2 liver cancer cells was also used to evaluate the effect of miR-122-5p-overexpressing hiPSCs or miR-122-5p-silencing hiPSCs on the expression of EMT markers. Results revealed that overexpression of miR-122-5p in hiPSCs induced hepatocyte-like characteristics, as evidenced by increased levels of AFP, ALB, and ASGPR. However, knockdown of miR-122-5p had the opposite effect. In the co-culture system, hiPSCs overexpressing miR-122-5p inhibited the EMT process of HepG2 cells, resulting in increased levels of mesenchymal markers and decreased levels of epithelial markers. Taken together, miR-122-5p promotes the differentiation of hiPSCs into hepatocyte-like cells and inhibits EMT process of liver cancer cells. Targeting miR-122-5p may be a novel approach to prevent liver cancer progression through cell therapy.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

E-cadherin inhibits the proliferation and migration of human colorectal cancer cells through Hippo signaling pathway. E-cadherin通过Hippo信号通路抑制人结直肠癌细胞的增殖和迁移。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-26 DOI: 10.4081/ejh.2025.4196

Zhijing Wang, Xiaohua Qin, Shanshan Liu, Yilei Wen, Bikan Lan, Hantao Liao, Haixian Wei

{"title":"E-cadherin inhibits the proliferation and migration of human colorectal cancer cells through Hippo signaling pathway.","authors":"Zhijing Wang, Xiaohua Qin, Shanshan Liu, Yilei Wen, Bikan Lan, Hantao Liao, Haixian Wei","doi":"10.4081/ejh.2025.4196","DOIUrl":"10.4081/ejh.2025.4196","url":null,"abstract":"E-cadherin (E-cad) is a crucial regulatory factor in rescue Epithelial-mesenchymal transition and is involved in the occurrence of various malignant tumor. However, the mechanisms by which E-cadherin regulates tumor metastasis in CRC remain unclear. We established sh-E-cad (silenced by short hairpin RNA) and rescue-E-cad (overexpressed by E-cad plasmid transfection) CRC cell lines to investigate the role of E-cad in CRC in vitro. Immunohistochemistry, clonogenic assays, scratch wound healing assays, CCK-8 assays, flow cytometry, Transwell assay, real time-PCR and Western blot were employed to investigate the underlying mechanisms by which E-cad involve the progression of CRC. In CRC tissues, E-cad expression was significantly reduced, while YAP expression was markedly elevated. Silencing E-cad induced a significant increase of clonogenic ability in CRC cells, which was reduced upon rescue of E-cad expression. Transwell assays indicate that low expression of E-cad enhances the cell migration, a finding corroborated by scratch wound healing experiments. CCK-8 results demonstrate that silencing E-cad promotes the proliferation of CRC cells. Importantly, we found that E-cad influences apoptosis rather than the cell cycle. Analysis of Hippo signaling pathway-related factors revealed that silencing E-cad resulted in significantly decreased expression of MST1/2 and LATS1/2, as well as reduced phosphorylation levels of YAP, while YAP expression was significantly increased. Additionally, immunofluorescence confirmed the nuclear translocation of YAP. Our study indicates that E-cad regulates the malignant progression of CRC via the Hippo signaling pathway, offering a potential new strategy for CRC treatment.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144152759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

miR-627-5p inhibits malignant progression of cervical cancer by targeting ANGPTL4. miR-627-5p 通过靶向 ANGPTL4 抑制宫颈癌的恶性进展

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 DOI: 10.4081/ejh.2025.4161

Xinghua Wu, Kai Lin, Chen Gao, Yinfang Ni, Li Zhang, Tailai Yang, Jinguo Chen

{"title":"miR-627-5p inhibits malignant progression of cervical cancer by targeting ANGPTL4.","authors":"Xinghua Wu, Kai Lin, Chen Gao, Yinfang Ni, Li Zhang, Tailai Yang, Jinguo Chen","doi":"10.4081/ejh.2025.4161","DOIUrl":"10.4081/ejh.2025.4161","url":null,"abstract":"In recent years, accumulating evidence has highlighted the critical role of miR-627-5p in the occurrence and progression of various cancers. However, its specific role and mechanism in cervical cancer (CC) remain unclear. This study aimed to elucidate the mechanism by which miR-627-5p inhibits the malignant progression of CC and assess its potential clinical implications. In C33A cells, the mRNA expression levels of ANGPTL4 and miR-627-5p were analyzed using qRT-PCR. The miR-627-5p mimics and their control (miR-NC) were transfected into C33A cells to determine whether miR-627-5p directly regulates ANGPTL4 expression. A comprehensive suite of assays, including CCK-8, migration, transwell, flow cytometry, and Western blotting, was conducted to evaluate how miR-627-5p modulates the malignant biological behavior of CC cells. Rescue experiments were performed by overexpressing ANGPTL4. In C33A cells, miR-627-5p expression was reduced, whereas ANGPTL4 expression was elevated. Further analysis confirmed that miR-627-5p negatively regulates ANGPTL4 by directly targeting its 3'-UTR. Functional assays demonstrated that miR-627-5p inhibits proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) while promoting apoptosis and S-phase arrest in C33A cells, effects that were reversed by ANGPTL4 overexpression. These findings highlight the potential of miR-627-5p as both a biomarker and a therapeutic target for CC. By inhibiting EMT and regulating ANGPTL4 expression, miR-627-5p may provide a novel avenue for improving therapeutic strategies, particularly in advanced or metastatic CC. Moreover, miRNA-based therapies, supported by advanced delivery systems such as nanoparticle carriers, could enhance the stability and precision of miR-627-5p applications. This study lays the groundwork for future research integrating miR-627-5p into precision medicine approaches for CC treatment.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Anatomical insights into the proximal aponeurosis of the long head of the biceps femoris. 股二头肌长头近端腱膜的解剖学观察。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-13 DOI: 10.4081/ejh.2025.4165

Carmela Julia Mantecón-Tagarro, Eri Nanizawa, Munekazu Naito, Shun Otsuka, Huub Maas, Yasuo Kawakami

{"title":"Anatomical insights into the proximal aponeurosis of the long head of the biceps femoris.","authors":"Carmela Julia Mantecón-Tagarro, Eri Nanizawa, Munekazu Naito, Shun Otsuka, Huub Maas, Yasuo Kawakami","doi":"10.4081/ejh.2025.4165","DOIUrl":"10.4081/ejh.2025.4165","url":null,"abstract":"The biceps femoris long head (BFlh) is prone to strain injuries, but its reasons remain unclear. This study analyzed the BFlh proximal intramuscular aponeurosis in donor samples (n=4) through morphometric, microscopic, and histological methods. Cross-sections were taken every 5% of the muscle belly to differentiate connective, adipose, and muscle tissues. The aponeurosis extended from the muscle surface, becoming intramuscular from 40-70% of the muscle belly, and ended distally. Quantitative analysis revealed significant reductions of size in both the cross-sectional area (CSA) and width of the aponeurosis at 50% of muscle length, with CSA ranging from 4.9 mm² to 13.4 mm² and widths from 6.8 mm to 12.4 mm across subjects. Dense connective tissue bundles were separated by adipose or loose connective tissues. The aponeurosis shape varied along the muscle, with T- and hook-shaped configurations, and small branches were observed distally. These findings reveal the BFlh proximal aponeurosis as a complex structure, potentially influencing its injury susceptibility.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12117529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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