Histochemistry and Cell Biology最新文献

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A simple immunohistochemical method for perinatal mammalian ovaries revealed different kinetics of oocyte apoptosis caused by DNA damage and asynapsis.
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-02-17 DOI: 10.1007/s00418-025-02358-5
Hiroshi Kogo, Akiko Iizuka-Kogo, Hanako Yamamoto, Maiko Ikezawa, Yukiko Tajika, Toshiyuki Matsuzaki
{"title":"A simple immunohistochemical method for perinatal mammalian ovaries revealed different kinetics of oocyte apoptosis caused by DNA damage and asynapsis.","authors":"Hiroshi Kogo, Akiko Iizuka-Kogo, Hanako Yamamoto, Maiko Ikezawa, Yukiko Tajika, Toshiyuki Matsuzaki","doi":"10.1007/s00418-025-02358-5","DOIUrl":"https://doi.org/10.1007/s00418-025-02358-5","url":null,"abstract":"<p><p>Oocytes with meiotic defects are assumed to be eliminated by apoptosis in the perinatal period. However, oocyte apoptosis caused by meiotic defects has not been well analyzed, partly because of the great technical demands of tissue sectioning perinatal ovaries. In the present study, we applied a squash method for immunohistochemical analysis of perinatal mouse ovaries as a substitute for tissue sectioning. As a result, we could show different kinetics of apoptosis caused by DMC1- and SPO11-deficiencies, indicating that DNA damage-induced apoptosis precedes asynapsis-induced apoptosis in mouse oocytes. Double-mutant analysis revealed that only asynapsis-induced apoptosis was significantly dependent on HORMAD2. The present method is simple, easy, and able to analyze a sufficient number of oocytes to detect infrequent events in a single specimen, accelerating detailed immunohistochemical analyses of mammalian ovaries during the fetal and perinatal periods.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"32"},"PeriodicalIF":2.1,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440760","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
FAK mediates mechanical signaling to maintain epithelial homeostasis through YAP/TAZ-TEADs.
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-02-07 DOI: 10.1007/s00418-025-02360-x
Yang Peng, Qiuyun Yuan, Shuting Zhou, Jianguo Gan, Zhengzhong Shen, Xiaoqiang Xia, Yuchen Jiang, Qianming Chen, Yao Yuan, Gu He, Qiang Wei, Xiaodong Feng
{"title":"FAK mediates mechanical signaling to maintain epithelial homeostasis through YAP/TAZ-TEADs.","authors":"Yang Peng, Qiuyun Yuan, Shuting Zhou, Jianguo Gan, Zhengzhong Shen, Xiaoqiang Xia, Yuchen Jiang, Qianming Chen, Yao Yuan, Gu He, Qiang Wei, Xiaodong Feng","doi":"10.1007/s00418-025-02360-x","DOIUrl":"10.1007/s00418-025-02360-x","url":null,"abstract":"<p><p>Epithelial homeostasis ensures that the epithelium can perform its normal physiological functions. Mechanical signaling response through integrin-mediated adhesions of the basement membrane (BM) is crucial for maintaining epithelial homeostasis. The essential mechanosensors YAP and the paralog TAZ (YAP/TAZ) have been shown to play a critical role in epithelial homeostasis, but the key regulator that mediates mechanical signaling to YAP/TAZ in maintaining epithelial homeostasis has not been fully understood. In this study, we noticed that mechanical signals correlated with YAP/TAZ activation and basal state maintenance in epithelial stem/progenitor cells through immunohistochemistry. Subsequently, we found that inhibition of focal adhesion kinase (FAK) suppressed YAP/TAZ activation in the human keratinocyte line HaCaT cells. Furthermore, inhibition of the interaction between YAP/TAZ and the transcriptional enhanced associate domains (TEADs) resulted in the differentiation of HaCaT cells. Finally, we used primary mouse epithelial cells to reconstruct the epithelium in vitro and found that FAK inhibition led to both a reduction in YAP/TAZ activity and an increase of differentiation in the basal layer cells. In conclusion, our findings reveal that FAK mediates mechanical signaling to maintain epithelial homeostasis via YAP/TAZ-TEADs.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"31"},"PeriodicalIF":2.1,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364442","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
Identifying CSNK1E as a therapeutic target in thyroid cancer among the core circadian clock genes. 在核心昼夜节律时钟基因中确定 CSNK1E 为甲状腺癌的治疗靶点。
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-02-04 DOI: 10.1007/s00418-025-02357-6
Shun-Yu Chi, Yi-Chiung Hsu, Chung-Hsin Tsai, Shih-Yuan Huang, Shao-Chiang Chang, Shih-Ping Cheng
{"title":"Identifying CSNK1E as a therapeutic target in thyroid cancer among the core circadian clock genes.","authors":"Shun-Yu Chi, Yi-Chiung Hsu, Chung-Hsin Tsai, Shih-Yuan Huang, Shao-Chiang Chang, Shih-Ping Cheng","doi":"10.1007/s00418-025-02357-6","DOIUrl":"https://doi.org/10.1007/s00418-025-02357-6","url":null,"abstract":"<p><p>Previous studies have shown that thyroid malignancies can alter the transcriptional oscillations of circadian clock genes. In this study, we screened the expression of core circadian clock genes in thyroid neoplasms and found that CSNK1E, NPAS2, and TIMELESS were upregulated, while ARNTL, CRY1, CRY2, PER2, and RORA were downregulated during the progression and dedifferentiation of thyroid cancer. Immunohistochemical analysis further confirmed an increase in CSNK1E expression parallel to the loss of tumor differentiation. To investigate the potential therapeutic implications, we treated thyroid cancer cell lines with two different CSNK1E inhibitors: PF670462 and IC261. Both inhibitors resulted in growth inhibition in monolayer and three-dimensional spheroid cultures. This growth inhibition was accompanied by G2/M cell cycle arrest and a decrease in CDK4 and cyclin D1 expression. Moreover, CSNK1E inhibitors suppressed cell migration and invasion and reduced the expression of epithelial-mesenchymal transition markers. In vivo experiments using xenograft models showed that the administration of IC261 significantly restrained tumor growth and decreased the Ki-67 index of the xenograft tumors. In conclusion, our study provides evidence of aberrant CSNK1E expression in thyroid cancer dedifferentiation and highlights the potential therapeutic value of targeting CSNK1E.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"30"},"PeriodicalIF":2.1,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189200","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
Distinct TYRO3 and PROS1 expression levels contribute to preeclampsia pathogenesis.
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-01-29 DOI: 10.1007/s00418-024-02351-4
Esma Kirimlioglu, Ertan Katirci, Mehmet Simsek
{"title":"Distinct TYRO3 and PROS1 expression levels contribute to preeclampsia pathogenesis.","authors":"Esma Kirimlioglu, Ertan Katirci, Mehmet Simsek","doi":"10.1007/s00418-024-02351-4","DOIUrl":"https://doi.org/10.1007/s00418-024-02351-4","url":null,"abstract":"<p><p>Preeclampsia (PE) is a severe placental complication occurring after the 20th week of pregnancy. PE is associated with inflammation and an increased immune reaction against the fetus. TYRO3 and PROS1 suppress inflammation by clearing apoptotic cells. Disruptions in TYRO3/PROS1 signaling may increase the risk of PE. This study investigated the role of TYRO3/PROS1 signaling in the development of PE using healthy placentae (HP) and preeclamptic placentae (PP) of six pregnant women each. Tissue morphology using hematoxylin and eosin (H&E), TYRO3, MERTK, PROS1, and GAS6 mRNA levels using qPCR and localization and expression levels of TYRO3 and PROS1 using immunohistochemical staining (IHC) were evaluated. The study results show that the levels of TYRO3, MERTK, PROS1 and GAS6 mRNA, as well as TYRO3 protein, increased in PE. TYRO3 expression was observed in extravillous trophoblast (EVTs) and syncytiotrophoblast cells (SCTs). PROS1 was observed in HP fetal vessels through IHC while absent in PP. The reduced presence of PROS1 in the cytotrophoblast layer in PE may indicate a compromised blood-placental barrier. The absence of PROS1 in fetal vessels may suggest potential complement activation and thrombosis. TYRO3, MERTK, PROS1 and GAS6 may help balance impaired inflammation, apoptosis, thrombosis, complement activation and the blood-placental barrier in PE.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"29"},"PeriodicalIF":2.1,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058987","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
Modulation of placental angiogenesis by metformin in a rat model of gestational diabetes.
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-01-27 DOI: 10.1007/s00418-025-02355-8
Basmah M Eldakhakhny, Fatma M Ghoneim, Mona F M Soliman, Salwa M Abo El-Khair, Ayman Z Elsamanoudy, Yousef M Almoghrabi, Passant M Mohie, Fatma E Hassan, Amany A Abd Elfattah
{"title":"Modulation of placental angiogenesis by metformin in a rat model of gestational diabetes.","authors":"Basmah M Eldakhakhny, Fatma M Ghoneim, Mona F M Soliman, Salwa M Abo El-Khair, Ayman Z Elsamanoudy, Yousef M Almoghrabi, Passant M Mohie, Fatma E Hassan, Amany A Abd Elfattah","doi":"10.1007/s00418-025-02355-8","DOIUrl":"https://doi.org/10.1007/s00418-025-02355-8","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) significantly disrupts placental structure and function, leading to complications such as intrauterine growth restriction (IUGR) and preeclampsia. This study aimed to investigate the effects of GDM on placental histology, angiogenesis, and oxidative stress, as well as evaluate metformin's protective role in mitigating these changes. A total of 60 pregnant Sprague-Dawley rats were divided into four groups: control, metformin-treated, GDM, and GDM with metformin. GDM was induced using streptozotocin (STZ) at 40 mg/kg, and metformin was administered at 200 mg/kg from gestational day (GD) 4 to GD17. Blood glucose and insulin levels were assessed, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was calculated. Placentae were weighed and subjected to histological, immunohistochemical, and molecular analyses, focusing on key angiogenesis markers (VEGF, VEGFR, CD31, KLF2) and oxidative stress indicators (MDA, eNOS). GDM increased placental weight, angiogenesis (elevated VEGF, VEGFR, CD31), and oxidative stress (elevated MDA, eNOS). Histopathological changes included villous edema, membrane rupture, and hemosiderin deposition. Metformin treatment reduced placental weight; normalized VEGF, KLF2, and PlGF expression; and improved placental architecture. Additionally, oxidative stress was significantly reduced in metformin-treated GDM rats. In conclusion, GDM induces placental abnormalities, promoting excessive angiogenesis and oxidative stress, potentially leading to IUGR and other complications. Metformin showed protective effects by reducing placental overgrowth and restoring vascular and oxidative balance. These findings suggest that metformin may play a therapeutic role in improving placental health in GDM pregnancies, warranting further investigation into its long-term effects on fetal development and maternal health.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"28"},"PeriodicalIF":2.1,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046663","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
Differentiation of stem cells into chondrocytes and their potential clinical application in cartilage regeneration.
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-01-25 DOI: 10.1007/s00418-025-02356-7
Julia Cieśla, Marcin Tomsia
{"title":"Differentiation of stem cells into chondrocytes and their potential clinical application in cartilage regeneration.","authors":"Julia Cieśla, Marcin Tomsia","doi":"10.1007/s00418-025-02356-7","DOIUrl":"https://doi.org/10.1007/s00418-025-02356-7","url":null,"abstract":"<p><p>Cartilage diseases and injuries are considered difficult to treat owing to the low regenerative capacity of this tissue. Using stem cells (SCs) is one of the potential methods of treating cartilage defects and creating functional cartilage models for transplants. Their ability to proliferate and to generate functional chondrocytes, a natural tissue environment, and extracellular cartilage matrix, makes SCs a new opportunity for patients with articular injuries or incurable diseases, such as osteoarthritis (OA). The review summarizes the most important scientific reports on biology and mechanisms of SC-derived chondrogenesis and sources of SCs for chondrogenic purposes. Additionally, it focuses on the genetic mechanisms, microRNA (miRNA) regulation, and epigenetic processes steering the chondrogenic differentiation of SCs. It also describes the attempts to create functional cartilage with tissue engineering using growth factors and scaffolds. Finally, it presents the challenges that researchers will have to face in the future to effectuate SC differentiation methods into clinical practice for treating cartilage diseases.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"27"},"PeriodicalIF":2.1,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143038176","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
The dynamic interaction of pediatric ALL cells and MSCs: influencing leukemic cell survival and modulating MSC β-catenin expression. 儿童ALL细胞和间充质干细胞的动态相互作用:影响白血病细胞存活和调节间充质干细胞β-catenin的表达
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-01-21 DOI: 10.1007/s00418-025-02353-w
Tuba Ozdemir-Sanci, Ilkay Piskin, Yasin Köksal, Sevil Cayli, Namik Y Ozbek, H Meltem Ozguner
{"title":"The dynamic interaction of pediatric ALL cells and MSCs: influencing leukemic cell survival and modulating MSC β-catenin expression.","authors":"Tuba Ozdemir-Sanci, Ilkay Piskin, Yasin Köksal, Sevil Cayli, Namik Y Ozbek, H Meltem Ozguner","doi":"10.1007/s00418-025-02353-w","DOIUrl":"10.1007/s00418-025-02353-w","url":null,"abstract":"<p><p>Bone marrow mesenchymal stromal cells (BM-MSCs) are integral components of the bone marrow microenvironment, playing a crucial role in supporting hematopoiesis. Recent studies have investigated the potential involvement of BM-MSCs in the pathophysiology of acute lymphoblastic leukemia (ALL). However, the exact contribution of BM-MSCs to leukemia progression remains unclear because of conflicting findings and limited characterization. In this study, we compared BM-MSCs derived from pediatric ALL patients with those from matched healthy donors (HDs). Our results indicate that while both ALL-MSCs and HD-MSCs meet the criteria established by the International Society for Cellular Therapy, they exhibit significant differences in proliferation and differentiation capacity. ALL-MSCs displayed markedly lower proliferation rates and reduced osteogenic/adipogenic differentiation potential compared to HD-MSCs. Furthermore, co-culture experiments revealed that MSCs enhance the survival of leukemic blasts through both soluble factors and direct cell-cell interactions, underscoring their anti-apoptotic properties. Importantly, our findings demonstrate that interactions with leukemic cells activate the Wnt/β-catenin signaling pathway in MSCs, suggesting a potential target for therapeutic intervention. Overall, this study enhances our understanding of the role of BM-MSCs in leukemia and highlights β-catenin as a promising target for future therapies.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"26"},"PeriodicalIF":2.1,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11750926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004630","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
mTORC1 regulates the proliferation of SOX9+ porcine skin-derived stem cells (pSDSCs) by promoting S6K phosphorylation. mTORC1通过促进S6K磷酸化调节SOX9+猪皮肤源性干细胞(pSDSCs)的增殖。
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-01-20 DOI: 10.1007/s00418-025-02354-9
Ming-Xin Zang, Geng Zhang, Ying Zhang, Sha-Sha Wang, Xiang-Wei Zhai, Na Zhao, Wei Ge, Jin-Wen Xie, Wei Shen, Shun-Feng Cheng
{"title":"mTORC1 regulates the proliferation of SOX9<sup>+</sup> porcine skin-derived stem cells (pSDSCs) by promoting S6K phosphorylation.","authors":"Ming-Xin Zang, Geng Zhang, Ying Zhang, Sha-Sha Wang, Xiang-Wei Zhai, Na Zhao, Wei Ge, Jin-Wen Xie, Wei Shen, Shun-Feng Cheng","doi":"10.1007/s00418-025-02354-9","DOIUrl":"https://doi.org/10.1007/s00418-025-02354-9","url":null,"abstract":"<p><p>Skin-derived stem cells (SDSCs) are a subtype of adult stem cells (ASCs) that are widely harvested and exempt from ethical restrictions in clinical applications. These cells possess capabilities for self-renewal, proliferation, and multi-lineage differentiation. Compared to model animals like rats and mice, pigs exhibit greater physiological similarity to humans. Porcine skin has very similar histological and physiological characteristics to human skin. Therefore, porcine skin is becoming increasingly significant as an in vitro model for research. In this study, porcine skin-derived stem cells (pSDSCs) were isolated and cultured in vitro for experiments. The expression of stemness-related gene SOX9 was detected. RNA sequencing (RNA-seq) results found that the mammalian target of rapamycin (mTOR) signaling pathway was significantly enriched in SOX9<sup>+</sup> pSDSCs. To investigate the role of the mTOR signaling pathway, we added rapamycin (RAPA), an inhibitor of the mTOR complex 1 (mTORC1), and found that the proliferation rate of SOX9<sup>+</sup> pSDSCs decreased significantly during culture. In addition, western blotting (WB) results demonstrated that mTORC1 promoted proliferation by phosphorylating S6 kinase (S6K) and then activating cyclin D1(CCND1) in SOX9<sup>+</sup> pSDSCs. These findings provide insights into the mechanisms of adult stem cell proliferation.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"25"},"PeriodicalIF":2.1,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004544","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
Seventy years of peroxisome research: current advances and future perspectives. 过氧化物酶体研究70年:当前进展与未来展望。
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-01-18 DOI: 10.1007/s00418-024-02349-y
Ruth E Carmichael, Silke Oeljeklaus, Luis D Cruz-Zaragoza, Rechal Kumar, Chloe Bolton, Markus Islinger, Markus Kunze, Jorgaq Pata, Celien Lismont, Beatriz S C Silva, Suzan Kors, Michael Schrader, Ralf Erdmann
{"title":"Seventy years of peroxisome research: current advances and future perspectives.","authors":"Ruth E Carmichael, Silke Oeljeklaus, Luis D Cruz-Zaragoza, Rechal Kumar, Chloe Bolton, Markus Islinger, Markus Kunze, Jorgaq Pata, Celien Lismont, Beatriz S C Silva, Suzan Kors, Michael Schrader, Ralf Erdmann","doi":"10.1007/s00418-024-02349-y","DOIUrl":"https://doi.org/10.1007/s00418-024-02349-y","url":null,"abstract":"","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"24"},"PeriodicalIF":2.1,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004547","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
Differential cell architecture and microenvironmental responses of pretumoral and tumoral cellular models exposed to coverslip-induced hypoxia. 肿瘤前和肿瘤细胞模型暴露于覆盖层诱导的缺氧的差异细胞结构和微环境反应。
IF 2.1 4区 生物学
Histochemistry and Cell Biology Pub Date : 2025-01-03 DOI: 10.1007/s00418-024-02350-5
Magdalena Millán, Felipe Parietti, Florencia Lamela, María Cecilia De Rossi, Belén Benítez, Valeria Levi, Manoela Domingues, Ronell Bologna-Molina, Miguel Arocena, Jimena Hochmann
{"title":"Differential cell architecture and microenvironmental responses of pretumoral and tumoral cellular models exposed to coverslip-induced hypoxia.","authors":"Magdalena Millán, Felipe Parietti, Florencia Lamela, María Cecilia De Rossi, Belén Benítez, Valeria Levi, Manoela Domingues, Ronell Bologna-Molina, Miguel Arocena, Jimena Hochmann","doi":"10.1007/s00418-024-02350-5","DOIUrl":"10.1007/s00418-024-02350-5","url":null,"abstract":"<p><p>The tumor microenvironment is an altered milieu that imposes multiple selective pressures leading to the survival and dissemination of aggressive and fit tumor cell subpopulations. How pre-tumoral and tumoral cells respond to changes in their microenvironment will determine the subsequent evolution of the tumor. In this study, we have subjected pre-tumoral and tumoral cells to coverslip-induced hypoxia, which recapitulates the intracellular hypoxia and extracellular acidification characteristic of the early tumor microenvironment, and we have used a combination of quantitative phase microscopy and epifluorescence to analyze diverse cellular responses to this altered environment. In normoxia, tumor cells showed differences in nuclear organization, as evidenced by decreased numbers of HP1 foci, and in hypoxia major changes in nuclear architecture were observed, with tumor cells significantly increasing the number of high dry mass density foci in the nucleus compared to pre-tumoral and non-tumoral cells. Conversely, compared to pre-tumoral and normal cells, mitochondrial ATP levels decayed markedly in tumor cells in hypoxia, whereas the activation of executioner caspases increased only in tumor cells in this condition. Therefore, in terms of cellular organization, metabolic changes and activation of cell death processes, tumor cells showed more dramatic responses to an altered microenvironment than their pre-tumoral and normal counterparts, responses which in turn could play fundamental roles in shaping future tumor development.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"163 1","pages":"23"},"PeriodicalIF":2.1,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921536","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
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