Tissue & cell最新文献_第7页

The effect of curcumin, catechin and resveratrol on viability, proliferation and cytotoxicity of human umbilical cord Wharton’s jelly derived mesenchymal stem cells

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-19 DOI: 10.1016/j.tice.2025.102742

Aishwarya Lakshminarayanan , Suresh Kannan , M. Kalaivani Kuppusamy , Kavitha Sankaranarayanan , Usharani Godla , Alan M. Punnoose

Introduction

Mesenchymal stem cells possess the capability to proliferate and differentiate into diverse lineages. Their beneficial properties have been explored widely to treat various disorders. Phytochemicals like curcumin, catechin and resveratrol have been evaluated for their medicinal values and have promising potential in treating numerous diseases. In this study, we have elucidated the in vitro survival, proliferative and cytotoxic effects of these phytochemicals at selected range of concentrations on human umbilical cord derived Wharton’s jelly mesenchymal stem cells (WJ-MSCs).

Methods

The human WJ-MSCs were extracted using explant culture method and characterized as per International Society for Cellular Therapy (ISCT) guidelines. To analyse the effect of different phytochemicals, the WJ-MSCs were treated with various concentrations ranging from 0.1 to 1000 µM and the viability, proliferative and toxicity effects were assayed using (3-(4,5-dimethylthioazolyl-2,5-diphenyltetrozolium bromide) MTT.

Results

Curcumin and catechin elicited no cytotoxic effect on WJ-MSCs after 48 hours of treatment between the concentrations ranging from 0.1 to 10 µM and the viability was maintained above 80 %. For both the phytochemicals, there was a significant decrease in the viability of WJ-MSCs after 50 µM. Resveratrol was well tolerated at higher doses till 100 µM with a viability above 90 % and cytotoxic effect was observed above 250 µM.

Conclusion

Curcumin, catechin and resveratrol, affect the viability and proliferation of WJ-MSCs differently at varying concentrations. This data will be useful in deciding the dose of phytochemicals when employed concomitantly with stem cells to increase their efficiency.

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引用次数: 0

Assessing diapocynin's different effects on osteosarcoma and breast cancer cells: An in vitro study

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-18 DOI: 10.1016/j.tice.2025.102741

Fernanda Cesar dos Santos , Matheus Menão Mochetti , Cíntia Kazuko Tokuhara , Adriano de Souza Pessoa , Kelly Karina Inacio , Mariana Liessa Rovis Sanches , Valdecir Farias Ximenes , Rodrigo Cardoso de Oliveira

Osteosarcoma is the most common primary bone cancer, accounting for approximately 5 % of new cancer cases globally. In contrast, breast cancer remains the most prevalent malignancy and a leading cause of cancer-related mortality among women. Given the limitations of current therapies, novel treatment strategies are urgently needed. This study evaluates the effects of diapocynin, a derivative of apocynin, on osteosarcoma (UMR-106) and breast cancer (MDA-MB-231) cell lines. Our results demonstrate a dose-dependent cytotoxicity of diapocynin in both cell types, with UMR-106 cells showing higher sensitivity than MDA-MB-231 cells. Notably, treatment with diapocynin induced significant morphological changes in both cell lines, and both IC25 and IC50 concentrations effectively inhibited cell migration, particularly in osteosarcoma cells. However, no significant changes were detected in matrix metalloproteinases −2 and −9 activity following treatment, suggesting that diapocynin may exert its effects through alternative pathways. These results highlight diapocynin as a promising candidate for cancer therapy, warranting further investigation into its mechanisms of action and potential clinical applications.

{"title":"Assessing diapocynin's different effects on osteosarcoma and breast cancer cells: An in vitro study","authors":"Fernanda Cesar dos Santos , Matheus Menão Mochetti , Cíntia Kazuko Tokuhara , Adriano de Souza Pessoa , Kelly Karina Inacio , Mariana Liessa Rovis Sanches , Valdecir Farias Ximenes , Rodrigo Cardoso de Oliveira","doi":"10.1016/j.tice.2025.102741","DOIUrl":"10.1016/j.tice.2025.102741","url":null,"abstract":"<div><div>Osteosarcoma is the most common primary bone cancer, accounting for approximately 5 % of new cancer cases globally. In contrast, breast cancer remains the most prevalent malignancy and a leading cause of cancer-related mortality among women. Given the limitations of current therapies, novel treatment strategies are urgently needed. This study evaluates the effects of diapocynin, a derivative of apocynin, on osteosarcoma (UMR-106) and breast cancer (MDA-MB-231) cell lines. Our results demonstrate a dose-dependent cytotoxicity of diapocynin in both cell types, with UMR-106 cells showing higher sensitivity than MDA-MB-231 cells. Notably, treatment with diapocynin induced significant morphological changes in both cell lines, and both IC25 and IC50 concentrations effectively inhibited cell migration, particularly in osteosarcoma cells. However, no significant changes were detected in matrix metalloproteinases −2 and −9 activity following treatment, suggesting that diapocynin may exert its effects through alternative pathways. These results highlight diapocynin as a promising candidate for cancer therapy, warranting further investigation into its mechanisms of action and potential clinical applications.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102741"},"PeriodicalIF":2.7,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047996","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

Exosome-derived Uc.339 as a potential biomarker for bone metastasis from pulmonary adenocarcinoma.

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-18 DOI: 10.1016/j.tice.2025.102747

Weiqiang Lai, Jinchang Huang, Xuwang Lai, Yuli Wang

This study explored the role of Uc.339, which is a highly expressed genomic sequence in tumor cell-derived exosomes, in mediating bone metastasis from lung adenocarcinoma. By integrating clinical samples, in vitro experiments, and in vivo murine models, we elucidated the molecular mechanisms underlying this process. Clinical blood samples from patients with lung adenocarcinoma revealed elevated Uc.339 expression in exosomes, particularly in those with bone metastasis. In vitro experiments using A549 cell-derived exosomes demonstrated an increase in osteoclast formation, implicating Uc.339 in bone microenvironment modulation. Mechanistically, Uc.339 functions as a decoy for miR-339-3p, disrupting the gene expression balance. In vivo experiments in a murine model confirmed disrupted bone microstructure in the presence of elevated Uc.339, alongside altered expression of key regulators, including SQSTM1, RANKL, nuclear factor kappa B, and miR-339-3p. Our findings underscore the systemic impact of Uc.339 in exosomes, suggesting its potential as both a biomarker and a mediator of bone metastasis. Moreover, the identified molecular alterations provide potential therapeutic targets for managing bone metastasis in patients with lung adenocarcinoma. This study contributes to a deeper understanding of the complex interplay between cancer cells and the bone microenvironment, paving the way for targeted interventions and improved clinical outcomes.

{"title":"Exosome-derived Uc.339 as a potential biomarker for bone metastasis from pulmonary adenocarcinoma.","authors":"Weiqiang Lai, Jinchang Huang, Xuwang Lai, Yuli Wang","doi":"10.1016/j.tice.2025.102747","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102747","url":null,"abstract":"<p><p>This study explored the role of Uc.339, which is a highly expressed genomic sequence in tumor cell-derived exosomes, in mediating bone metastasis from lung adenocarcinoma. By integrating clinical samples, in vitro experiments, and in vivo murine models, we elucidated the molecular mechanisms underlying this process. Clinical blood samples from patients with lung adenocarcinoma revealed elevated Uc.339 expression in exosomes, particularly in those with bone metastasis. In vitro experiments using A549 cell-derived exosomes demonstrated an increase in osteoclast formation, implicating Uc.339 in bone microenvironment modulation. Mechanistically, Uc.339 functions as a decoy for miR-339-3p, disrupting the gene expression balance. In vivo experiments in a murine model confirmed disrupted bone microstructure in the presence of elevated Uc.339, alongside altered expression of key regulators, including SQSTM1, RANKL, nuclear factor kappa B, and miR-339-3p. Our findings underscore the systemic impact of Uc.339 in exosomes, suggesting its potential as both a biomarker and a mediator of bone metastasis. Moreover, the identified molecular alterations provide potential therapeutic targets for managing bone metastasis in patients with lung adenocarcinoma. This study contributes to a deeper understanding of the complex interplay between cancer cells and the bone microenvironment, paving the way for targeted interventions and improved clinical outcomes.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"102747"},"PeriodicalIF":2.7,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256828","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

Titanium dioxide-induced fibrotic liver model and the therapeutic effect of resveratrol by modulation of α-SMA and 8-oHdG expressions, oxidative stress, and inflammation

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-18 DOI: 10.1016/j.tice.2025.102748

Feyza Başak , Tansu Kuşat , Yusuf Ersan , Tahir Kahraman

The research sought to assess the therapeutic impact of resveratrol by biochemical, immunohistochemical, and histopathological analyses in a TiO₂-induced liver fibrosis model. Titanium dioxide (100 mg/kg body weight) was delivered for 15 days to induce liver fibrosis, either alone or in conjunction with resveratrol (30 mg/kg body weight) therapy for the same duration. Resveratrol has been identified as a crucial therapeutic drug that provides an alternative treatment method for TiO₂-induced liver fibrosis by mitigating inflammation, oxidative stress, and the expressions of α-SMA and 8-OHdG. Resveratrol treatment mitigated TiO₂-induced liver fibrosis by repairing hepatocellular injury and decreasing plasma AST, ALT, and ALP levels. Resveratrol improves the activity of superoxide dismutase (SOD) and catalase (CAT), crucial enzymes for antioxidant defense, and elevates glutathione peroxidase (GSH-Px) levels, so augmenting antioxidant function. Furthermore, resveratrol decreased hepatic inflammation (IL-6 and IL-1β) and oxidative stress markers. Furthermore, histological alterations and immunohistochemistry expression of α-SMA and 8-OhdG were reinstated after resveratrol administration in the TiO₂-induced liver fibrosis model. Our research indicates that resveratrol administration effectively protects against liver fibrosis produced by TiO₂.

{"title":"Titanium dioxide-induced fibrotic liver model and the therapeutic effect of resveratrol by modulation of α-SMA and 8-oHdG expressions, oxidative stress, and inflammation","authors":"Feyza Başak , Tansu Kuşat , Yusuf Ersan , Tahir Kahraman","doi":"10.1016/j.tice.2025.102748","DOIUrl":"10.1016/j.tice.2025.102748","url":null,"abstract":"<div><div>The research sought to assess the therapeutic impact of resveratrol by biochemical, immunohistochemical, and histopathological analyses in a TiO<sub>2</sub>-induced liver fibrosis model. Titanium dioxide (100 mg/kg body weight) was delivered for 15 days to induce liver fibrosis, either alone or in conjunction with resveratrol (30 mg/kg body weight) therapy for the same duration. Resveratrol has been identified as a crucial therapeutic drug that provides an alternative treatment method for TiO<sub>2</sub>-induced liver fibrosis by mitigating inflammation, oxidative stress, and the expressions of α-SMA and 8-OHdG. Resveratrol treatment mitigated TiO<sub>2</sub>-induced liver fibrosis by repairing hepatocellular injury and decreasing plasma AST, ALT, and ALP levels. Resveratrol improves the activity of superoxide dismutase (SOD) and catalase (CAT), crucial enzymes for antioxidant defense, and elevates glutathione peroxidase (GSH-Px) levels, so augmenting antioxidant function. Furthermore, resveratrol decreased hepatic inflammation (IL-6 and IL-1β) and oxidative stress markers. Furthermore, histological alterations and immunohistochemistry expression of α-SMA and 8-OhdG were reinstated after resveratrol administration in the TiO<sub>2</sub>-induced liver fibrosis model. Our research indicates that resveratrol administration effectively protects against liver fibrosis produced by TiO<sub>2</sub>.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102748"},"PeriodicalIF":2.7,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029641","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

Mesua ferrea L. extract inhibits cell invasion and tumor growth in breast cancer in vitro and in vivo

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-17 DOI: 10.1016/j.tice.2025.102750

Zhi-Ying Liu , Ge Ge , Shuang-Shuang Ma , Xi-Ya Chen , Yue Cong , Shu-Yun Wang , Ya-Ping Guo

Mesua ferrea L. was commonly used in Uyghur medicine, and the flowering buds of M. ferrea extract exhibited significant inhibitory effects on the proliferation of breast cancer cells in our preliminary research; however, the underlying active components remain to be elucidated. In this study, firstly, we extracted the flowering buds of M. ferrea with methanol and obtained eleven bioactive sub-fractions (MF-P-1–MF-P-11), and MF-P-5 showed the strongest inhibitory activity against MDA-MB-231 and 4T1 cells. Subsequently, 52 compounds from MF-P-5 were identified by UPLC Q-TOF MS/MS. In addition, ten compounds (MF1–MF10) from MF-P-5 were separated and identified, and MF5 could inhibit MDA-MB-231 and 4T1 cells proliferation as MTT and colony formation assay, suppress the migration of MDA-MB-231 and 4T1 cells by means of wound healing assay, reduce the expression level of E-cadherin, and induce MDA-MB-231 and 4T1 cells apoptosis by Annexin V-FITC/PI double staining assay and up-regulate the expression of Bax and down-regulate the expression of PARP. Ultimately, we evaluated the effects of MF-P-5 on breast cancer via MDA-MB-231 cell xenograft in nude mice. The results of tumor volume and weight and immunohistochemistry revealed that MF-P-5 could significantly inhibit the growth of MDA-MB-231 cells in vivo. Besides, the expression levels of E-cadherin significantly increased and MMP-2 decreased. The above results suggested that MF-P-5 could suppress the invasion of breast cancer cells in vivo. Furthermore, the expression level of Bcl-2 was prominently reduced which revealed that MF-P-5 stimulated the mitochondrial apoptosis pathway in vivo. As a result, MF5 could inhibit MDA-MB-231 and 4T1 cells proliferation, migration and tumor growth in vitro and MF-P-5 could suppress tumor growth in vivo which had laid a theoretical foundation for further clinical application.

{"title":"Mesua ferrea L. extract inhibits cell invasion and tumor growth in breast cancer in vitro and in vivo","authors":"Zhi-Ying Liu , Ge Ge , Shuang-Shuang Ma , Xi-Ya Chen , Yue Cong , Shu-Yun Wang , Ya-Ping Guo","doi":"10.1016/j.tice.2025.102750","DOIUrl":"10.1016/j.tice.2025.102750","url":null,"abstract":"<div><div><em>Mesua ferrea</em> L. was commonly used in Uyghur medicine, and the flowering buds of <em>M. ferrea</em> extract exhibited significant inhibitory effects on the proliferation of breast cancer cells in our preliminary research; however, the underlying active components remain to be elucidated. In this study, firstly, we extracted the flowering buds of <em>M. ferrea</em> with methanol and obtained eleven bioactive sub-fractions (MF-P-1–MF-P-11), and MF-P-5 showed the strongest inhibitory activity against MDA-MB-231 and 4T1 cells. Subsequently, 52 compounds from MF-P-5 were identified by UPLC Q-TOF MS/MS. In addition, ten compounds (MF1–MF10) from MF-P-5 were separated and identified, and MF5 could inhibit MDA-MB-231 and 4T1 cells proliferation as MTT and colony formation assay, suppress the migration of MDA-MB-231 and 4T1 cells by means of wound healing assay, reduce the expression level of E-cadherin, and induce MDA-MB-231 and 4T1 cells apoptosis by Annexin V-FITC/PI double staining assay and up-regulate the expression of Bax and down-regulate the expression of PARP. Ultimately, we evaluated the effects of MF-P-5 on breast cancer via MDA-MB-231 cell xenograft in nude mice. The results of tumor volume and weight and immunohistochemistry revealed that MF-P-5 could significantly inhibit the growth of MDA-MB-231 cells <em>in vivo</em>. Besides, the expression levels of E-cadherin significantly increased and MMP-2 decreased. The above results suggested that MF-P-5 could suppress the invasion of breast cancer cells <em>in vivo</em>. Furthermore, the expression level of Bcl-2 was prominently reduced which revealed that MF-P-5 stimulated the mitochondrial apoptosis pathway <em>in vivo</em>. As a result, MF5 could inhibit MDA-MB-231 and 4T1 cells proliferation, migration and tumor growth <em>in vitro</em> and MF-P-5 could suppress tumor growth <em>in vivo</em> which had laid a theoretical foundation for further clinical application.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102750"},"PeriodicalIF":2.7,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143024914","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

MOSPD1 facilitates fatty acid metabolism and gastric cancer progression by promoting the MAPK pathway

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-17 DOI: 10.1016/j.tice.2025.102752

Chengliang Wang, Yunping Qiu, Xiao Zheng, Shuhui Chen, Chao He

Background

Motile sperm domain containing 1 (MOSPD1) is overexpressed in colorectal, prostate, and breast cancers, but its role in gastric cancer (GC) progression remains unclear.

Methods

The effect of MOSPD1 was evaluated using cell viability, colony formation, wound healing, and Transwell assays. Triglyceride and lipid levels were measured in GC cells. Western blotting was used to examine protein expression. A mouse model of subcutaneous tumor xenotransplantation was used to evaluate the effects of MOSPD1 knockdown on GC cells.

Results

MOSPD1 expression in GC tissues and cells was higher than in normal tissues and cells. MOSPD1 knockdown decreased the proliferation, migration, and invasion of GC cells and the growth of subcutaneous tumors. MOSPD1 overexpression increased the proliferation, migration, and invasion of GC cells. Levels of triglyceride, lipid, and fatty acid synthesis-related enzymes (ACLY, ACC1, and FASN) were downregulated in MOSPD1 knockdown cells and upregulated in MOSPD1 overexpressed cells. MOSPD1 knockdown inhibited the phosphorylation of ERK, JNK, and P38 in GC cells and subcutaneous tumors. MOSPD1 overexpression promoted the phosphorylation of ERK, JNK, and P38 in GC cells.

Conclusions

High MOSPD1 expression facilitates fatty acid metabolism and GC progression by activating the MAPK pathway. Thus, MOSPD1 may be a potential therapeutic target for GC.

{"title":"MOSPD1 facilitates fatty acid metabolism and gastric cancer progression by promoting the MAPK pathway","authors":"Chengliang Wang, Yunping Qiu, Xiao Zheng, Shuhui Chen, Chao He","doi":"10.1016/j.tice.2025.102752","DOIUrl":"10.1016/j.tice.2025.102752","url":null,"abstract":"<div><h3>Background</h3><div>Motile sperm domain containing 1 (MOSPD1) is overexpressed in colorectal, prostate, and breast cancers, but its role in gastric cancer (GC) progression remains unclear.</div></div><div><h3>Methods</h3><div>The effect of MOSPD1 was evaluated using cell viability, colony formation, wound healing, and Transwell assays. Triglyceride and lipid levels were measured in GC cells. Western blotting was used to examine protein expression. A mouse model of subcutaneous tumor xenotransplantation was used to evaluate the effects of MOSPD1 knockdown on GC cells.</div></div><div><h3>Results</h3><div>MOSPD1 expression in GC tissues and cells was higher than in normal tissues and cells. MOSPD1 knockdown decreased the proliferation, migration, and invasion of GC cells and the growth of subcutaneous tumors. MOSPD1 overexpression increased the proliferation, migration, and invasion of GC cells. Levels of triglyceride, lipid, and fatty acid synthesis-related enzymes (ACLY, ACC1, and FASN) were downregulated in MOSPD1 knockdown cells and upregulated in MOSPD1 overexpressed cells. MOSPD1 knockdown inhibited the phosphorylation of ERK, JNK, and P38 in GC cells and subcutaneous tumors. MOSPD1 overexpression promoted the phosphorylation of ERK, JNK, and P38 in GC cells.</div></div><div><h3>Conclusions</h3><div>High MOSPD1 expression facilitates fatty acid metabolism and GC progression by activating the MAPK pathway. Thus, MOSPD1 may be a potential therapeutic target for GC.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102752"},"PeriodicalIF":2.7,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047328","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

Down-regulation of platelet-derived growth factor receptor β in pericytes increases blood-brain barrier permeability and significantly enhances α-synuclein in a Parkinson’s Disease 3D cell model in vitro under hyperglycemic condition

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-17 DOI: 10.1016/j.tice.2025.102751

Ting Wang , Meng-yan Li , Zhong Pei , Qiu-Xia Chen , Qiu-sheng Cheng , Ze Li

Background

Parkinson's Disease (PD) often presents with a compromised blood-brain barrier (BBB), which hyperglycemia may exacerbate. Pericytes, a key cell for BBB integrity, are potential therapeutic targets for neurodegenerative disorders. Few studies have developed 3D PD cell models incorporating neurovascular units (NVU) through the co-culture of human endothelial, pericytes, astrocytes, and SH-SY5Y cells to evaluate BBB impairment and the role of pericytes under hyperglycemic condition.

Method

A 3D PD like cell model was developed using 6-OHDA-affected SH-SY5Y cells, combined with endothelial cells, pericytes, and astrocytes through the Real Architecture for Tissue (RAFT) 3D co-culture system. PD incorporating reduced (30 % and 89 %) PDGFRβ NVU (RPN) with or without hyperglycemic model (HM) were also established. BBB permeability to sodium fluorescein was assessed, and BBB impairment was evaluated using BBB-associated proteins (ZO-1, CD54, CD144), cell-specific proteins (CD31, GFAP, PDGFRβ, CD13), tyrosine hydroxylase (TH), α-synuclein, oligomeric α-synuclein, and α-synuclein (ser9).

Results

PD 3D cell models incorporating RPN with or without hyperglycemia were successfully established in vitro. Graduately increased BBB impairment was observed in PD, PD with RPN, and PD with RPN combined with HM, indicated by decreased BBB-associated and cell-specific proteins, reduced TH, and increased α-synuclein, oligomeric α-synuclein, and α-synuclein (ser9) compared to the NVU model.

Conclusion

Reduced pericyte PDGFRβ could increase BBB permeability, accelerate PD progression, and exacerbate under hyperglycemic condition.

{"title":"Down-regulation of platelet-derived growth factor receptor β in pericytes increases blood-brain barrier permeability and significantly enhances α-synuclein in a Parkinson’s Disease 3D cell model in vitro under hyperglycemic condition","authors":"Ting Wang , Meng-yan Li , Zhong Pei , Qiu-Xia Chen , Qiu-sheng Cheng , Ze Li","doi":"10.1016/j.tice.2025.102751","DOIUrl":"10.1016/j.tice.2025.102751","url":null,"abstract":"<div><h3>Background</h3><div>Parkinson's Disease (PD) often presents with a compromised blood-brain barrier (BBB), which hyperglycemia may exacerbate. Pericytes, a key cell for BBB integrity, are potential therapeutic targets for neurodegenerative disorders. Few studies have developed 3D PD cell models incorporating neurovascular units (NVU) through the co-culture of human endothelial, pericytes, astrocytes, and SH-SY5Y cells to evaluate BBB impairment and the role of pericytes under hyperglycemic condition.</div></div><div><h3>Method</h3><div>A 3D PD like cell model was developed using 6-OHDA-affected SH-SY5Y cells, combined with endothelial cells, pericytes, and astrocytes through the Real Architecture for Tissue (RAFT) 3D co-culture system. PD incorporating reduced (30 % and 89 %) PDGFRβ NVU (RPN) with or without hyperglycemic model (HM) were also established. BBB permeability to sodium fluorescein was assessed, and BBB impairment was evaluated using BBB-associated proteins (ZO-1, CD54, CD144), cell-specific proteins (CD31, GFAP, PDGFRβ, CD13), tyrosine hydroxylase (TH), α-synuclein, oligomeric α-synuclein, and α-synuclein (ser9).</div></div><div><h3>Results</h3><div>PD 3D cell models incorporating RPN with or without hyperglycemia were successfully established in <em>vitro</em>. Graduately increased BBB impairment was observed in PD, PD with RPN, and PD with RPN combined with HM, indicated by decreased BBB-associated and cell-specific proteins, reduced TH, and increased α-synuclein, oligomeric α-synuclein, and α-synuclein (ser9) compared to the NVU model.</div></div><div><h3>Conclusion</h3><div>Reduced pericyte PDGFRβ could increase BBB permeability, accelerate PD progression, and exacerbate under hyperglycemic condition.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102751"},"PeriodicalIF":2.7,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029638","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

Curculigoside exhibits multiple therapeutic efﬁcacy to induce apoptosis and ferroptosis in osteosarcoma via modulation of ROS and tumor microenvironment

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-16 DOI: 10.1016/j.tice.2025.102745

Ziyang Ma , Yirong Wang , Xiaoyu Zhang , Shi Ding , Jian Fan , Tian Li , Xin Xiao , Jing Li

Objective

Patients with osteosarcoma (OS) exhibit metastasis upon diagnosis, and the condition frequently acquires resistance to traditional chemotherapy treatments, failing the therapy. The objective of this research was to examine the impact of curculigoside (Cur), a key phenolic compound discovered in the rhizome of C. orchioides Gaertn, on OS cells and the surrounding tumor environment.

Methods

We assessed the impact of curculigoside on tumor inhibition in four osteosarcoma cell lines and mice tumor xenograft models using various techniques including cell viability assay, wound healing assay, cell apoptosis analysis, immunofluorescent staining, and IHC. Moreover, we created a mini-PDX model by utilizing freshly obtained primary OS cells from surgically removed OS tissues to evaluate the possible clinical use of Cur.

Result

The results of our study show that Cur triggers cell death in OS cells and enhances the maturation of RAW264.7 cells. By effectively inhibiting the growth of OS cells, these actions mechanistically trigger the catastrophic buildup of unbound iron and uncontrolled lipid peroxidation, ultimately resulting in ferroptosis. Moreover, additional validation of Cur's substantial antineoplastic impact is obtained through in vivo experiments employing xenograft and mini-PDX models.

Conclusions

To sum up, this research is the initial one to exhibit the anti-tumor effects of Cur on OS using various methods, indicating that Cur shows potential as a viable approach for treating OS.

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引用次数: 0

Collagen-based hydrogel derived from amniotic membrane loaded with quercetin accelerates wound healing by improving stereological parameters and reducing inflammation in a diabetic rat model 胶原基水凝胶来源于负载槲皮素的羊膜，通过改善体力学参数和减少糖尿病大鼠模型的炎症加速伤口愈合。

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-16 DOI: 10.1016/j.tice.2025.102743

Xin Xiang , Weijun Peng , Qi Lu , Shiqi Ma , Jinfeng Wang , Jinling Ma , Xiaokai Wei , Mengmeng Li , Hongfeng Wang

In clinical practice, there is a demand for innovative wound healing methods to tackle full thickness skin injuries, especially in those with diabetes. In this study, we examined if collagen-based hydrogel from amniotic membrane (CHAM) loaded with quercetin could enhance healing in diabetic rats. Sixty diabetic rats were randomly divided into the control group, CHAM group, quercetin group, and CHAM+Quercetin group. Sampling took place on days 4 and 8 for additional evaluations. Our findings showed that the rates of wound contraction, volumes of new epidermis and dermis, fibroblast and blood vessel counts, collagen deposition, and concentrations of TGF-β1 and VEGF cytokines were significantly higher in the treatment groups compared to the control group, with these changes being more pronounced in the CHAM+Quercetin group. This is while the counts of neutrophils and macrophages, along with the concentration levels of IL-6, IL-1β, and TNF-α cytokines dropped more noticeably in the CHAM+Quercetin group in comparison to the other groups. In summary, it was determined that the combination of CHAM and quercetin significantly enhances diabetic wound healing.

在临床实践中，需要创新的伤口愈合方法来解决全层皮肤损伤，特别是糖尿病患者。在这项研究中，我们检测了负载槲皮素的羊膜胶原基水凝胶（CHAM）是否能促进糖尿病大鼠的愈合。将60只糖尿病大鼠随机分为对照组、CHAM组、槲皮素组和CHAM+槲皮素组。在第4天和第8天进行抽样以进行进一步评价。我们的研究结果显示，与对照组相比，治疗组的伤口收缩率、新表皮和真皮层体积、成纤维细胞和血管计数、胶原沉积、TGF-β1和VEGF细胞因子浓度显著高于对照组，这些变化在CHAM+槲皮素组更为明显。与其他组相比，CHAM+槲皮素组的中性粒细胞和巨噬细胞计数以及IL-6、IL-1β和TNF-α细胞因子的浓度水平下降更为明显。综上所述，我们确定CHAM和槲皮素联合使用可显著促进糖尿病创面愈合。

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引用次数: 0

Granisetron ameliorates doxorubicin-evoked nephrotoxicity via modulation of Nrf2 and TLR4/p38 MAPK/NLRP3 signals in rats

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-15 DOI: 10.1016/j.tice.2025.102744

Marwa M. Khalaf , Emad H.M. Hassanein , Hamada S. Qebesy , Abdullatif A. Ahmed , Heba M. Mahmoud

Doxorubicin (DOX) is an anthracycline chemotherapy employed in treating malignancies. Unfortunately, the clinical application of DOX is limited due to its nephrotoxicity. Granisetron (GRAN) is a 5-HT3 receptor blocker used widely to manage post-chemotherapy nausea and vomiting with anti-inflammatory, anti-oxidant, and anti-apoptotic bioactivities. We plan to examine the renoprotective effect of GRAN against DOX-associated renal toxicity. In this investigation, twenty-four adult male Wistar rats were allocated to control, DOX (30 mg/kg, i.p), and GRAN (2.5 mg/kg, p.o) + DOX groups. GRAN attenuated renal impairment induced by DOX in rats by decreasing the BUN, creatinine, KIM-1, and Cys-C levels, and such finding is supported by attenuating histological alterations caused by DOX. GRAN combated oxidative stress proved by decreasing MDA content and elevating GSH and CAT levels mediated by Nrf2 activation. GRAN suppressed inflammation evidenced by decreasing IL-6 and TNF-α levels mediated by downregulation of inflammatory sensitive controllers TLR-4, NLRP3, and p38 MAPK. GRAN prevented apoptosis by controlling renal expression of BAX, caspase-3 and Bcl2. Therefore, GRAN holds promise agent against DOX-induced renal toxicity by upregulating Nrf2 and suppressing apoptosis and inflammatory cascadeTLR4/p38 MAPK/ NLRP3.

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引用次数: 0