Tissue engineering (TE) combines scaffolds, cells, and bioactive chemicals in order to create tissues. The objective is to restore or sustain tissue functionality and expedite the recovery of damaged tissues or organs in a controlled laboratory environment. This study aimed to evaluate the properties and biocompatibility of decellularized sheep kidney scaffolds (DKS) and to explore the differentiation potential of adipose-derived mesenchymal stem cells (ADSCs) into renal cells. After decellularizing sheep kidneys using freeze-drying and detergent techniques, we conducted histological studies, DNA quantification, and ultrastructural evaluations using scanning electron microscopy (SEM). Furthermore, to assay the feasibility and attachment of stem cells to the decellularized scaffolds, ADSCs were cultured on the scaffolds and subjected to the MTT assay. The expression of the pax2 gene was analyzed using real-time PCR to determine the differentiation of MSCs into kidney cells. DNA quantitation revealed a significant reduction in the quantity of DNA present in the scaffold tissue compared to the control kidney tissue. Ultrastructural examination confirmed the preservation of the decellularized scaffold's ultrastructure. Histological analysis demonstrated the complete removal of nuclear material from the scaffold. Additionally, Pax2 gene expression was significantly increased in ADSC cells cultured on the scaffold compared to the control group. The results demonstrate that the produced scaffolds are well-suited for regenerative medicine, exhibiting excellent biocompatibility and providing a conducive environment for the differentiation of ADSCs.
{"title":"Evaluation of decellularized sheep kidney scaffolds for renal tissue engineering: Biocompatibility and stem cell differentiation potential","authors":"Maryam Jahanvar , Saber Zahri , Arash Abdolmaleki , Asadollah Asadi","doi":"10.1016/j.tice.2024.102594","DOIUrl":"10.1016/j.tice.2024.102594","url":null,"abstract":"<div><div>Tissue engineering (TE) combines scaffolds, cells, and bioactive chemicals in order to create tissues. The objective is to restore or sustain tissue functionality and expedite the recovery of damaged tissues or organs in a controlled laboratory environment. This study aimed to evaluate the properties and biocompatibility of decellularized sheep kidney scaffolds (DKS) and to explore the differentiation potential of adipose-derived mesenchymal stem cells (ADSCs) into renal cells. After decellularizing sheep kidneys using freeze-drying and detergent techniques, we conducted histological studies, DNA quantification, and ultrastructural evaluations using scanning electron microscopy (SEM). Furthermore, to assay the feasibility and attachment of stem cells to the decellularized scaffolds, ADSCs were cultured on the scaffolds and subjected to the MTT assay. The expression of the <em>pax2</em> gene was analyzed using real-time PCR to determine the differentiation of MSCs into kidney cells. DNA quantitation revealed a significant reduction in the quantity of DNA present in the scaffold tissue compared to the control kidney tissue. Ultrastructural examination confirmed the preservation of the decellularized scaffold's ultrastructure. Histological analysis demonstrated the complete removal of nuclear material from the scaffold. Additionally, Pax2 gene expression was significantly increased in ADSC cells cultured on the scaffold compared to the control group. The results demonstrate that the produced scaffolds are well-suited for regenerative medicine, exhibiting excellent biocompatibility and providing a conducive environment for the differentiation of ADSCs.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102594"},"PeriodicalIF":2.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628773","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}
Pub Date : 2024-11-05DOI: 10.1016/j.tice.2024.102604
Mustafa Oguz Cumaoglu , Mustafa Makav , Serpil Dag , Ayfer Yildiz Uysal , Lale Baser , Tyler W. LeBaron , Duried Alwazeer
Gentamicin-induced nephrotoxicity primarily results from renal inflammatory cascades and increased oxidative stress. This study aims to examine the effects of hydrogen-rich water (HRW) on gentamicin-induced renal damage in rats. Thirty-two rats were equally divided into four groups, including control (no treatment), hydrogen, gentamicin, and gentamicin+hydrogen. At the end of one week, all animals were euthanized following ethical rules, and blood and tissue samples were analyzed for examining Malondialdehyde (MDA), glutathione (GSH), Tumor Necrosis Factor-Alfa (TNF-α), Tumor Necrosis Factor-Beta (TNF-β), Interleukin 6 (IL-6), endoglin, endocan, urea, creatinine, Na+, and K+ parameters. Levels of 8-Hydroxyguanosine (8-OHdG), MDA, and Bax were immunohistochemically analyzed. Data showed that while MDA (control P<0.0001, H2P<0.0001, Genta+H2P<0.0007), TNF-α (control P<0.0002, H2P<0.0040, Genta+H2P<0.0381), IL-6 (control P<0.0044, H2P<0.0070, Genta+H2P<0.0109), endocan (control P<0.0460, H2P<0.0286, Genta+H2P<0.0452), and endoglin (control P<0.0131, H2P<0.0164, Genta+H2P<0.0397), urea (control P<0.0024, H2P<0.0001, Genta+H2P<0.0180), and creatinine parameters (control P<0.0017, H2P<0.0178, Genta+H2P<0.0011) increased in the gentamicin group compared to the other groups, a decrease in these parameters was observed in the gentamicin+hydrogen group compared to the gentamicin group. The Genta group had greater levels of TNF-β than the control (P<0.0042) and H2 groups (P<0.0268). GSH content was higher in the hydrogen group compared to the gentamicin group. Immunohistochemically, 8-OHdG, MDA, and Bax expressions increased in the gentamicin group compared to the control group, whereas they decreased in the gentamicin+hydrogen group compared to the gentamicin group. Hydrogen may be an alternative treatment for oxidative stress-induced nephrotoxicity.
{"title":"Combating oxidative stress and inflammation in gentamicin-induced nephrotoxicity using hydrogen-rich water","authors":"Mustafa Oguz Cumaoglu , Mustafa Makav , Serpil Dag , Ayfer Yildiz Uysal , Lale Baser , Tyler W. LeBaron , Duried Alwazeer","doi":"10.1016/j.tice.2024.102604","DOIUrl":"10.1016/j.tice.2024.102604","url":null,"abstract":"<div><div>Gentamicin-induced nephrotoxicity primarily results from renal inflammatory cascades and increased oxidative stress. This study aims to examine the effects of hydrogen-rich water (HRW) on gentamicin-induced renal damage in rats. Thirty-two rats were equally divided into four groups, including control (no treatment), hydrogen, gentamicin, and gentamicin+hydrogen. At the end of one week, all animals were euthanized following ethical rules, and blood and tissue samples were analyzed for examining Malondialdehyde (MDA), glutathione (GSH), Tumor Necrosis Factor-Alfa (TNF-α), Tumor Necrosis Factor-Beta (TNF-β), Interleukin 6 (IL-6), endoglin, endocan, urea, creatinine, Na<sup>+</sup>, and K<sup>+</sup> parameters. Levels of 8-Hydroxyguanosine (8-OHdG), MDA, and Bax were immunohistochemically analyzed. Data showed that while MDA (control <em>P</em><0.0001, H<sub>2</sub> <em>P</em><0.0001<em>, </em>Genta+H<sub>2</sub> <em>P</em><0.0007), TNF-α (control <em>P</em><0.0002, H<sub>2</sub> <em>P</em><0.0040, <em></em>Genta+H<sub>2</sub> <em>P</em><0.0381), IL-6 (control <em>P</em><0.0044<em>,</em> H<sub>2</sub> <em>P<</em>0.0070<em>, </em>Genta+H<sub>2</sub> <em>P</em><0.0109), endocan (control <em>P</em><0.0460<em>,</em> H<sub>2</sub> <em>P</em><0.0286, <em></em>Genta+H<sub>2</sub> <em>P</em><0.0452), and endoglin (control <em>P</em><0.0131<em>,</em> H<sub>2</sub> <em>P</em><0.0164, <em></em>Genta+H<sub>2</sub> <em>P</em><0.0397), urea (control <em>P</em><0.0024<em>,</em> H<sub>2</sub> <em>P</em><0.0001<em>, </em>Genta+H<sub>2</sub> <em>P</em><0.0180), and creatinine parameters (control <em>P</em><0.0017<em>,</em> H<sub>2</sub> <em>P</em><0.0178, <em></em>Genta+H<sub>2</sub> <em>P</em><0.0011<em>)</em> increased in the gentamicin group compared to the other groups<em>,</em> a decrease in these parameters was observed in the gentamicin+hydrogen group compared to the gentamicin group<em>.</em> The Genta group had greater levels of TNF-β than the control (<em>P</em><0.0042) and H2 groups (<em>P</em><0.0268). GSH content was higher in the hydrogen group compared to the gentamicin group. Immunohistochemically, 8-OHdG, MDA, and Bax expressions increased in the gentamicin group compared to the control group, whereas they decreased in the gentamicin+hydrogen group compared to the gentamicin group. Hydrogen may be an alternative treatment for oxidative stress-induced nephrotoxicity.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102604"},"PeriodicalIF":2.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628769","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}
Pub Date : 2024-11-05DOI: 10.1016/j.tice.2024.102602
Sally M. Safwat , Dalia M. Abdel Ghaffar , Mamdouh Eldesoqui , Sally Abdallah Mostafa , Eman A.E. Farrag , Fardous El-Senduny , Basma Osman , Eman Mohamad El Nashar , Shaker Hassan Alshehri , A. Alhefzi , Mohammed Saeed Alasmry , Omar Aboubakr Elnashar , Zienab Helmy Eldken
Background
Muscle tissue is essential for overall well-being that declines with age and different illnesses. Glucocorticoids, despite being efficient in treating inflammation, can induce muscle weakness (known as glucocorticoid-induced myopathy) by affecting protein breakdown and synthesis. Glucocorticoids have a negative impact on satellite cells, which play a role in muscle regeneration. Platelet rich plasma (PRP), containing concentrated growth factors, has a potential role in enhancing tissue repair and could be used to ameliorates combat muscle wasting caused by glucocorticoids.
Aim
The purpose of this study was to identify how PRP can affect dexamethasone-induced myopathy in a rat model.
Methods
Twenty-four male rats were divided into four equal groups: control, PRP, steroid (dexamethasone) treated for induction of myopathy, and steroid then treated with PRP for three weeks. Skeletal muscle contractile properties, protein content of the muscle, oxidative stress markers, histological structure, myogenin gene expression and immunohistochemical expression of Myo-D, Pax-7 and LC3 were assessed.
Results
dexamethasone caused significant muscle weakness, decreased protein content, increased oxidative stress, decreased expression of myogenic genes and upregulated LC3 expression. PRP administration significantly improved muscle function, increased protein content, reduced oxidative stress, and upregulated myogenic genes. Histological results confirmed these findings. Additionally, PRP decreased autophagy marker LC3 expression and increased muscle stem cell markers MyoD and Pax7.
Conclusion
These results suggested that PRP could effectively prevent and reverse dexamethasone-induced muscle atrophy by promoting muscle protein synthesis, reducing oxidative stress, decreasing autophagy, and enhancing muscle stem cell activity. This study supports the potential role of PRP as a therapeutic strategy for muscle wasting disorders.
{"title":"Platelet-rich plasma ameliorates dexamethasone-induced myopathy by suppressing autophagy and enhancing myogenic potential through modulation of Myo-D, Pax-7, and myogenin expression","authors":"Sally M. Safwat , Dalia M. Abdel Ghaffar , Mamdouh Eldesoqui , Sally Abdallah Mostafa , Eman A.E. Farrag , Fardous El-Senduny , Basma Osman , Eman Mohamad El Nashar , Shaker Hassan Alshehri , A. Alhefzi , Mohammed Saeed Alasmry , Omar Aboubakr Elnashar , Zienab Helmy Eldken","doi":"10.1016/j.tice.2024.102602","DOIUrl":"10.1016/j.tice.2024.102602","url":null,"abstract":"<div><h3>Background</h3><div>Muscle tissue is essential for overall well-being that declines with age and different illnesses. Glucocorticoids, despite being efficient in treating inflammation, can induce muscle weakness (known as glucocorticoid-induced myopathy) by affecting protein breakdown and synthesis. Glucocorticoids have a negative impact on satellite cells, which play a role in muscle regeneration. Platelet rich plasma (PRP), containing concentrated growth factors, has a potential role in enhancing tissue repair and could be used to ameliorates combat muscle wasting caused by glucocorticoids.</div></div><div><h3>Aim</h3><div>The purpose of this study was to identify how PRP can affect dexamethasone-induced myopathy in a rat model.</div></div><div><h3>Methods</h3><div>Twenty-four male rats were divided into four equal groups: control, PRP, steroid (dexamethasone) treated for induction of myopathy, and steroid then treated with PRP for three weeks. Skeletal muscle contractile properties, protein content of the muscle, oxidative stress markers, histological structure, myogenin gene expression and immunohistochemical expression of Myo-D, Pax-7 and LC3 were assessed.</div></div><div><h3>Results</h3><div>dexamethasone caused significant muscle weakness, decreased protein content, increased oxidative stress, decreased expression of myogenic genes and upregulated LC3 expression. PRP administration significantly improved muscle function, increased protein content, reduced oxidative stress, and upregulated myogenic genes. Histological results confirmed these findings. Additionally, PRP decreased autophagy marker LC3 expression and increased muscle stem cell markers MyoD and Pax7.</div></div><div><h3>Conclusion</h3><div>These results suggested that PRP could effectively prevent and reverse dexamethasone-induced muscle atrophy by promoting muscle protein synthesis, reducing oxidative stress, decreasing autophagy, and enhancing muscle stem cell activity. This study supports the potential role of PRP as a therapeutic strategy for muscle wasting disorders.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102602"},"PeriodicalIF":2.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628798","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}
Pub Date : 2024-11-04DOI: 10.1016/j.tice.2024.102603
Shufeng Gao, Xintao Wang, Yun Huang, Longgui You
Background
Calreticulin (CALR) is a multifunctional calcium-binding protein. Recent studies have revealed that CALR contributes to tumor development and promotes cancer cell proliferation. However, how CALR affects the development of laryngeal squamous cell carcinoma (LSCC) remains mysterious. Thus, this study aimed to explore the effect of CALR on LSCC development and uncover its underlying mechanisms.
Methods
CALR expression in LSCC cell lines and tissues was examined by qRT-PCR and western blot analysis and its functional role was detected via in vivo and in vitro assays. Cell proliferation was discriminated with CCK-8 and colony formation assays, while apoptosis was analyzed using flow cytometry. Autophagy levels were measured via LC3 immunofluorescence, and western blot assay was conducted to assess apoptosis- and autophagy-related proteins. Additionally, a mouse xenograft model was employed to determine the impact of CALR knockdown on tumor growth.
Results
We found that CALR knockdown reduced LSCC cell viability and proliferation while enhancing apoptosis, whereas CALR overexpression showed opposite effects. In vivo experiments verified that CALR knockdown suppressed tumor growth. In addition, elevated CALR expression induced autophagy in LSCC cells, while autophagy inhibitor 3-MA (2.5 mM) reversed the anti-apoptosis effects of CALR overexpression.
Conclusion
Our study identifies CALR as an oncogene in LSCC, where it promotes tumor progression by inducing autophagy and inhibiting apoptosis. Targeting CALR or modulating autophagy may represent novel therapeutic strategies for LSCC.
{"title":"Calreticulin-driven autophagy enhances cell proliferation in laryngeal squamous cell carcinoma","authors":"Shufeng Gao, Xintao Wang, Yun Huang, Longgui You","doi":"10.1016/j.tice.2024.102603","DOIUrl":"10.1016/j.tice.2024.102603","url":null,"abstract":"<div><h3>Background</h3><div>Calreticulin (CALR) is a multifunctional calcium-binding protein. Recent studies have revealed that CALR contributes to tumor development and promotes cancer cell proliferation. However, how CALR affects the development of laryngeal squamous cell carcinoma (LSCC) remains mysterious. Thus, this study aimed to explore the effect of CALR on LSCC development and uncover its underlying mechanisms.</div></div><div><h3>Methods</h3><div>CALR expression in LSCC cell lines and tissues was examined by qRT-PCR and western blot analysis and its functional role was detected via <em>in vivo</em> and <em>in vitro</em> assays. Cell proliferation was discriminated with CCK-8 and colony formation assays, while apoptosis was analyzed using flow cytometry. Autophagy levels were measured via LC3 immunofluorescence, and western blot assay was conducted to assess apoptosis- and autophagy-related proteins. Additionally, a mouse xenograft model was employed to determine the impact of CALR knockdown on tumor growth.</div></div><div><h3>Results</h3><div>We found that CALR knockdown reduced LSCC cell viability and proliferation while enhancing apoptosis, whereas CALR overexpression showed opposite effects. <em>In vivo</em> experiments verified that CALR knockdown suppressed tumor growth. In addition, elevated CALR expression induced autophagy in LSCC cells, while autophagy inhibitor 3-MA (2.5 mM) reversed the anti-apoptosis effects of CALR overexpression.</div></div><div><h3>Conclusion</h3><div>Our study identifies CALR as an oncogene in LSCC, where it promotes tumor progression by inducing autophagy and inhibiting apoptosis. Targeting CALR or modulating autophagy may represent novel therapeutic strategies for LSCC.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102603"},"PeriodicalIF":2.7,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648836","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}
Pub Date : 2024-11-04DOI: 10.1016/j.tice.2024.102606
Bindu Kumari Yadav , Riya Manoj Kataria
Skin cancer is an uncontrolled proliferation of abnormal skin cells that is usually caused by damaging UV radiation. Skin cancer is classified into two types: non-melanoma skin cancer and melanoma skin cancer. The entire studies focus on cytotoxic effect of prepared 5-Flurouracil loaded chitosan nanoparticle using A375 and A431 skin cancer cell line. In-vitro cell cytotoxicity assay, DAPI test of prepared formulation was conducted to observe the cytotoxic effect. The cell cytotoxicity investigation revealed that nanoparticles had higher cytotoxicity, inducing greater apoptosis within 72 h. The experimental results show that the produced nanoparticle is a good candidate for use as a 5-FU carrier in the treatment of skin cancer.
{"title":"Impact of 5-Flurouracil loaded chitosan nanoparticle on A375 and A431 cell line for the therapy of skin cancer","authors":"Bindu Kumari Yadav , Riya Manoj Kataria","doi":"10.1016/j.tice.2024.102606","DOIUrl":"10.1016/j.tice.2024.102606","url":null,"abstract":"<div><div>Skin cancer is an uncontrolled proliferation of abnormal skin cells that is usually caused by damaging UV radiation. Skin cancer is classified into two types: non-melanoma skin cancer and melanoma skin cancer. The entire studies focus on cytotoxic effect of prepared 5-Flurouracil loaded chitosan nanoparticle using A375 and A431 skin cancer cell line. <em>In-vitro</em> cell cytotoxicity assay, DAPI test of prepared formulation was conducted to observe the cytotoxic effect. The cell cytotoxicity investigation revealed that nanoparticles had higher cytotoxicity, inducing greater apoptosis within 72 h. The experimental results show that the produced nanoparticle is a good candidate for use as a 5-FU carrier in the treatment of skin cancer.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102606"},"PeriodicalIF":2.7,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628778","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}
Pub Date : 2024-11-02DOI: 10.1016/j.tice.2024.102601
Ahmet Turk , Tuba Ozcan Metin , Tuncay Kuloglu , Mustafa Yilmaz , Gokhan Artas , I. Hanifi Ozercan , Serhat Hancer
Introduction
Breast cancer is one of the most common malignant tumors and a leading cause of cancer-related death in women. Research is focusing on biomarkers linked to breast cancer, particularly two novel proteins: isthmin-1 (ISM-1) and spexin (SPX), which require further investigation.
Material and methods
The study involved 20 healthy controls and 60 patients with invasive ductal carcinoma, categorized into three groups: Grade I (n=20), Grade II (n=20), and Grade III (n=20). Levels of ISM-1 and SPX in tissue were analyzed using immunohistochemistry alongside the clinicopathologic data of patients.
Results
There were no statistically significant differences in age, menopausal status, ER, PR, and Cerb-B2 values across grades (p>0.05). Tumor diameters showed a significant increase in Grade I compared to Grade II (p<0.05), while no significant difference was noted between Grade II and Grade III, although diameters were larger in Grade III compared to Grade I (p<0.05). Notably, ISM-1 immunoreactivity decreased, and SPX immunoreactivity increased significantly across all grades compared to normal tissue (p<0.05), with no significant differences between tumor grades for these markers (p>0.05).
Conclusions
This study presents new findings on ISM-1 and SPX expression in invasive ductal breast carcinoma. The decrease in ISM-1 and increase in SPX suggest a need for further research into the relationship between adipokines and tumor development in breast cancer.
{"title":"Isthmin-1 and spexin as promising novel biomarker candidates for invasive ductal breast carcinoma","authors":"Ahmet Turk , Tuba Ozcan Metin , Tuncay Kuloglu , Mustafa Yilmaz , Gokhan Artas , I. Hanifi Ozercan , Serhat Hancer","doi":"10.1016/j.tice.2024.102601","DOIUrl":"10.1016/j.tice.2024.102601","url":null,"abstract":"<div><h3>Introduction</h3><div>Breast cancer is one of the most common malignant tumors and a leading cause of cancer-related death in women. Research is focusing on biomarkers linked to breast cancer, particularly two novel proteins: isthmin-1 (ISM-1) and spexin (SPX), which require further investigation.</div></div><div><h3>Material and methods</h3><div>The study involved 20 healthy controls and 60 patients with invasive ductal carcinoma, categorized into three groups: Grade I (n=20), Grade II (n=20), and Grade III (n=20). Levels of ISM-1 and SPX in tissue were analyzed using immunohistochemistry alongside the clinicopathologic data of patients.</div></div><div><h3>Results</h3><div>There were no statistically significant differences in age, menopausal status, ER, PR, and Cerb-B2 values across grades (p>0.05). Tumor diameters showed a significant increase in Grade I compared to Grade II (p<0.05), while no significant difference was noted between Grade II and Grade III, although diameters were larger in Grade III compared to Grade I (p<0.05). Notably, ISM-1 immunoreactivity decreased, and SPX immunoreactivity increased significantly across all grades compared to normal tissue (p<0.05), with no significant differences between tumor grades for these markers (p>0.05).</div></div><div><h3>Conclusions</h3><div>This study presents new findings on ISM-1 and SPX expression in invasive ductal breast carcinoma. The decrease in ISM-1 and increase in SPX suggest a need for further research into the relationship between adipokines and tumor development in breast cancer.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102601"},"PeriodicalIF":2.7,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628781","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}
Pub Date : 2024-10-31DOI: 10.1016/j.tice.2024.102593
Maguie El Boustani , Nayla Mouawad , Monah Abou Alezz
Colorectal cancer (CRC) affects approximately a million people annually with a mortality rate of 50 %, accounting for 8 % of cancer-related deaths globally. Molecular characterization by The Cancer Genome Atlas could be useful in these tumor subtypes to reveal "druggable" genes. Our study focuses on the significance of the AP3M2 gene (adaptor-related protein complex 3 subunit mu 2) as a potential oncogene by employing RNA interference to inactivate AP3M2. AP3M2, inplicated in protein trafficking to lysosomes pathway and specialized organelles in neuronal cells, was amplified in CRC cell lines. The Knockdown of AP3M2 significantly reduced the viability of three CRC cell lines HCT-116, CACO2, and HT29. Intriguingly, our findings revealed an interaction between AP3M2 expression and autophagy-related genes, as well as reactive oxygen species (ROS) levels in CRC cell lines. These results suggest that targeting AP3M2 could provide a powerful strategy for CRC treatment through autophagy-ROS mechanism.
{"title":"AP3M2: A key regulator from the nervous system modulates autophagy in colorectal cancer","authors":"Maguie El Boustani , Nayla Mouawad , Monah Abou Alezz","doi":"10.1016/j.tice.2024.102593","DOIUrl":"10.1016/j.tice.2024.102593","url":null,"abstract":"<div><div>Colorectal cancer (CRC) affects approximately a million people annually with a mortality rate of 50 %, accounting for 8 % of cancer-related deaths globally. Molecular characterization by The Cancer Genome Atlas could be useful in these tumor subtypes to reveal \"druggable\" genes. Our study focuses on the significance of the AP3M2 gene (adaptor-related protein complex 3 subunit mu 2) as a potential oncogene by employing RNA interference to inactivate AP3M2. AP3M2, inplicated in protein trafficking to lysosomes pathway and specialized organelles in neuronal cells, was amplified in CRC cell lines. The Knockdown of AP3M2 significantly reduced the viability of three CRC cell lines HCT-116, CACO2, and HT29. Intriguingly, our findings revealed an interaction between AP3M2 expression and autophagy-related genes, as well as reactive oxygen species (ROS) levels in CRC cell lines. These results suggest that targeting AP3M2 could provide a powerful strategy for CRC treatment through autophagy-ROS mechanism.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102593"},"PeriodicalIF":2.7,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568524","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}
Pub Date : 2024-10-30DOI: 10.1016/j.tice.2024.102599
Fu Han Wang , Eskandar Qaed , Waleed Aldahmash , Mueataz A. Mahyoub , Zhongyuan Tang , Peng Chu , Ze Yao Tang
Hepatic ischemia/reperfusion (HI/R) presents significant challenges in surgical liver transplantation and hepatic ischemic shock, with few effective clinical preventive measures available. This study explores the potential protective effects and underlying mechanisms of phosphocreatine (PCr) in the context of HI/R. We established an in vitro ischemia/reperfusion model using hepatocellular carcinoma HepG2 cells and normal liver L02 cells. For in vivo assessments, C57BL/6 mice were subjected to the HI/R model to evaluate the impact of PCr on liver protection. PCr pretreatment significantly improved liver cell survival rates, maintained mitochondrial membrane potential (MMP), reduced apoptosis, and alleviated oxidative damage and inflammatory responses. Importantly, PCr exerted its protective effects by downregulating TLR4 and activating the Akt signaling pathway, which suppressed inflammation, mitigated oxidative stress, inhibited apoptosis, and modulated key biomarkers, including ALT, AST, IL-6, IL-1β, TNF-α, SOD, MDA, and reactive oxygen species (ROS). Western blot analyses demonstrated PCr's anti-inflammatory effects through the regulation of UCP2, Cyp-D, Cyt-C, and PGC-1α, thereby preserving mitochondrial structure and function, maintaining MMP, and regulating membrane pores. Transmission electron microscopy further highlighted PCr's role in sustaining mitochondrial integrity. In conclusion, our findings suggest that PCr helps maintain mitochondrial homeostasis by intervening in the TLR4 inflammatory pathway and activating the Akt signaling pathway, ultimately reducing liver injury. This study offers new insights and potential treatment strategies for HI/R, providing valuable guidance for future clinical applications.
{"title":"Phosphocreatine ameliorates hepatocellular apoptosis mediated by protecting mitochondrial damage in liver ischemia/reperfusion injury through inhibiting TLR4 and Agonizing Akt Pathway","authors":"Fu Han Wang , Eskandar Qaed , Waleed Aldahmash , Mueataz A. Mahyoub , Zhongyuan Tang , Peng Chu , Ze Yao Tang","doi":"10.1016/j.tice.2024.102599","DOIUrl":"10.1016/j.tice.2024.102599","url":null,"abstract":"<div><div>Hepatic ischemia/reperfusion (HI/R) presents significant challenges in surgical liver transplantation and hepatic ischemic shock, with few effective clinical preventive measures available. This study explores the potential protective effects and underlying mechanisms of phosphocreatine (PCr) in the context of HI/R. We established an in vitro ischemia/reperfusion model using hepatocellular carcinoma HepG2 cells and normal liver L02 cells. For in vivo assessments, C57BL/6 mice were subjected to the HI/R model to evaluate the impact of PCr on liver protection. PCr pretreatment significantly improved liver cell survival rates, maintained mitochondrial membrane potential (MMP), reduced apoptosis, and alleviated oxidative damage and inflammatory responses. Importantly, PCr exerted its protective effects by downregulating TLR4 and activating the Akt signaling pathway, which suppressed inflammation, mitigated oxidative stress, inhibited apoptosis, and modulated key biomarkers, including ALT, AST, IL-6, IL-1β, TNF-α, SOD, MDA, and reactive oxygen species (ROS). Western blot analyses demonstrated PCr's anti-inflammatory effects through the regulation of UCP2, Cyp-D, Cyt-C, and PGC-1α, thereby preserving mitochondrial structure and function, maintaining MMP, and regulating membrane pores. Transmission electron microscopy further highlighted PCr's role in sustaining mitochondrial integrity. In conclusion, our findings suggest that PCr helps maintain mitochondrial homeostasis by intervening in the TLR4 inflammatory pathway and activating the Akt signaling pathway, ultimately reducing liver injury. This study offers new insights and potential treatment strategies for HI/R, providing valuable guidance for future clinical applications.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102599"},"PeriodicalIF":2.7,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560561","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}
Pub Date : 2024-10-29DOI: 10.1016/j.tice.2024.102600
Nikita Lykov , Huiling Wang , Mogellah John Panga, Zhanxiang Du, Ziyi Chen, Shitian Chen, Lin Zhu, Ye Zhao
The Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) play complex roles in liver health, influencing processes such as fibrosis, cancer development, and regeneration. WW domain binding protein-2 (WBP2) primarily enhances the co-translational activity of YAP/TAZ, which is crucial for the progression of liver diseases. Despite existing knowledge, the specific functions of WBP2 and its interactions with YAP remain inadequately understood. This study investigates the expression levels of WBP2 in zebrafish embryos and its molecular interaction with YAP. We employed morpholino-mediated knockdown of wbp2 and yap, followed by assessments of liver histology, immunofluorescence, and co-immunoprecipitation. Subsequently, RNA sequencing analyses were conducted to elucidate the signaling pathways and mechanisms underlying the interplay between YAP and WBP2 in liver injury. Our findings highlight the significant interaction between WBP2 and YAP, emphasizing their potential as therapeutic targets for liver diseases.
{"title":"Evaluating the involvement and mutual interaction of wbp2 and yap in embryogenesis with an emphasis on liver function in zebrafish embryos","authors":"Nikita Lykov , Huiling Wang , Mogellah John Panga, Zhanxiang Du, Ziyi Chen, Shitian Chen, Lin Zhu, Ye Zhao","doi":"10.1016/j.tice.2024.102600","DOIUrl":"10.1016/j.tice.2024.102600","url":null,"abstract":"<div><div>The Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) play complex roles in liver health, influencing processes such as fibrosis, cancer development, and regeneration. WW domain binding protein-2 (WBP2) primarily enhances the co-translational activity of YAP/TAZ, which is crucial for the progression of liver diseases. Despite existing knowledge, the specific functions of WBP2 and its interactions with YAP remain inadequately understood. This study investigates the expression levels of WBP2 in zebrafish embryos and its molecular interaction with YAP. We employed morpholino-mediated knockdown of <em>wbp2</em> and <em>yap</em>, followed by assessments of liver histology, immunofluorescence, and co-immunoprecipitation. Subsequently, RNA sequencing analyses were conducted to elucidate the signaling pathways and mechanisms underlying the interplay between YAP and WBP2 in liver injury. Our findings highlight the significant interaction between WBP2 and YAP, emphasizing their potential as therapeutic targets for liver diseases.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102600"},"PeriodicalIF":2.7,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560563","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}
Pub Date : 2024-10-29DOI: 10.1016/j.tice.2024.102598
Meenu Singh, Yeshvandra Verma, SV S. Rana
Aims
Present study demonstrates dose and time dependent effects of NiONPs (<30 nm) on the ovaries of Wistar rat.
Methods
Female rats were gavaged NiONPs or NiOMPs (5 mg/kg b.w.) for 24 h, 15 days and 30 days, euthanized and ovaries thus removed were analyzed for nickel bioaconcentration and processed for scanning electron microscopy. Serum samples were analyzed to compare the effects of nickel nano & microparticles on progesterone and estradiol values.
Results
Results confirmed the bioaccumulation of Ni in ovarian tissue. Its concentration was higher in NiONPs treated rats than NiOMPs treated rats. Progesterone level increased whereas estradiol values decreased in NiONPs and NiOMPs treated rats. SEM results also exhibited dose dependent effects on the morphology of corpoluteal complex. The structural changes varied from formation of blebs to distorted microvilli and germinal epithelium.
Conclusion
It is hypothesized that NiONPs/NiOMPs are biodegraded into smaller fragments that conjugate with amino acids and or alter downstream signaling pathways, generate ROS and modulate protein structure activity relationships. Finally, these processes manifest into morphological alterations in the ovary. Biopersistence of nickel in female reproductive system may compromise with fertility and reproductive performance of exposed population.
{"title":"Dose and time dependent morphodynamic changes in the ovary of nano-nickel treated rats A SEM study","authors":"Meenu Singh, Yeshvandra Verma, SV S. Rana","doi":"10.1016/j.tice.2024.102598","DOIUrl":"10.1016/j.tice.2024.102598","url":null,"abstract":"<div><h3>Aims</h3><div>Present study demonstrates dose and time dependent effects of NiONPs (<30 nm) on the ovaries of Wistar rat.</div></div><div><h3>Methods</h3><div>Female rats were gavaged NiONPs or NiOMPs (5 mg/kg b.w.) for 24 h, 15 days and 30 days, euthanized and ovaries thus removed were analyzed for nickel bioaconcentration and processed for scanning electron microscopy. Serum samples were analyzed to compare the effects of nickel nano & microparticles on progesterone and estradiol values.</div></div><div><h3>Results</h3><div>Results confirmed the bioaccumulation of Ni in ovarian tissue. Its concentration was higher in NiONPs treated rats than NiOMPs treated rats. Progesterone level increased whereas estradiol values decreased in NiONPs and NiOMPs treated rats. SEM results also exhibited dose dependent effects on the morphology of corpoluteal complex. The structural changes varied from formation of blebs to distorted microvilli and germinal epithelium.</div></div><div><h3>Conclusion</h3><div>It is hypothesized that NiONPs/NiOMPs are biodegraded into smaller fragments that conjugate with amino acids and or alter downstream signaling pathways, generate ROS and modulate protein structure activity relationships. Finally, these processes manifest into morphological alterations in the ovary. Biopersistence of nickel in female reproductive system may compromise with fertility and reproductive performance of exposed population.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102598"},"PeriodicalIF":2.7,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560562","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号