Glial cells missing 2 (GCM2) has been identified as an essential factor for parathyroid differentiation, and GCM2 silencing in parathyroid cells decreases calcium-sensing receptor (CaSR) expression. However, the role of GCM2 in parathyroid differentiation from induced pluripotent stem cells (iPSCs) is unclear. Here, we investigated the role of GCM2 in parathyroid differentiation from iPSCs using the Tet-On 3 G system. We confirmed that iPS cells transfected with GCM2/TRE3G and pCMV-Tet3G vectors express GCM2 in a doxycycline-dependent manner. Though parathyroid glands derive from the endoderm and differentiate via the third pharyngeal arch (PPE), overexpression of GCM2 in iPSCs significantly abolished the suppression of OCT4 and SOX2, suggesting inhibition of endodermal differentiation. GCM2 overexpression at the stage of differentiation into the third PPE also increased the expression levels of CaSR and parathyroid hormone, and increased the number of CaSR+/EpCAM+ cells. These results suggest that GCM2 regulates parathyroid differentiation after endoderm differentiation rather than at an earlier stage.
{"title":"The role of glial cells missing 2 in induced pluripotent stem cell parathyroid differentiation","authors":"Tadashi Kato , Ryusuke Nakatsuka , Rong Zhang , Yasushi Uemura , Hiromi Yamashita , Yoshikazu Matsuoka , Yasumasa Shirouzu , Tatsuya Fujioka , Fumiyuki Hattori , Hiroaki Ogata , Akiko Sakashita , Hirokazu Honda , Hirofumi Hitomi","doi":"10.1016/j.tice.2024.102634","DOIUrl":"10.1016/j.tice.2024.102634","url":null,"abstract":"<div><div>Glial cells missing 2 (GCM2) has been identified as an essential factor for parathyroid differentiation, and GCM2 silencing in parathyroid cells decreases calcium-sensing receptor (CaSR) expression. However, the role of GCM2 in parathyroid differentiation from induced pluripotent stem cells (iPSCs) is unclear. Here, we investigated the role of GCM2 in parathyroid differentiation from iPSCs using the Tet-On 3 G system. We confirmed that iPS cells transfected with GCM2/TRE3G and pCMV-Tet3G vectors express GCM2 in a doxycycline-dependent manner. Though parathyroid glands derive from the endoderm and differentiate via the third pharyngeal arch (PPE), overexpression of GCM2 in iPSCs significantly abolished the suppression of <em>OCT4</em> and <em>SOX2</em>, suggesting inhibition of endodermal differentiation. GCM2 overexpression at the stage of differentiation into the third PPE also increased the expression levels of CaSR and parathyroid hormone, and increased the number of CaSR<sup>+</sup>/EpCAM<sup>+</sup> cells. These results suggest that GCM2 regulates parathyroid differentiation after endoderm differentiation rather than at an earlier stage.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"92 ","pages":"Article 102634"},"PeriodicalIF":2.7,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142747167","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 : 2024-11-21DOI: 10.1016/j.tice.2024.102633
Tao Zhang, Long Zhao, Xiaoping Tang
We elucidate the role of the BNC1 gene in glioma and its potential mechanism. The expression levels of BNC1 in patients with glioma or corresponding cell lines were down-regulated. High BNC1 expression increased survival rate in patients with glioma. BNC1 gene reduced cell proliferation, and enhanced ferroptosis of glioma cells through the induction of TCF21/PI3K signaling pathway. Meanwhile, BNC1 gene could decline tumor proliferation in mice model of glioma. The ferroptosis inhibitor alleviated the impact of BNC1 on glioma ferroptosis, while the ferroptosis agonist weakened the effect of BNC1 on glioma ferroptosis. SiTCF21 also declined the effects of BNC1 on ferroptosis of glioma. The enhanced expression of TCF21 also inhibited the effect of BNC1 on ferroptosis of glioma. BNC1 protein interlinked with TCF21 protein, and bioluminescence imaging demonstrated that BNC1 enhanced TCF21 expression in the brain tissue of the mouse model of glioma. In conclusion, BNC1 reduced cell proliferation, and increased ferroptosis of glioma cells by TCF21/PI3K signaling pathway, may be a feasible strategy to treat glioma.
{"title":"Down-regulated BNC1 promotes glioma by inhibiting ferroptosis via TCF21/PI3K signaling pathway BNC1TCF21PI3K","authors":"Tao Zhang, Long Zhao, Xiaoping Tang","doi":"10.1016/j.tice.2024.102633","DOIUrl":"10.1016/j.tice.2024.102633","url":null,"abstract":"<div><div>We elucidate the role of the <em>BNC1</em> gene in glioma and its potential mechanism. The expression levels of <em>BNC1</em> in patients with glioma or corresponding cell lines were down-regulated. High <em>BNC1</em> expression increased survival rate in patients with glioma. <em>BNC1</em> gene reduced cell proliferation, and enhanced ferroptosis of glioma cells through the induction of <em>TCF21</em>/<em>PI3K</em> signaling pathway. Meanwhile, <em>BNC1</em> gene could decline tumor proliferation in mice model of glioma. The ferroptosis inhibitor alleviated the impact of <em>BNC1</em> on glioma ferroptosis, while the ferroptosis agonist weakened the effect of <em>BNC1</em> on glioma ferroptosis. Si<em>TCF21</em> also declined the effects of <em>BNC1</em> on ferroptosis of glioma. The enhanced expression of <em>TCF21</em> also inhibited the effect of <em>BNC1</em> on ferroptosis of glioma. <em>BNC1</em> protein interlinked with <em>TCF21</em> protein, and bioluminescence imaging demonstrated that <em>BNC1</em> enhanced <em>TCF21</em> expression in the brain tissue of the mouse model of glioma. In conclusion, <em>BNC1</em> reduced cell proliferation, and increased ferroptosis of glioma cells by <em>TCF21</em>/<em>PI3K</em> signaling pathway, may be a feasible strategy to treat glioma.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102633"},"PeriodicalIF":2.7,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721554","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 : 2024-11-21DOI: 10.1016/j.tice.2024.102630
Indyaswan Tegar Suryaningtyas , Jae-Young Je
Non-alcoholic fatty liver disease (NAFLD) is a progressive condition, advancing from simple hepatic lipid accumulation to inflammation, fibrosis, and increased risk of mortality. This study explores the therapeutic efficacy of bioactive peptides PIISVYWK (P1) and FSVVPSPK (P2) in ameliorating NAFLD in both oleic acid-treated HepG2 cells and high-fat diet (HFD)-induced mice. Our findings demonstrated that P1 and P2 significantly reduced hepatic fat deposition, enhanced lipolysis by promoting the release of free glycerol and free fatty acids, and suppressed key de novo lipogenesis-related proteins, including peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer-binding protein α (C/EBPα), sterol regulatory element-binding protein 1 (SREBP-1), and fatty acid synthase (FAS). Furthermore, both peptides stimulated fatty acid oxidation via phosphorylation of AMP-activated protein kinase (AMPK) and hormone-sensitive lipase (HSL). Notably, reductions in body and liver weight, along with improved cholesterol profiles and liver function markers (alanine transaminase and aspartate aminotransferase), were observed in HFD mice. Additionally, P1 and P2 significantly attenuated the production of pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in both in vitro and in vivo models. Collectively, these results highlight the potent therapeutic potential of P1 and P2 in mitigating NAFLD progression, offering a promising intervention for this increasingly prevalent metabolic disorder.
{"title":"Therapeutic effects of blue mussel-derived peptides (PIISVYWK and FSVVPSPK) on non-alcoholic fatty liver disease by modulating lipid metabolism and inflammation in high-fat diet-induced mice","authors":"Indyaswan Tegar Suryaningtyas , Jae-Young Je","doi":"10.1016/j.tice.2024.102630","DOIUrl":"10.1016/j.tice.2024.102630","url":null,"abstract":"<div><div>Non-alcoholic fatty liver disease (NAFLD) is a progressive condition, advancing from simple hepatic lipid accumulation to inflammation, fibrosis, and increased risk of mortality. This study explores the therapeutic efficacy of bioactive peptides PIISVYWK (P1) and FSVVPSPK (P2) in ameliorating NAFLD in both oleic acid-treated HepG2 cells and high-fat diet (HFD)-induced mice. Our findings demonstrated that P1 and P2 significantly reduced hepatic fat deposition, enhanced lipolysis by promoting the release of free glycerol and free fatty acids, and suppressed key <em>de novo</em> lipogenesis-related proteins, including peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer-binding protein α (C/EBPα), sterol regulatory element-binding protein 1 (SREBP-1), and fatty acid synthase (FAS). Furthermore, both peptides stimulated fatty acid oxidation via phosphorylation of AMP-activated protein kinase (AMPK) and hormone-sensitive lipase (HSL). Notably, reductions in body and liver weight, along with improved cholesterol profiles and liver function markers (alanine transaminase and aspartate aminotransferase), were observed in HFD mice. Additionally, P1 and P2 significantly attenuated the production of pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in both <em>in vitro</em> and <em>in vivo</em> models. Collectively, these results highlight the potent therapeutic potential of P1 and P2 in mitigating NAFLD progression, offering a promising intervention for this increasingly prevalent metabolic disorder.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102630"},"PeriodicalIF":2.7,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695839","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 : 2024-11-20DOI: 10.1016/j.tice.2024.102626
Mohammad-Sadegh Lotfi , Mohammad Sheibani , Majid Jafari-Sabet
Quercetin, a natural flavonoid, has been extensively researched for its potential in promoting bone regeneration and tissue engineering. This review aimed to provide a comprehensive overview of the applications of quercetin-based biomaterials in bone regeneration and tissue engineering. The review discusses several studies that have integrated quercetin into biomaterials such as electrospun fibers, hydrogels, microspheres, and nanoparticles. These biomaterials are engineered to imitate the natural extracellular matrix of bone, creating an environment conducive to cell attachment, growth, and differentiation.
The investigations presented emphasize the potential of quercetin-derived biomaterials in improving bone regeneration, decreasing oxidative stress and inflammation, and facilitating bone tissue restoration. These biomaterials have demonstrated the ability to facilitate cell encapsulation, maintain consistent quercetin release patterns, and have been applied in a range of uses such as bone grafts, implants, and tissue engineering scaffolds. Biomaterials derived from quercetin are utilized in the treatment of bone-related disorders, including osteoporosis and bone defects. These materials enhance bone regeneration by providing a scaffold for new bone growth, promoting the development of new bone tissue, and improving the mechanical properties of bone tissue.
{"title":"Quercetin-based biomaterials for enhanced bone regeneration and tissue engineering","authors":"Mohammad-Sadegh Lotfi , Mohammad Sheibani , Majid Jafari-Sabet","doi":"10.1016/j.tice.2024.102626","DOIUrl":"10.1016/j.tice.2024.102626","url":null,"abstract":"<div><div>Quercetin, a natural flavonoid, has been extensively researched for its potential in promoting bone regeneration and tissue engineering. This review aimed to provide a comprehensive overview of the applications of quercetin-based biomaterials in bone regeneration and tissue engineering. The review discusses several studies that have integrated quercetin into biomaterials such as electrospun fibers, hydrogels, microspheres, and nanoparticles. These biomaterials are engineered to imitate the natural extracellular matrix of bone, creating an environment conducive to cell attachment, growth, and differentiation.</div><div>The investigations presented emphasize the potential of quercetin-derived biomaterials in improving bone regeneration, decreasing oxidative stress and inflammation, and facilitating bone tissue restoration. These biomaterials have demonstrated the ability to facilitate cell encapsulation, maintain consistent quercetin release patterns, and have been applied in a range of uses such as bone grafts, implants, and tissue engineering scaffolds. Biomaterials derived from quercetin are utilized in the treatment of bone-related disorders, including osteoporosis and bone defects. These materials enhance bone regeneration by providing a scaffold for new bone growth, promoting the development of new bone tissue, and improving the mechanical properties of bone tissue.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102626"},"PeriodicalIF":2.7,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721557","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 : 2024-11-19DOI: 10.1016/j.tice.2024.102624
Nima Rastegar-Pouyani , Mohadeseh Haji Abdolvahab , Mohammad Amin Farzin , Hamed Zare , Prashant Kesharwani , Amirhossein Sahebkar
Cancer-associated fibroblasts (CAFs) are a heterogeneous cell population within the tumor that have recently come into the spotlight. By extracellular matrix (ECM) remodeling and robust cross-talk with cancer cells via different secretions such as cytokines, chemokines, and growth factors, CAFs contribute to cancer progression and poorer prognoses in patients. Novel candidates have been developed to inhibit CAFs; however, due to safety and efficacy issues, none have successfully passed clinical trials. Despite these shortcomings, one concept embraced by many researchers is to repurpose non-oncology drugs with potential anti-cancer properties for cancer treatment. One such example is pirfenidone (PFD), an oral anti-fibrotic medication, primarily administered for idiopathic pulmonary fibrosis. Emerging evidence suggests that PFD has promising anti-cancer effects, mainly manifesting through targeting CAFs. With inhibitory effects on CAFs, PFD restricts cancer proliferation, metastasis, immunosuppression, drug resistance, and tumor stiffness. To improve efficacy and minimize adverse effects, several innovative approaches have been proposed for targeting CAFs via PFD. Interestingly, combination therapy comprising PFD and chemotherapeutics e.g. doxorubicin has shown synergistic anti-cancer effects while protecting normal tissue. Furthermore, novel drug delivery systems, e.g. biomimetic liposomes and multilayer core-shell nanoparticles, have enhanced the pharmacokinetic properties of PFD and further increased its intratumoral delivery. Single-cell RNA sequencing (scRNA-seq) has also been suggested to characterize different subpopulations of CAFs and design precise PFD-based therapeutic strategies. Herein, we discuss the promising anti-cancer effects of PFD via inhibition of CAFs. We then provide findings on novel PFD-based approaches to target CAFs using combination therapy, nanocarrier-based drug delivery, and scRNA-seq.
{"title":"Targeting cancer-associated fibroblasts with pirfenidone: A novel approach for cancer therapy","authors":"Nima Rastegar-Pouyani , Mohadeseh Haji Abdolvahab , Mohammad Amin Farzin , Hamed Zare , Prashant Kesharwani , Amirhossein Sahebkar","doi":"10.1016/j.tice.2024.102624","DOIUrl":"10.1016/j.tice.2024.102624","url":null,"abstract":"<div><div>Cancer-associated fibroblasts (CAFs) are a heterogeneous cell population within the tumor that have recently come into the spotlight. By extracellular matrix (ECM) remodeling and robust cross-talk with cancer cells <em>via</em> different secretions such as cytokines, chemokines, and growth factors, CAFs contribute to cancer progression and poorer prognoses in patients. Novel candidates have been developed to inhibit CAFs; however, due to safety and efficacy issues, none have successfully passed clinical trials. Despite these shortcomings, one concept embraced by many researchers is to repurpose non-oncology drugs with potential anti-cancer properties for cancer treatment. One such example is pirfenidone (PFD), an oral anti-fibrotic medication, primarily administered for idiopathic pulmonary fibrosis. Emerging evidence suggests that PFD has promising anti-cancer effects, mainly manifesting through targeting CAFs. With inhibitory effects on CAFs, PFD restricts cancer proliferation, metastasis, immunosuppression, drug resistance, and tumor stiffness. To improve efficacy and minimize adverse effects, several innovative approaches have been proposed for targeting CAFs <em>via</em> PFD. Interestingly, combination therapy comprising PFD and chemotherapeutics <em>e.g.</em> doxorubicin has shown synergistic anti-cancer effects while protecting normal tissue. Furthermore, novel drug delivery systems, e.g. biomimetic liposomes and multilayer core-shell nanoparticles, have enhanced the pharmacokinetic properties of PFD and further increased its intratumoral delivery. Single-cell RNA sequencing (scRNA-seq) has also been suggested to characterize different subpopulations of CAFs and design precise PFD-based therapeutic strategies. Herein, we discuss the promising anti-cancer effects of PFD <em>via</em> inhibition of CAFs. We then provide findings on novel PFD-based approaches to target CAFs using combination therapy, nanocarrier-based drug delivery, and scRNA-seq.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102624"},"PeriodicalIF":2.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711131","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 : 2024-11-19DOI: 10.1016/j.tice.2024.102632
Ming Du , Xinyu Li , Bayinnamula , Na Wang , Yuanyi Liu, Lei Zhang, Yiping Zhao, Manglai Dugarjaviin
An important method for preserving equine germplasm is the cryopreservation of equine oocytes. Due to its ease, rapidity and affordability, vitrification freezing has taken over as the primary method of horse oocyte cryopreservation. The vitrification cryoprotectants utilized in this investigation were Ethylene glycol (E), Dimethyl sulfoxide (D), Sucrose (S), and Ficoll (F). According to the oocyte volume alteration, the treatment time was 39 s in equilibrium solution ED10 (10 % EG + 10 % DMSO), 32 s in equilibrium solution ED15 (15 % EG + 15 % DMSO), while 20 s in equilibrium solution ED20 (20 % EG + 20 % DMSO). We prepared three kinds of cryosolutions EDFS30 (E15 %+D15 %+70 %FS), EDFS35 (E17.5 % + D17.5 % + 65 %FS), EDFS40 (E20 % + D20 % + 60 %FS) according to the proportion of protectant components. Among 27 freezing protocols, we selected protocol ED10 (39 s) + EDFS30 + 80 s which has the highest in vitro culture maturation rate of 19.3 % while protocol ED20 (20 s) + EDFS40 + 120 s is the worst. Apoptosis gene analysis revealed that BAX, BID, BOK, and TP53 expression was substantially higher in oocytes from the ED20 (20 s) + EDFS40 + 120 s group than in oocytes from the ED10 (39 s) + EDFS30 + 80 s and control groups (p<0.01). This study investigated several vitrification schemes for equine oocytes.
{"title":"Optimization of vitrification methods for equine oocytes","authors":"Ming Du , Xinyu Li , Bayinnamula , Na Wang , Yuanyi Liu, Lei Zhang, Yiping Zhao, Manglai Dugarjaviin","doi":"10.1016/j.tice.2024.102632","DOIUrl":"10.1016/j.tice.2024.102632","url":null,"abstract":"<div><div>An important method for preserving equine germplasm is the cryopreservation of equine oocytes. Due to its ease, rapidity and affordability, vitrification freezing has taken over as the primary method of horse oocyte cryopreservation. The vitrification cryoprotectants utilized in this investigation were Ethylene glycol (E), Dimethyl sulfoxide (D), Sucrose (S), and Ficoll (F). According to the oocyte volume alteration, the treatment time was 39 s in equilibrium solution ED10 (10 % EG + 10 % DMSO), 32 s in equilibrium solution ED15 (15 % EG + 15 % DMSO), while 20 s in equilibrium solution ED20 (20 % EG + 20 % DMSO). We prepared three kinds of cryosolutions EDFS30 (E15 %+D15 %+70 %FS), EDFS35 (E17.5 % + D17.5 % + 65 %FS), EDFS40 (E20 % + D20 % + 60 %FS) according to the proportion of protectant components. Among 27 freezing protocols, we selected protocol ED10 (39 s) + EDFS30 + 80 s which has the highest in vitro culture maturation rate of 19.3 % while protocol ED20 (20 s) + EDFS40 + 120 s is the worst. Apoptosis gene analysis revealed that BAX, BID, BOK, and TP53 expression was substantially higher in oocytes from the ED20 (20 s) + EDFS40 + 120 s group than in oocytes from the ED10 (39 s) + EDFS30 + 80 s and control groups (<em>p</em><0.01). This study investigated several vitrification schemes for equine oocytes.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102632"},"PeriodicalIF":2.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693685","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 : 2024-11-18DOI: 10.1016/j.tice.2024.102629
Mahmoud A. Mahmoud , Mustafa M. Ibrahim
During routine veterinary inspection of fish from fishing boats, fish auction yards, and fish landing stations, as well as the large fish market for detection of fish diseases, abnormalities and/or overgrowth in body surfaces and evaluation of hygienic conditions and fish quality at El-Jubail Province, Saudi Arabia., external neoplastic overgrowths were observed in two fish species, giant sea catfish (Arius thalassinus) and Delagoa threadfin bream (Nemipterus bipunctatu). In both fishes, the neoplasms appeared as bony masses, and it was hard in its consistency. In the giant sea catfish (Arius thalassinus), the tumor appeared as three multifocal hard swellings at different locations (in the head region, at the dorsal fin, and near the caudal fin). The tumor mass in the head region of this fish was observed at the base of the right angle of the lower jaw, and it was hard, bony, nodular to round, and of 0.7 cm in diameter. The second one was observed at the dorsal fin and appeared as a small oval to rod hard mass of 0.5 cm in diameter, while the third mass appeared as a large and irregular wart-shaped bony swelling, about 3 cm in diameter, that extended laterally on the left aspect of the caudal peduncle near the caudal fin. In radiographic examination, the neoplasm appeared small, round to large, irregular, dense bony overgrowth with variable sizes. In histopathological examination, evidences of fibro-osteosarcoma associated with prominent multiple rounded eosinophilic apoptotic bodies in the neoplastic bony trabeculae were observed. On the other side, the Delagoa threadfin bream (Nemipterus bipunctatus) showed only one yellowish to reddish, pedunculated, irregular, and very hard swelling at the base of the median site of the dorsal fin, and it was firmly connected to the spine of the dorsal fin; it was about 1 cm high with a wide base of 0.5 cm. In histopathological examination, the bony neoplastic masses in this fish appeared with massive edematous fibrous connective tissue and newly formed blood capillaries; abnormal mitosis, hemorrhages, and hemosiderin pigment deposition in the central and peripheral parts of the neoplasm were observed. New bone formation was confirmed using histochemical staining. Our results indicated that these two species are vulnerable to fibro-osteosarcoma. Further environmental investigations as well as immunohistochemical and molecular studies are required to indicate the potential impact of the environmental pollution on the incidence of the neoplasms in this locality and to correlate the cellular evidence of the neoplasms to a specific fish species.
{"title":"Osteogenic sarcomas in two fish species giant sea catfish (Arius thalassinus), and Delagoa threadfin bream (Nemipterus bipunctatu) caught from Saudi Arabia, the Arabian Gulf","authors":"Mahmoud A. Mahmoud , Mustafa M. Ibrahim","doi":"10.1016/j.tice.2024.102629","DOIUrl":"10.1016/j.tice.2024.102629","url":null,"abstract":"<div><div>During routine veterinary inspection of fish from fishing boats, fish auction yards, and fish landing stations, as well as the large fish market for detection of fish diseases, abnormalities and/or overgrowth in body surfaces and evaluation of hygienic conditions and fish quality at El-Jubail Province, Saudi Arabia., external neoplastic overgrowths were observed in two fish species, giant sea catfish (<em>Arius thalassinus</em>) and Delagoa threadfin bream (<em>Nemipterus bipunctatu</em>). In both fishes, the neoplasms appeared as bony masses, and it was hard in its consistency. In the giant sea catfish (<em>Arius thalassinus</em>), the tumor appeared as three multifocal hard swellings at different locations (in the head region, at the dorsal fin, and near the caudal fin). The tumor mass in the head region of this fish was observed at the base of the right angle of the lower jaw, and it was hard, bony, nodular to round, and of 0.7 cm in diameter. The second one was observed at the dorsal fin and appeared as a small oval to rod hard mass of 0.5 cm in diameter, while the third mass appeared as a large and irregular wart-shaped bony swelling, about 3 cm in diameter, that extended laterally on the left aspect of the caudal peduncle near the caudal fin. In radiographic examination, the neoplasm appeared small, round to large, irregular, dense bony overgrowth with variable sizes. In histopathological examination, evidences of fibro-osteosarcoma associated with prominent multiple rounded eosinophilic apoptotic bodies in the neoplastic bony trabeculae were observed. On the other side, the Delagoa threadfin bream (<em>Nemipterus bipunctatus</em>) showed only one yellowish to reddish, pedunculated, irregular, and very hard swelling at the base of the median site of the dorsal fin, and it was firmly connected to the spine of the dorsal fin; it was about 1 cm high with a wide base of 0.5 cm. In histopathological examination, the bony neoplastic masses in this fish appeared with massive edematous fibrous connective tissue and newly formed blood capillaries; abnormal mitosis, hemorrhages, and hemosiderin pigment deposition in the central and peripheral parts of the neoplasm were observed. New bone formation was confirmed using histochemical staining. Our results indicated that these two species are vulnerable to fibro-osteosarcoma. Further environmental investigations as well as immunohistochemical and molecular studies are required to indicate the potential impact of the environmental pollution on the incidence of the neoplasms in this locality and to correlate the cellular evidence of the neoplasms to a specific fish species.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102629"},"PeriodicalIF":2.7,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695818","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 : 2024-11-17DOI: 10.1016/j.tice.2024.102620
Ying Yang
Diabetic retinopathy (DR) has been proven to be a leading cause of blindness. This study aimed to investigate the effect of Yes-associated protein 1 (YAP1) on the hypoxia-induced DR mice retinal microvascular endothelial cells (MRMECs) model. The hypoxia-induced DR MRMECs model was generated by treating in hypoxia circumstance (5 % CO2 and 3 % O2) for 48 h. This study constructed YAP1 overexpression and taurine-upregulated gene 1 (TUG1) silencing lentiviral vectors, both of which were used to infect the DR MRMECs model. Quantitative real-time PCR (qRT-PCR) was used to amplify the YAP1, TUG1, vascular endothelial growth factor A (VEGFA), and miR-144–3p gene. Western blot was used to identify the expression of YAP1 and VEGFA. The CCK-8 assay was used to evaluate proliferation and the flow cytometry assay was used to determine apoptosis of MRMECs. Cell migration and tube formation were also evaluated. The results showed that YAP1 overexpression and TUG1 silencing lentivirus were successfully constructed. YAP1 overexpression significantly promoted, but TUG1 silence inhibited cell proliferation and migration compared to DR MRMECs model (P<0.05). YAP1 markedly promoted TUG1/VEGFA and reduced miR-144–3p gene transcription compared to those of the DR MRMECs model (P<0.05). YAP1 overexpression and TUG1 silence demonstrated the opposite effects on VEGFA expression. YAP1 overexpression obviously promoted tube formation of MRMECs. In conclusion, overexpression of YAP1 promoted cell proliferation, cell migration, TUG1 and VEGFA expression, and reduced the transcription of the miR-144–3p gene in DR MRMECs. Overexpression of YAP1 aggravated the progress of DR in MRMECs by activating the TUG1/miR-144–3p/VEGFA signaling pathway.
{"title":"YAP1 overexpression aggravates the progress of diabetic retinopathy by activating the TUG1/miR-144–3p/VEGFA signaling pathway in the hypoxia-induced DR MRMECs model","authors":"Ying Yang","doi":"10.1016/j.tice.2024.102620","DOIUrl":"10.1016/j.tice.2024.102620","url":null,"abstract":"<div><div>Diabetic retinopathy (DR) has been proven to be a leading cause of blindness. This study aimed to investigate the effect of Yes-associated protein 1 (YAP1) on the hypoxia-induced DR mice retinal microvascular endothelial cells (MRMECs) model. The hypoxia-induced DR MRMECs model was generated by treating in hypoxia circumstance (5 % CO<sub>2</sub> and 3 % O<sub>2</sub>) for 48 h. This study constructed YAP1 overexpression and taurine-upregulated gene 1 (TUG1) silencing lentiviral vectors, both of which were used to infect the DR MRMECs model. Quantitative real-time PCR (qRT-PCR) was used to amplify the YAP1, TUG1, vascular endothelial growth factor A (VEGFA), and miR-144–3p gene. Western blot was used to identify the expression of YAP1 and VEGFA. The CCK-8 assay was used to evaluate proliferation and the flow cytometry assay was used to determine apoptosis of MRMECs. Cell migration and tube formation were also evaluated. The results showed that YAP1 overexpression and TUG1 silencing lentivirus were successfully constructed. YAP1 overexpression significantly promoted, but TUG1 silence inhibited cell proliferation and migration compared to DR MRMECs model (<em>P</em><0.05). YAP1 markedly promoted TUG1/VEGFA and reduced miR-144–3p gene transcription compared to those of the DR MRMECs model (<em>P</em><0.05). YA<em>P</em>1 overexpression and TUG1 silence demonstrated the opposite effects on VEGFA expression. YAP1 overexpression obviously promoted tube formation of MRMECs. In conclusion, overexpression of YAP1 promoted cell proliferation, cell migration, TUG1 and VEGFA expression, and reduced the transcription of the miR-144–3p gene in DR MRMECs. Overexpression of YAP1 aggravated the progress of DR in MRMECs by activating the TUG1/miR-144–3p/VEGFA signaling pathway.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"92 ","pages":"Article 102620"},"PeriodicalIF":2.7,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142747168","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 : 2024-11-17DOI: 10.1016/j.tice.2024.102627
Dan Wu, Shuyu Li, Meng Chen, Shujing Zhang, Qian Wang
C1q/tumor necrosis factor-related protein-6 (CTRP6) has multiple protective effects against cardiovascular diseases. Myofibroblast differentiation plays a critical role in cardiac fibrosis under various cardiac pathological conditions. The aim of the present study was to determine the effects of CTRP6 on cardiac fibrosis, and to identify the possible mechanisms of action. Toward this end, we measured the expression of fibrotic markers, including collagen I, collagen III, CTGF, and TGFβ1, and assessed the effects of CTRP6 on cardiac fibroblast differentiation into myofibroblasts. CTRP6 inhibited the expression of the angiotensin II (Ang II)-induced myofibroblast markers α-SMA and SM22, and of profibrotic molecules, including collagen I, collagen III, CTGF, TGFβ1, MMP2, MMP9, and TIMP1. Furthermore, CTRP6 significantly attenuated the proliferation and migration of cardiac fibroblasts incubated with Ang II and activated the phosphorylation of AMP-activated protein kinase (AMPK). Incubation with an AMPK inhibitor reversed the subsequent inhibitory effects of CTRP6 on Ang II-induced myofibroblast differentiation. Therefore, CTRP6 suppresses cardiac fibrosis by inhibition of myofibroblast differentiation via AMPK pathway activation, suggesting CTRP6 as a target for the treatment of cardiac fibrosis.
C1q/肿瘤坏死因子相关蛋白-6（CTRP6）对心血管疾病具有多种保护作用。在各种心脏病理条件下，肌成纤维细胞分化在心脏纤维化中起着关键作用。本研究旨在确定 CTRP6 对心脏纤维化的影响，并找出可能的作用机制。为此，我们测量了纤维化标志物的表达，包括胶原 I、胶原 III、CTGF 和 TGFβ1，并评估了 CTRP6 对心脏成纤维细胞分化为肌成纤维细胞的影响。CTRP6抑制了血管紧张素II（Ang II）诱导的肌成纤维细胞标记物α-SMA和SM22的表达，以及包括胶原蛋白I、胶原蛋白III、CTGF、TGFβ1、MMP2、MMP9和TIMP1在内的促纤维化分子的表达。此外，CTRP6 还能明显减少与 Ang II 培养的心脏成纤维细胞的增殖和迁移，并激活 AMP 激活蛋白激酶（AMPK）的磷酸化。用 AMPK 抑制剂孵育可逆转 CTRP6 随后对 Ang II 诱导的肌成纤维细胞分化的抑制作用。因此，CTRP6通过激活AMPK通路抑制肌成纤维细胞分化，从而抑制心脏纤维化，这表明CTRP6是治疗心脏纤维化的一个靶点。
{"title":"C1q/tumor necrosis factor-related protein-6 suppresses the angiotensin II-induced differentiation of cardiac fibroblasts to myofibroblasts via activation of the AMPK pathway","authors":"Dan Wu, Shuyu Li, Meng Chen, Shujing Zhang, Qian Wang","doi":"10.1016/j.tice.2024.102627","DOIUrl":"10.1016/j.tice.2024.102627","url":null,"abstract":"<div><div>C1q/tumor necrosis factor-related protein-6 (CTRP6) has multiple protective effects against cardiovascular diseases. Myofibroblast differentiation plays a critical role in cardiac fibrosis under various cardiac pathological conditions. The aim of the present study was to determine the effects of CTRP6 on cardiac fibrosis, and to identify the possible mechanisms of action. Toward this end, we measured the expression of fibrotic markers, including collagen I, collagen III, CTGF, and TGFβ1, and assessed the effects of CTRP6 on cardiac fibroblast differentiation into myofibroblasts. CTRP6 inhibited the expression of the angiotensin II (Ang II)-induced myofibroblast markers α-SMA and SM22, and of profibrotic molecules, including collagen I, collagen III, CTGF, TGFβ1, MMP2, MMP9, and TIMP1. Furthermore, CTRP6 significantly attenuated the proliferation and migration of cardiac fibroblasts incubated with Ang II and activated the phosphorylation of AMP-activated protein kinase (AMPK). Incubation with an AMPK inhibitor reversed the subsequent inhibitory effects of CTRP6 on Ang II-induced myofibroblast differentiation. Therefore, CTRP6 suppresses cardiac fibrosis by inhibition of myofibroblast differentiation via AMPK pathway activation, suggesting CTRP6 as a target for the treatment of cardiac fibrosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102627"},"PeriodicalIF":2.7,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711130","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 : 2024-11-16DOI: 10.1016/j.tice.2024.102614
Ola Mohammed Youssef , Nermeen Hosney Lashine , Mohammad El-Nablaway , Mona Ibrahim El-yamany , Manar Monir Youssef , Dina Abdalla Arida
Over time, Parkinson disease (PD) develops as a neurological illness. The goal of this study was to see whether ferulic acid has any neuroprotective benefits on the cerebellum of rats that have Parkinson's disease brought on by rotenone poisoning. A total of twenty-four male albino rats, in good condition, weighed between 200 and 250 g and nine to ten weeks old, were employed in the investigation. The control group received 1 ml of sunflower oil intraperitoneally (i.p.) each day. Rats' motor performance was considerably worse when given rotenone than it was in the control group. Rats given Ferulic Acid (FA) showed a substantial drop in the amount of glutathione (GSH) in the cerebellum. Moreover, the injection of FA resulted in a significant reduction in the optical density (OD) of the immune-positive reaction for α-synuclein, and the area percentage of BCL-2 and NF-kB immunological positive response. FA therapy, surprisingly, enhanced the OD of TH immunopositive response and apoptotic regulators (BCL2) in the cerebellum. Furthermore, FA boosted BCL2 expression, confirming the antiapoptotic effects of FA. Based on these results, FA is probably a good candidate to treat neurodegenerative diseases brought on by long-term exposure to rotenone.
{"title":"Ferulic acid mitigated rotenone toxicity -Evoked Parkinson in rat model by featuring apoptosis, oxidative stress, and neuroinflammation signaling","authors":"Ola Mohammed Youssef , Nermeen Hosney Lashine , Mohammad El-Nablaway , Mona Ibrahim El-yamany , Manar Monir Youssef , Dina Abdalla Arida","doi":"10.1016/j.tice.2024.102614","DOIUrl":"10.1016/j.tice.2024.102614","url":null,"abstract":"<div><div>Over time, Parkinson disease (PD) develops as a neurological illness. The goal of this study was to see whether ferulic acid has any neuroprotective benefits on the cerebellum of rats that have Parkinson's disease brought on by rotenone poisoning. A total of twenty-four male albino rats, in good condition, weighed between 200 and 250 g and nine to ten weeks old, were employed in the investigation. The control group received 1 ml of sunflower oil intraperitoneally (i.p.) each day. Rats' motor performance was considerably worse when given rotenone than it was in the control group. Rats given Ferulic Acid (FA) showed a substantial drop in the amount of glutathione (GSH) in the cerebellum. Moreover, the injection of FA resulted in a significant reduction in the optical density (OD) of the immune-positive reaction for α-synuclein, and the area percentage of BCL-2 and NF-kB immunological positive response. FA therapy, surprisingly, enhanced the OD of TH immunopositive response and apoptotic regulators (BCL2) in the cerebellum. Furthermore, FA boosted BCL2 expression, confirming the antiapoptotic effects of FA. Based on these results, FA is probably a good candidate to treat neurodegenerative diseases brought on by long-term exposure to rotenone.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102614"},"PeriodicalIF":2.7,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693682","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}
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