Journal of Molecular Histology最新文献

{"title":"Preliminary assessment of cardiovascular effects and chemoinformatic analysis of total aqueous extract and fractions from Inula viscosa leaves","authors":"Fatima El hajji, Zineb Hakkou, Ayman M. Al-Qaaneh, Moulay Hfid Youssoufi, Zachee Louis Evariste Akissi, Sevser Sahpaz, Chaimae Alla, Amal Zahi, Sanae Abid, Sergey Shityakov, Abderrahim Ziyyat, Hassane Mekhfi, Mohamed Bnouham, Abdelkhaleq Legssyer","doi":"10.1007/s10735-025-10408-4","DOIUrl":"10.1007/s10735-025-10408-4","url":null,"abstract":"<div><p><i>Inula viscosa</i> (L.) Aiton [<i>Dittrichia viscosa</i> (L.) Greuter] (Asteraceae) is an evergreen perennial herb that grows in different regions of the Mediterranean Basin. It has been particularly used for the treatment of hypertension and diabetes in the Eastern and South-East regions of Morocco. To assess the cardiovascular effects of total aqueous extract and various fractions of <i>Inula viscosa</i> leaves in rat-isolated hearts and aortic rings, and to investigate the potential mechanisms of action of the most active extract(s). In Langendorff's isolated heart system, heart rate (HR) and left ventricular developed pressure (LVDP) were measured for three increasing concentrations of TAE, DCMF, EAF, BF, and AF (0.003, 0.03, and 0.3 mg/mL). Propranolol (1.5 × 10⁻<sup>5</sup> M) and Verapamil (2 × 10⁻<sup>7</sup> M) were used to investigate the potential mechanisms of action of both EAF and BF. In isolated intact aortic rings, four cumulative concentrations of EAF and BF (0.0001, 0.001, 0.01, and 1 mg/mL) were tested for their vasorelaxant effects. The role of the endothelium in the vasorelaxant effect of EAF was examined by denuding aortic rings. To explore the involvement of the nitric oxide (NO) pathway, β-adrenergic receptors, calcium channels, and the sarco/endoplasmic reticulum Ca<sup>2</sup>⁺-ATPase (SERCA) pump, intact aortic rings were preincubated with L-NAME (10⁻<sup>4</sup> M), Propranolol hydrochloride (10⁻<sup>6</sup> M), Verapamil hydrochloride (10⁻<sup>5</sup> M), and Thapsigargin (10⁻<sup>7</sup> M), respectively. The hypotensive effects of both BF (125 mg/kg) and EAF (125 mg/kg) were evaluated indirectly using the tail-cuff method in normotensive rats. Additionally, the antioxidant activity, as well as the total phenolic and flavonoid contents of all prepared extracts, were determined. To further investigate the antioxidant properties, computational analysis was conducted to determine the bond dissociation energies of the hydroxyl groups on the B-ring of luteolin and quercetin, which are present in EAF and BF, respectively. Finally, an UHPLC analysis was performed for BF. In isolated perfused hearts, TAE induced a dose-dependent positive inotropic effect, accompanied by mild bradycardia. EAF exhibited both positive inotropic and chronotropic effects in a concentration-dependent manner. BF demonstrated a highly dose-dependent, selective positive inotropic effect (LVDP = 76.5 ± 19.2% vs. control at 0.3 mg/mL) with no significant impact on HR. Our findings suggest that BF acts independently of β-adrenoreceptor-dependent pathways, whereas EAF may exert its effects through β-agonistic activity. Additionally, Ca<sup>2</sup>⁺ channels may play a role in the effects of both fractions. In phenylephrine-precontracted thoracic arteries, both BF and EAF induced concentration-dependent vasorelaxation, with EAF producing the most potent vasorelaxant effect (E<sub>max</sub> = 84.16 ± 3.68%). EAF mediates an endothelium-independen","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143845705","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}

{"title":"Mesenchymal stem cells and their exosomes: a novel approach to skin regeneration via signaling pathways activation","authors":"Maryam Kananivand,&nbsp;Fatemeh Nouri,&nbsp;Mohammad Hasan Yousefi,&nbsp;Ali Pajouhi,&nbsp;Hakimeah Ghorbani,&nbsp;Hamed Afkhami,&nbsp;Zahra Sadat Razavi","doi":"10.1007/s10735-025-10394-7","DOIUrl":"10.1007/s10735-025-10394-7","url":null,"abstract":"<div><p>Accelerating wound healing is a crucial objective in surgical and regenerative medicine. The wound healing process involves three key stages: inflammation, cell proliferation, and tissue repair. Mesenchymal stem cells (MSCs) have demonstrated significant therapeutic potential in promoting tissue regeneration, particularly by enhancing epidermal cell migration and proliferation. However, the precise molecular mechanisms underlying MSC-mediated wound healing remain unclear. This review highlights the pivotal role of MSCs and their exosomes in wound repair, with a specific focus on critical signaling pathways, including PI3K/Akt, WNT/β-catenin, Notch, and MAPK. These pathways regulate essential cellular processes such as proliferation, differentiation, and angiogenesis. Moreover, in vitro and in vivo studies reveal that MSCs accelerate wound closure, enhance collagen deposition, and modulate immune responses, contributing to improved tissue regeneration. Understanding these mechanisms provides valuable insights into MSC-based therapeutic strategies for enhancing wound healing.</p><h3>Graphical abstract</h3><p>Effects of mesenchymal stem cell and its derived-exosome treatment on skin regeneration and tissue repair via activation of different signaling pathways</p><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818105","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}

{"title":"Quercetin prevents sarcopenia by reversing oxidative stress and mitochondrial damage","authors":"Jianwei Sun,&nbsp;Haibing Liu,&nbsp;Ying Yan,&nbsp;Fei Fang","doi":"10.1007/s10735-025-10411-9","DOIUrl":"10.1007/s10735-025-10411-9","url":null,"abstract":"<div><p>This study investigates the effectiveness of quercetin (QUE) in preventing sarcopenia via the PI3K/AKT signaling pathway. Thirty SD rats were categorized into three groups: a young control group (Y), an old control group (O), and an old QUE-supplemented group (O + QUE). Body weight and grip strength were monitored weekly during the experiment. Soleus and gastrocnemius muscle weights, gastrocnemius tissue pathological examination, cell apoptosis, and mitochondrial damage were evaluated using HE, TUNEL staining, electron microscopy, and JC-1 staining. Biochemical assays and molecular biology techniques (qPCR and Western blot) were used to assess oxidative stress markers and the expression of sarcopenia-related genes and proteins. QUE supplementation increased muscle weight and improved grip strength in aged rats. Furthermore, QUE supplementation alleviated tissue damage, apoptosis, enhanced antioxidant capacity, and decreased damage to oxidative stress and mitochondria in the gastrocnemius of old rats. Molecular assessments revealed downregulation of muscle degradation markers (MuRF1, Atrogen-1, Bnip3) and upregulation of PI3K/AKT pathway proteins, suggesting a mechanistic pathway through which QUE mitigates sarcopenia. QUE maybe modulate the PI3K/AKT pathway to alleviate oxidative stress, mitochondrial damage, and muscle degradation due to aging, highlighting its potential as a therapeutic agent against sarcopenia.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818104","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}

{"title":"Synergistic salvation: HIIT and herbal allies reverse NAFLD damage in rats","authors":"Ehsan Arabzadeh,&nbsp;Amir Sarshin,&nbsp;Foad Feizolahi,&nbsp;Majid Mohabbat,&nbsp;Mohammad-Ali Soleiman-Fallah,&nbsp;Alireza Rahimi,&nbsp;Anatoli Petridou,&nbsp;Zahra Emami,&nbsp;Helena Tajik,&nbsp;Reza Bozorg Omid,&nbsp;Amir Maleki,&nbsp;Hamid Ekrami Ogholbag,&nbsp;Ali Khademi,&nbsp;Mehdi Zargani","doi":"10.1007/s10735-025-10413-7","DOIUrl":"10.1007/s10735-025-10413-7","url":null,"abstract":"<div><p>Fatty liver disease is a build-up of fats in the liver that can damage the organ and lead to serious complications. This study aimed to investigate the effects of exercise training and supplementation (milk thistle, chicory and cumin) on liver metabolites related to its function and health in rats with non-alcoholic fatty liver disease (NAFLD). Forty adult male Wistar rats with an average weight of 215 ± 10 g were divided into a control group fed on the basal diet and four experimental groups fed with high-fat diet (HFD) for 6 weeks to induce non-alcoholic fatty liver disease (NAFLD). The 4 NAFLD groups were subdivided and treated with (a) plain HFD, (b) high-intensity interval training (HIIT), (c) supplement (milk thistle, chicory, and cumin), and (d) combined HIIT and supplementation for 4 weeks. The induction of NAFLD through HFD yielded dyslipidemia, liver tissue damage, increased malondialdehyde, uncoupling protein 2 (UCP2), and phosphatidylinositol-3 kinase (PI3K), as well as decreased superoxide dismutase (SOD) and peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α) in liver tissue (<i>p</i> &lt; 0.05). The 4 weeks intervention with either HIIT, supplement or especially the combined application of both, reversed these factors (<i>p</i> &lt; 0.05) through changes in their concentrations in a direction indicative of enhanced liver health and function. HIIT beside supplementation (milk thistle, chicory, and cumin) improved indices related to oxidative stress, lipid profile, and the expression of PI3K, UCP2, PGC-1α genes expression and PGC-1α protein content, making it potentially promising in the treatment of liver damage caused by HFD.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10413-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143778116","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}

{"title":"A comprehensive assessment of smokeless tobacco (Shammah) extract: unraveling the effects on hematological parameters, antioxidant defense mechanisms, and organ health in rats","authors":"Mabrouk A. Abo-Zaid,&nbsp;Mohammed Abdulaziz Alfattah,&nbsp;Nabila Fathi Elashmawy,&nbsp;Hanan Ahmed Hamdi,&nbsp;Bedor Ali Yatimi,&nbsp;Latifah Abdu Hakami,&nbsp;Amira Ahmed Malhan,&nbsp;Tawfiq AlFaifi,&nbsp;Abadi M. Mashlawi,&nbsp;Sultan Areshi,&nbsp;Ali Hassan Amin,&nbsp;Khalid M. Elazab,&nbsp;Mohamed Fawzy Ramadan,&nbsp;Ahmed Hanafy Ismail","doi":"10.1007/s10735-025-10403-9","DOIUrl":"10.1007/s10735-025-10403-9","url":null,"abstract":"<div><p>\u0000 Shammah, also known as smokeless tobacco, is a form of tobacco product consumed without combustion, commonly used in various cultures, particularly in the Middle East and parts of Africa. The experiment was conducted in four groups control male and female, also treated male and female. The administration of Shammah extract induced significant hematological, biochemical, and histopathological changes in both female and male rats. Treated females showed a decrease in total leukocyte count (TLC) to 9900, while treated males increased to 14,525. Lymphocyte percentage decreased by 9.5% in females and 6.02% in males, with neutrophil counts rising by 24.6% and 20.5%, respectively. Eosinophil levels surged by 240% in females and 50.3% in males. Hemoglobin levels decreased by 12.4–13.1% in females, while males showed a non-significant increase to 15.68. Malondialdehyde (MDA) levels increased to 1.57 in females (57% increase) and 1.93 in males (70.8% increase). Antioxidant enzymes decreased, with superoxide dismutase (SOD) at 3.53 (116.2% decrease) in females and 3.90 (45.8% decrease) in males. Kidney function assessments revealed elevated urea levels of 36.35 (84.8% increase) in females and 43.17 (131.2% increase) in males, alongside creatinine levels of 1.28 (75.3% increase) in females and 1.56 (90.2% increase) in males. Histopathological examinations showed untreated livers with a typical structure, while treated livers exhibited infiltrative cell aggregations, venous congestion, hemorrhage, and edema. Treated kidneys showed severe glomerular atrophy and degeneration. Spleens from treated groups had blending of white and red pulp, while brains displayed hemorrhage and distorted neurons in males, and ghost neurons in females. Treated testes exhibited dilated blood vessels, edema, and reduced spermatogenesis, while treated ovaries showed cyst formation and vacuolar degeneration. These findings indicate significant oxidative stress and organ damage associated with Shammah extract exposure.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143778132","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}

{"title":"piR-38,736 promotes gastric cancer cell proliferation by downregulating SMAD4 expression","authors":"Dongmei Liu,&nbsp;Chenghai Wang,&nbsp;Hongshan Ge,&nbsp;Hong Yu","doi":"10.1007/s10735-025-10412-8","DOIUrl":"10.1007/s10735-025-10412-8","url":null,"abstract":"<div><p>PIWI-interacting RNAs (piRNAs) play an important role in cancer development and progression. Although recent studies had advanced our understanding of the functions of various piRNAs in cancer, the specific role of piR-38736 in gastric cancer remained poorly understood. This study aimed to investigate the clinical significance and underlying mechanisms of piR-38736 in gastric cancer. This study found that piR-38736 was significantly upregulated in gastric cancer cells and tissues. Positive piR-38736 expression was closely correlated with larger tumor size and medium to poor differentiation. Survival analysis revealed that patients with positive piR-38736 expression had significantly shorter survival times compared to those with negative expression. Knockdown of piR-38736 markedly inhibited cell proliferation and tumor growth in gastric cancer. Furthermore, piR-38736 was found to directly bind to the 3′ untranslated region (UTR) of SMAD4 mRNA, resulting in significant downregulation of SMAD4 at both the mRNA and protein levels upon overexpression of piR-38,736. In conclusion, these findings indicate that piR-38,736 promotes cell proliferation and tumor growth in gastric cancer by downregulating SMAD4 expression. piR-38,736 may serve as a prognostic biomarker and a potential therapeutic target for gastric cancer. Further studies are required to fully elucidate the underlying mechanisms of piR-38,736 and explore its clinical implications in gastric cancer management.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10412-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761728","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}

{"title":"PBK as a novel biomarker performed excellent diagnostic and prognostic value in HCC associated with immune infiltration and methylation","authors":"Beibei Lv,&nbsp;Fenna Zhang,&nbsp;Xinyi Zhang,&nbsp;Ziyi Wang,&nbsp;Shuai Hao,&nbsp;Na Ye,&nbsp;Na He","doi":"10.1007/s10735-024-10324-z","DOIUrl":"10.1007/s10735-024-10324-z","url":null,"abstract":"<div><p>Diagnostic and prognosis of hepatocellular carcinoma (HCC) remain major challenge in clinic. This study aimed to explore a gene signature for diagnosis and prognosis prediction of HCC followed by mechanism investigation. Differentially expressed genes (DEGs) in HCC were screened using TCGA. With specific formula, clinic features of prognosis associated DEGs were calculated to obtained a specific model followed by Kaplan–Meier analysis. Protein–protein interaction (PPI) were predicted using STRING and associations between hub gene and clinic features were analyzed using R software. The hub gene was silenced in HCC cell lines followed by cell behaviors analyses. A prognosis associated 14-gene model was identified in this study which could significantly distinguish samples into high-risk and low-risk groups. PBK, BUB1, NUF2, and CDCA8 were the key nodes involved in the 14 gene-coded PPI with high diagnostic values, and only PBK was an independent risk factor of disease specific survival (DSS) of HCC. Moreover, higher PBK was positively correlated with pathological and histological grades, higher AFP, and infiltrations of Th2, T helper cells and aDC of HCC, but negatively correlated with the killer immune cells. Dysregulated methylation might contribute to the higher expression of PBK and silencing PBK significantly suppressed the proliferation, growth, migration, and invasion of HCC cells. PBK, BUB1, NUF2, and CDCA8 played crucial role in prognosis associated 14-gene model with high diagnostic values. Methylation dysregulation-induced PBK accumulation might promote the development of HCC via modulating immune surveillance.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-024-10324-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761783","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}

{"title":"L6H21 stabilizing gut barrier improves EtOH-LPS-induced hepatic steatosis and injury in mice","authors":"Li Ren,&nbsp;Xiaoxia Kong,&nbsp;Chen Mi,&nbsp;Fengyuan Li,&nbsp;Tuo Shao,&nbsp;Zhiming Hao","doi":"10.1007/s10735-025-10410-w","DOIUrl":"10.1007/s10735-025-10410-w","url":null,"abstract":"<div><p>This study aimed to investigate the role of (E)-2,3-dimethoxy-4′-methoxychalcone (L6H21) in alcoholic liver disease (ALD) by considering the connection among alcohol intake, gut microbiota-related intestinal endothelial barrier dysfunction, and ALD. Male C57BL/6J mice (8 weeks old) were randomly assigned to 8 experimental groups (<i>n</i> = 5/group), including those fed a control isocaloric liquid diet (Control), a Lieber-DeCarli liquid alcohol diet with 5% ethanol (EtOH group), and mice in the EtOH + LPS group or LPS group receiving LPS on Day 10. Other four groups (L6H21 group, LPS + L6H21 group, EtOH + L6H21 group, EtOH + LPS + L6H21 group) received L6H21 treatment at 10 mg/kg body weight/day via oral gavage starting from the experiment’s onset. Histological analysis (liver and ileum) and biochemical assays (serum and hepatic tissues) were performed in mice, while real-time PCR, Western blots, and immunofluorescence staining were used to investigate underlying mechanisms. In mice, EtOH-LPS induction led to significant increases in hepatic steatosis, hepatic inflammation, and serum ALT and AST levels. L6H21 treatment significantly reversed these changes. Furthermore, L6H21 treatment also reduced serum total cholesterol and hepatic triglyceride levels. In the intestine, L6H21 suppressed alcohol- and LPS-induced mucosal lesions and bacterial translocation, restored tight junction protein function, inhibited inflammation, and attenuated ROS production. L6H21 represents a promising therapeutic candidate for the intervention of ALD.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761781","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}

{"title":"Evaluating TGF-β1 gene expression and promoter polymorphism in cervical cancer progression","authors":"Pavan Kumar Poleboyina,&nbsp;Akbar Pasha,&nbsp;S. K. Heena,&nbsp;Sneha Malleswari Poleboyina,&nbsp;Smita C. Pawar","doi":"10.1007/s10735-025-10402-w","DOIUrl":"10.1007/s10735-025-10402-w","url":null,"abstract":"<div><p>This study aims to investigate the TGF-β1 gene, which has significant prognostic value for early detection and diagnosis of cervical cancer, as well as TGF-β1 gene mRNA and protein expression and the association of promoter region (−509 C&gt;T) polymorphisms with cervical cancer (CC) development. Transcriptome analysis, immunohistochemistry, and RT-PCR were conducted to determine the gene expression of TGF-β1. The PCR-SSCP and Sanger sequencing methods were employed to test and validate the TGF-β1 −509C&gt;T promoter polymorphism in cervical squamous cell carcinoma in comparison to control samples. TGF-β1 is a cytokine that plays a role in tumorigenesis as well as physiological and pathological processes. It appeared as one of the most over-expressed genes identified through the clariom D transcriptome microarray, which describes its role in cancer progression. The results showed a significant TGF-β1 upregulation in CC compared to normal cervical tissue was confirmed using immunohistochemistry and real-time PCR. The levels of TGF-β1 were also determined using a receiver operating characteristic (ROC) curve to distinguish diseased from normal individuals. TGF-β1 ROC showed good selectivity in distinguishing malignant CC from non-malignant cervical tissues. The −509 C&gt;T promoter polymorphism in the TGF-β1 gene is found to be significantly more common in the disease group, and in-silico analysis (using the AliBaba2.0 gene regulation tool) confirms its correlation to the loss of myogenin transcription factor binding site, may resulting in TGF-β1 overexpression.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761687","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}

{"title":"Blue light-emitting diode promotes mineralization of stem cells from the apical papilla via cryptochrome 1/Wnt/β-catenin signaling","authors":"Lin Ye,&nbsp;Hao Li,&nbsp;Wantong Zhang,&nbsp;Yan Zhou,&nbsp;Xiaorong Lan,&nbsp;Yao Wang","doi":"10.1007/s10735-025-10400-y","DOIUrl":"10.1007/s10735-025-10400-y","url":null,"abstract":"<div><p>This study aimed to determine whether low-intensity blue LED light (4 J/cm²) promotes mineralization of stem cells from the apical papilla (SCAPs) by modulating <i>CRY1</i> expression and to elucidate the underlying molecular mechanisms. SCAPs identity was validated using flow cytometry. In a controlled experimental design, SCAPs were exposed to blue LED light, followed by quantitative assessment of <i>CRY1</i> and osteogenic markers (Runx2, OSX, DSPP, DMP-1) via qRT-PCR, Western blotting, and osteogenic staining. To investigate the role of <i>CRY1</i> in SCAPs osteogenic differentiation, <i>CRY1</i> was overexpressed using lentiviral transfection. Additionally, the Wnt/β-catenin pathway was analyzed using specific inhibitors (XAV-939) to elucidate the underlying molecular mechanisms. Blue LED irradiation reduced <i>CRY1</i> mRNA expression to 80% (day 7) and 45% (day 14) of control levels. <i>CRY1</i> overexpression significantly increased <i>CRY1</i> mRNA and protein levels (<i>P</i> &lt; 0.001) but decreased ALP activity and ARS staining (<i>P</i> &lt; 0.001). Blue LED treatment restored mineralization parameters to 80% of control levels. Key osteogenic genes (DMP-1, DSPP, Runx2, OSX) showed lower mRNA and protein levels in the <i>CRY1</i> overexpression group compared to controls. Blue LED exposure increased these levels to 60–74% (mRNA) and 45–67% (protein) of control values. In the Wnt/β-catenin pathway, <i>CRY1</i> overexpression elevated GSK-3β and reduced p-GSK-3β, β-catenin, and nuclear β-catenin levels. Blue LED treatment restored these levels to 33–54% of control values, indicating pathway activation. Inhibition of the Wnt/β-catenin pathway (using XAV-939) abolished differences in osteogenic gene expression and mineralization between <i>CRY1</i> overexpression and blue LED-treated groups, confirming its critical role. Blue LED light at 4 J/cm² enhances SCAPs mineralization by modulating <i>CRY1</i> expression and activating the Wnt/β-catenin pathway. These findings provide mechanistic insights into photobiomodulation (PBM) in bone regeneration and highlight its potential for tissue engineering and regenerative medicine.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749210","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}