The aim of this study was to investigate the regenerative effect of lyophilized dental follicle mesenchymal stem cells (DF-MSCs) combined with rat platelet-rich fibrin (PRF) on geriatric skin wounds. Human DF-MSCs which were isolated from the wisdom teeth of healthy donors and PRF were mixed and incubated in a 37 °C incubator for 1–2 h containing 1 million cells in 150 mg PRF. The mixture was suspended in a freeze-drying solution and then lyophilized. Wounds were created on the back skin of Wistar albino rats using a 6 mm punch. Lyophilized DF-MSCs, PRF, or PRF + DF-MSCs were applied to the wounds of rats. On the 15th day, the wound area was histopathologically evaluated in rats. Blood samples from rats were analyzed for total antioxidant status (TAOS), and inflammatory cytokine levels using ELISA. In both young and geriatric rats treated with lyophilized PRF + DF-MSCs, wound area began to significantly decrease from the 10th day compared to the untreated group (p < 0.05). Histopathological examination revealed that in the lyophilized PRF + DF-MSCs treated groups, epithelial integrity and scarless healing significantly increased compared to the untreated groups (p < 0.05). There were no significant differences in TAOS, total oxidant status (TOS), tumor necrosis factor (TNF), interleukin-6 (IL6), and hydroxyproline levels in serum samples from young rats on the 15th day. In geriatric rats, hydroxyproline (HYPS) levels were increased in the DF-MSC and PRF + DF-MSC groups (p < 0.01), TNF was significantly elevated in PRF geriatric group and IL6 was increased in the PRF group compared to the control group (p = 0.01). Lyophilized PRF + DF-MSCs, which is a shelf-stable and ready-to-use product, hold promise, especially for traumatic wounds in geriatric individuals with longer healing times.

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Background/aims: Ulcerative colitis (UC) is a chronic inflammatory disease affecting the colon. Mesenchymal stem cells (MSCs) are candidates for use in inflammatory diseases with their tissue regeneration and anti-inflammatory capabilities. Chemokine receptor overexpression on MSCs is an effective strategy for the migration of MSCs into inflammatory tissue in high amounts. In this study, the anti-inflammatory and regenerative effects of genetically CCR2 overexpressed gingiva MSCs (GMSCs) on the inflamed colon in UC were studied. Materials and methods: GMSCs were transduced with a lentiviral vector for CCR2 overexpression. The UC experimental model was induced with a single intrarectal administration of 4% w/w acetic acid. Colon tissues were analyzed for IFN or IL-17 secreting CD4+ T lymphocytes via flow cytometry and lymphocytic infiltration, fibrosis, and ulcers by histopathologic evaluation. Homing analysis of GMSCs was done by analyzing fluorescence intensity under the fluorescence microscope. Results: GMSCs and CCR2⁺GMSCs equally downregulated colonic IFN-γ or IL-17 secreting CD4+ T lymphocytes ratios compared to the untreated group (p < 0.05). Fluorescence intensity of labeled cells was significantly high in colon tissues of CCR2⁺GMSCs administered rats (61.2 ± 13.7%) compared to GMSCs administered rats (19.6 ± 9.8%) (p < 0.05). In addition, mucosal integrity significantly increased and fibrosis and ulcers notably decreased in CCR2⁺GMSCs administered rats compared to GMSCs administered rats (p < 0.05). Conclusion: The overexpression of CCR2 on GMSCs increases migration to the inflammatory colon tissue, which has a high regenerative effect in UC. Overexpression of CCR2 on GMSCs may be an alternative to cellular therapies in UC.

Squamous cell carcinoma (SCC) is the second most common skin cancer and it often occurs in sun-exposed areas such as head and neck skin. Invasive SCC located on breast skin is a rare entity and may clinically mimic breast cancer. We report a case of a 39 years old female with a non-eroded, vegetative, growing lesion on the right breast skin, initially mimicking breast cancer both clinically and histopathologically. After surgery with clear margins, adjuvant radiotherapy was administered, by considering the pathological risk factors for recurrence. At 14 months, the patient is disease-free and under regular follow-up. Invasive SCC of the breast skin is a rare entity and may have different etiology/behavior or directly develop de novo when compared to SCCs located on sun-exposed skin. Medical history and physical examination in conjunction with histopathological examination of the biopsy specimen are critical for the accuracy of the diagnosis and the correct treatment decision in patients presenting with a mass invading breast skin.

This study aimed to evaluate the mRNA and protein levels of SMURF1 and SMURF2 in breast cancer and to elucidate their potential biological roles through in silico analyses. Tumor and adjacent normal tissue samples were collected from 30 newly diagnosed breast cancer patients who underwent mastectomy. The mRNA expression levels of SMURF1 and SMURF2 were analyzed by quantitative PCR (qPCR), and their protein expression patterns were evaluated using immunohistochemistry (IHC). In addition, protein–protein interaction (PPI) and functional enrichment analyses were performed via the STRING database to identify potential molecular interactions and biological pathways associated with these genes. The mRNA expression level of SMURF1 was significantly downregulated in tumor tissues compared to normal breast tissues (p = 0.002), whereas no significant difference was observed in SMURF2 mRNA expression (p = 0.981). IHC results revealed that SMURF1 and SMURF2 protein levels did not differ significantly between tumor and normal samples. The in silico analysis demonstrated that SMURF1 and SMURF2 interact with multiple proteins involved in key signaling pathways, particularly the TGF-β/BMP and Wnt/β-catenin pathways. The findings suggest that the downregulation of SMURF1 in breast cancer may contribute to tumor progression by enhancing Wnt/β-catenin signaling activity. The interactions of SMURF1 and SMURF2 with TGF-β/BMP pathway regulators indicate that these genes may play dual roles in both tumor-suppressive and oncogenic mechanisms, depending on the cellular context.