Mitochondrial dynamics and mitophagy are indispensable for cellular homeostasis in hormonally regulated tissues such as the endometrium and placenta. Decidualization of endometrial stromal cells (ESCs) into decidual cells (DCs) requires extensive mitochondrial remodeling, yet how ovarian steroids regulate this process in vivo and in vitro remains incompletely understood. This study elucidates the modulation of mitochondrial fusion, fission, and mitophagy by estrogen (E2) and progesterone (P4) across the menstrual cycle and during pregnancy. Endometrial tissues were collected from women at early (EP) and late (LP) proliferative, and early (ES), mid (MS), and late (LS) secretory phases, while placental tissues were obtained from first-trimester (FP) and term pregnancies (TP). The expression of MFN2 and OPA1 (fusion), Drp1, Fis1, and MFF (fission), and Pink1 and Parkin (mitophagy) was assessed by immunohistochemistry in vivo. In vitro, the effects of E2 and P4 on these markers were examined in ESCs and DCs using western blotting. Mitochondrial morphology was evaluated by transmission electron microscopy and morphometry. In vivo, FP-DCs exhibited increased expression of fission- and mitophagy-related proteins, while in vitro P4 treatment was associated with increased Drp1 expression in FP-DCs. Collectively, these findings suggest that mitochondrial dynamics- and mitophagy-related protein changes accompany ESC-to-DC differentiation, with P4-associated Drp1 regulation potentially contributing to early pregnancy adaptation. Understanding these processes may provide insight into mechanisms relevant to implantation failure and pregnancy loss. The table summarizes stage-specific in vivo immunoreactivity patterns of proteins associated with mitochondrial fusion, fission-related regulators, and mitophagy across the menstrual cycle and pregnancy (↑ increase, ↓ decrease, ns no significant difference). The schematic provides a concise overview of our working model, highlighting progesterone-associated stages in which coordinated changes in fission- and mitophagy-related regulators were observed in decidual cells. Created in BioRender. Sezer, Z. (2026) https://BioRender.com/zt5kb56 . Created in BioRender. https://BioRender.com/3t0y3w8
This study investigated the effects of different doses of dexamethasone on the regeneration of muscle fibers, electric organ cells, and electroreceptors in the amputated tails of the black ghost knifefish, Apteronotus albifrons (Linnaeus 1766). The relative gene expression of sox3 was analyzed to assess neural regeneration. Four groups of fish were exposed to dexamethasone concentrations of 0 (control), 1, 2, and 3 mg/L, with water replaced every 48 h to maintain drug stability. The results revealed that dexamethasone significantly downregulated sox3 expression. A significant decrease (p < 0.05) in relative expression levels was observed at the 1, 2, and 3 mg/L doses (0.134 ± 0.022, 0.061 ± 0.034, and 0.003 ± 0.002, respectively) compared to the control group (0.920 ± 0.252). These findings were supported by histological sections, which showed a reduced regeneration rate and lower growth percentages of neural and muscle tissues. Specifically, the neural tissue regeneration percentages were 28.40
Epidermodysplasia verruciformis (EV) is characterized by susceptibility to cutaneous β-human papillomaviruses, persistent viral lesions, and an increased risk of cutaneous squamous cell carcinoma (cSCC). We investigated whether expression of Toll-like receptors 3, 4, 5, and 9 (TLR3, TLR4, TLR5, and TLR9) differs across histological states within EV. Immunoreactivity was quantified by digital H-score using QuPath in 97 specimens from 28 patients, comprising 13 lesion-free skin samples, 15 flat warts, and 69 cSCCs. Prespecified comparisons evaluated flat wart versus lesion-free skin, cSCC versus non-neoplastic tissue, and invasive versus in situ cSCC, with invasive tumor differentiation assessed secondarily. Patient-clustered generalized estimating equations and false-discovery-rate (FDR) correction were used for inference. After correction for multiple testing, TLR9 H-scores were higher in flat warts than in lesion-free skin (β = 60.58; q = 0.0332). Compared with non-neoplastic tissue, cSCC showed lower TLR3 (β = −81.40; q = 0.00745), higher TLR4 (β = 55.59; q = 0.04793), and lower TLR9 expression (β = −34.80; q = 0.03412). TLR5 showed a nominal increase in cSCC that did not meet the FDR threshold. None of the four receptors differed significantly between invasive and in situ cSCC, and no differentiation trend remained significant after FDR correction. These findings show receptor-specific differences in TLR expression across histological states of EV, particularly involving TLR3, TLR4, and TLR9, although the diagnostic and prognostic significance of these tissue patterns remains to be established.
Pulmonary fibrosis is a chronic progressive disease, caused by numerous factors, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Damage to the alveolar epithelial barrier (formed by junctions between alveolar epithelial cells I) has been described as a key mechanism of early fibrosis and therefore could be crucial for COVID-19-associated sequelae. The integrity of adherens junctions is regulated by p120 catenin and is crucial for barrier regulation in epithelial-mesenchymal-transition-driven diseases such as fibrogenesis and cancer. Abundance and expression of p120 catenin and intercellular contact regulating proteins (caveolin-1, P2X7R) were investigated retrospectively in COVID-19 lungs (acute, chronic) compared with healthy controls and interstitial lung disease of different etiologies (n = 6). p120 Catenin was further investigated in early injury models using profibrotic agents in murine lung and human alveolar epithelial cell culture. p120 Catenin abundance was higher in chronic COVID-19 compared with acute COVID-19, suggesting a role in fibrotic development. The interacting proteins caveolin-1 and P2X7R were simultaneously decreased in COVID-19, indicating a role in early pathophysiology. Early epithelial damage showed no changes in p120 catenin and its phospho-Y228 site in cell culture whereas p120 catenin was reduced in murine lung culture. Thus, alterations in and interactions between p120 catenin and caveolae associated proteins may represent a potential mechanism underlying COVID-19-induced pulmonary fibrosis.
