Histochemistry and Cell Biology最新文献

The raphe pallidus (RPa), a part of the caudal medullary raphe nucleus, has been suggested to participate in respiratory regulation. Therefore, hypoxia and hypercapnia are expected to affect the expression of Fos, a marker of cellular activation, in the RPa; however, there is currently no consensus on Fos expression in the RPa under hypoxic and hypercapnic conditions. The present study investigated the distribution of Fos expression in the RPa of rats exposed to hypoxia (10% O₂), hypercapnia (8% CO₂), and hypercapnic hypoxia (10% O₂ and 8% CO₂) for 2 h. To confirm whether activation of the RPa affects respiratory function, an electrical stimulation was applied to the RPa of anesthetized rats. The stimulation induced a significant increase in the respiratory rate, which was similar to the respiratory changes induced by hypoxia. An immunohistochemical analysis revealed two types of cells in the RPa: serotonin-immunoreactive neurons and SOX9-immunoreactive astrocytes. Hypoxia significantly increased Fos immunoreactivity in astrocytes in the rostral region of the RPa, but did not affect Fos immunoreactivity in serotonergic neurons. In contrast, hypercapnia and hypercapnic hypoxia did not affect Fos immunoreactivity in either cell type in any region. These results suggest that astrocytes in the RPa are specifically activated by hypoxia and actively contribute to the respiratory response to hypoxia.

Exosomes are small membrane-bound nanovesicles that are secreted by cells when multivesicular bodies merge with the plasma membrane. These particles have been demonstrated to carry specific proteins, lipids and genetic components that are exclusive to each cell type. These compounds can be selectively taken up by cells in close proximity or at a distance, even after being released, thus altering their biological response. Therefore, the regulated manufacturing of exosomes, the exact makeup of their contents and their capacity to selectively interact with particular cells are highly important in the field of biology because of the immense potential of exosomes as noninvasive diagnostic biomarkers and therapeutic nanocarriers. This review presents a comprehensive examination and evaluation of the most recent progress in comprehending the regulatory mechanisms of exosome formation, the molecular composition of exosomes and the approaches utilised in exosome research. Furthermore, this review focuses on the potential use of exosomes as promising markers for the diagnosis and prognosis of medical conditions, owing to their specific associations with cellular lineage and state. In addition, the potential role of exosomes as vehicles for the delivery of medicines and genes for therapeutic applications is unraveled. The study of exosomes is currently in a nascent phase. Acquiring a thorough understanding of the subcellular constituents and processes implicated in exosome generation, together with their specific cell targeting, can yield valuable insights into their physiological roles.

Quantifying myofiber size is essential for assessing the health and function of skeletal muscle. Although several ImageJ plugins are currently available for myofiber segmentation and size quantification, significant challenges remain-most notably limited accuracy and poor compatibility with hematoxylin and eosin (H&E)-stained skeletal muscle cross sections. In this study, we introduce MyoAnalyst, an ImageJ plugin designed to enable automated analysis of both immunofluorescence (IF)- and H&E-stained skeletal muscle cross sections. Compared to existing ImageJ plugins, MyoAnalyst delivers enhanced segmentation sensitivity and superior boundary delineation accuracy across both healthy and injured muscle tissue stained with IF. Importantly, it also supports fully automated analysis of H&E-stained sections. With its intuitive graphical interface and batch processing capabilities, MyoAnalyst provides a potentially efficient tool for myofiber size quantification in both research and clinical settings.

Oxidative stress is known to have a detrimental effect on wound healing following oral mucosal injuries. Exogenous antioxidant administration to restore redox balance has been proposed as a therapeutic approach to support wound healing after oral surgery. In our study, we evaluated the relative effectiveness of melatonin and alpha-lipoic acid in palatal wound healing, as well as the potential synergistic effect of their combined treatment. A full-thickness wound model was created on the palatal mucosa of 64 Wistar rats with a 5-mm punch biopsy. Experimental groups were intraperitoneally administered 60 mg/kg/day alpha-lipoic acid, 30 mg/kg/day melatonin, or their combination. The rats were sacrificed 5 and 10 days later to evaluate the wound healing, and palatal tissue samples were evaluated macroscopically, histologically, and immunohistochemically. On day 10, all experimental groups exhibited a significant reduction in wound surface area compared with the control group, with the combined group showing the greatest reduction. There was no significant difference between groups in granulation tissue amount and leukocyte density in hematoxylin-eosin-stained samples. Masson trichrome staining showed that collagen production was significantly higher in the combined group on day 10. Vascular endothelial growth factor (VEGF) immunoreactivity in wound edges was found to be increased in the combined group, being significant on day 5. Filaggrin expression was significantly higher on both days in the wound beds of all treatment groups, with the combined group exerting the highest increase. Our study shows that combined treatment of melatonin and alpha-lipoic acid may improve palatal wound healing process.

Telocytes are specialized interstitial cells characterized by their unique structure, which features a relatively small cell body and long cytoplasmic projections, called telopodes. Formerly referred to as interstitial Cajal-like cells, telocytes are capable of forming a complex communication network between various stromal and epithelial cell types. Despite their positive staining for CD34 and vimentin antibodies, the mesenchymal origin of these cells, as well as whether telocytes should be considered distinct cell populations or just a subpopulation of other stromal cells, remains uncertain. Telocytes have been shown to perform various functions, ranging from establishing complex three-dimensional networks, serving as an important component of stem cell niches and playing a huge role in the formation of tissue barriers, to serving as one of the key regulators of cell differentiation, having immune functions, and taking part in angiogenesis and even in organ morphogenesis. The functional diversity exhibited by telocytes in different tissues makes their study more complicated, and the exact molecular mechanisms underlying their function remain inadequately understood. As a new and intriguing field of research, telocytes hold considerable promise for improving our understanding of connective tissue physiology.

Type 1 diabetes mellitus (T1DM) is associated with oxidative stress and inflammation in the liver, which contribute to hepatocellular damage. However, the molecular mechanisms driving this process remain poorly understood. ADAMTS-13, a metalloprotease involved in vascular homeostasis, has been implicated in tissue remodeling and apoptosis. This study explores the potential link between ADAMTS-13 and apoptosis in T1DM-induced liver injury. Diabetes was induced in Wistar albino rats via streptozotocin (STZ) injection, and liver tissues were examined using immunohistochemical staining for ADAMTS-13 and apoptotic markers, including caspase-3, caspase-8, caspase-9, and TNFR1. Expression levels were compared between diabetic and control groups to assess correlations with apoptotic pathways. ADAMTS-13 expression was significantly elevated in the diabetic group. Apoptotic markers also showed a significant increase (p < 0.05). Notably, caspase-9 expression was more prominent in hepatocytes, indicating activation of the intrinsic apoptotic pathway, while caspase-8 and TNFR1 were predominantly expressed in sinusoidal and vascular endothelial cells, suggesting involvement of the extrinsic pathway. This study is the first to demonstrate a link between ADAMTS-13 expression and apoptosis in T1DM-related liver injury. These findings suggest that ADAMTS-13 may play a role in modulating apoptotic responses, although its exact function remains to be clarified. Further mechanistic studies are warranted to determine whether ADAMTS-13 directly influences apoptosis or represents an adaptive response to hepatic stress. Additionally, the results highlight the potential of ADAMTS-13 as a biomarker for diabetes-associated liver dysfunction.

Extracellular matrix reorganization, a concurrent process of endometrial decidualization, has garnered widespread recognition. However, our understanding of this process remains limited. In this study, we aimed to investigate the expression, spatial distribution, and reorganization of fibrillar collagens, elastin, and lysyl oxidases within the decidua. Using second harmonic generation imaging, we successfully recorded fibrillar collagen reorganization between preimplantation and decidualized endometrium. Upon embryo implantation, the fibrillar collagens align themselves parallel to the direction of embryo invasion. Furthermore, we employed confocal imaging analysis to reveal distinct expression and spatial distribution patterns of elastin and lysyl oxidase-like enzymes. Elastin expression begins to manifest surrounding the implanting embryo, extends into the decidua, and exhibits a high concentration in the mesometrial region after gestational day 8. All lysyl oxidase-like enzymes are localized within the decidua, although they exhibit varying expression patterns. To gain further insights, we utilized an in vitro stromal cell decidualization model and provided compelling evidence that stromal cells serve as the primary source of the extracellular matrix components during endometrial decidualization. Additionally, we demonstrated that the genes encoding factors involved in the synthesis, processing, and assembly of fibrillar collagen and elastic fibers exhibit differential expression patterns during in vitro decidualization. Genes such as asporin, decorin, thrombospondin 2, fibulin 2, fibulin 5, and lysyl oxidase show significant induction during in vitro decidualization. In summary, our comprehensive analysis provides a detailed evaluation of the expression, spatial distribution, and reorganization of fibrillar collagens, elastin, and lysyl oxidases during the process of endometrial decidualization.

Ascl1 (Mash1), a bHLH transcription factor, is widely expressed by neuronal progenitors. The gene plays a key role in the differentiation of the autonomic nervous system, i.e., sympathetic, parasympathetic, and enteric ganglia; all of which are derived from neural crest cells. In Ascl1-null mutants, defective development of these ganglia is induced. The differentiation of neuroendocrine cells, including the carotid body, ultimobranchial body and thyroid C cells, the neuroepithelial body in the lung, and the adrenal medulla, is also controlled by Ascl1. Although the carotid body glomus cells and adrenal medulla are derived from neural crest, the ultimobranchial body is from pharyngeal endoderm and the neuroepithelial body is from endodermal epithelium. A targeted mutation of Ascl1 results in complete loss or failure in differentiation of these neuroendocrine cells. Furthermore, the development of olfactory epithelium and bulbus is regulated by Ascl1. In the central nervous system, Ascl1 is expressed in the arcuate and ventromedial nuclei, telencephalon, and dopaminergic neurons such as locus coeruleus and nucleus tractus solitarius. The elimination or atrophy of these regions are induced in Ascl1-null mutants. All cells and tissues affected by the deficiency of Ascl1 express catecholamines and/or serotonin. The Phox2b or/and Hes1 genes are required for regulation of Ascl1 expression. Phox2b stimulates the expression of Ascl1, whereas Hes1 represses gene expression.