Browsing by Subject "Connexin 43"

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    Connexin 43: its regulatory role in testicular junction dynamics and spermatogenesis
    (F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Weider, Karola; Bergmann, Martin; Brehm, Ralph
    Spermatogenesis is an intensely regulated process of germ cell development which takes place in the seminiferous tubules of the testis. In addition to known endocrine and autocrine/paracrine signaling pathways, there is now strong evidence that direct intercellular communication via gap junction channels and their specific connexins represents an important mechanism in the regulation of spermatogenesis. Another possibility is that connexins may indirectly regulate the spermatogenic process through modulation of tight and adherens junction proteins, further main structural components of the Sertoli-Sertoli junctional complexes at the blood-testis barrier site. The present review is focused on connexin 43 and updates its possible roles and functions in testicular junction dynamics and in the initiation and maintenance of spermatogenesis. In addition, testicular phenotypes of recently generated (1) conventional connexin 43 knockout mice, (2) connexin 43 knockin mice and (3) transgenic mice exhibiting a cell-specific (conditional) connexin 43 knockout will be discussed.
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    Gestational protein restriction: Study of the probable effects on cardiac muscle structure and function in adult rats
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Amer, Mona G.; Mohamed, Nader M.; Shaalan, Aly A.M.
    Intrauterine growth restriction (IUGR) has been linked to heart disease in adulthood. This study aimed to examine the effect of gestational protein restriction during fetal and early postnatal life on the cardiac muscle structure and function in adult offspring. Pregnant female rats were randomly divided into two dietary groups: normal-protein diet (NP) and low-protein diet (LP). Fifteen male offspring from each group were included in the study. Offspring body weights were recorded at birth and monthly from weaning until 24 weeks of age while systolic blood pressure was measured weekly. At the end of the experiment, hearts were weighed and processed for light and electron microscopy and immunohistochemical study. Immunohistochemical staining for localization of inducible nitric oxide synthase (iNOS) and connexin 43 proteins was performed. The gestational protein restriction induced deleterious effects on adult offspring including decreased birth weight, heart weight, and heart rate, and increased systolic blood pressure. Histologically, the number of cardiomyocytes decreased and cardiac fibrosis increased. Signs of degeneration at both structural and ultra-structural levels of cardiomyocytes were also seen. The iNOS was up regulated in LP offspring which was a promoter for apoptosis, while connexin 43 was down regulated which would affect heart conductivity and contractility. Our results demonstrate that adult offspring body weight and cardiac muscle structure and function can be programmed by maternal gestational nutrition. These adverse outcomes suggest the criticality of dietary behavior during pregnancy on long-term offspring cardiac health.
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    N-cadherin, beta-catenin and connexin 43 expression in astrocytic tumours of various grades
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Reszec, J.; Szkudlarek, M.; Hermanowicz, A.; Bernaczyk, P.S.; Mariak, Z.; Chyczewsk, L.
    Introduction: Astrocytic tumors are the most common primary brain tumors, but little is known about their etiology and prognostic factors. N-cadherin and beta-catenin are adhesive proteins, and are often overexpressed in many types of cancers, including breast or colorectal cancer, resulting in better prognosis. Connexin 43 is a gap junction protein involved in cellcell signaling pathway taking part in the process of carcinogenesis. The aim of the study was to evaluate Ncadherin, beta-catenin and connexin 43 expression in astrocytic tumors of various grades. Materials and methods: We examined 131 cases of astrocytic tumors, including 26 cases of diffuse astrocytoma (group I), 44 anaplasic astrocytomas (group II) and 61 glioblastoma cases (group III) - primary and secondary. To evaluate N-cadherin, beta-catenin and connexin 43 expression, we used immunohistochemical reaction with specific antibodies (Santa Cruz Biotechnology). The obtained results were correlated with clinical and morphological features. Results: Beta-catenin expression was observed in 69.3% of diffuse astrocytomas, 75% of anaplastic astrocytomas, and 82% of glioblastoma cases. Ncadherin expression was observed in 92.3% of diffuse astrocytomas, 90.1% of anaplastic astrocytomas, and in all glioblastoma cases. Connexin 43 was observed in 76.9% of diffuse astrocytomas, and in all cases of anaplastic astrocytomas and glioblastomas. Beta-catenin expression was significant within the nucleus of neoplastic cells in groups I and II. In group III, staining was observed only in the cellular membranes. Ncadherin and connexin 43 expression was observed only in the cells’ membranes. In glioblastomas, both primary and secondary, all protein expression was significant within the cells surrounding the necroses and blood vessels and weak or absent in the tumor’s margins. Conclusion: Our study shows that beta-catenin nuclear expression in group of diffuse astrocytomas and anaplastic astrocytomas is evidence for transcriptional function of beta-catenin in those groups. Strong Ncadherin and connexin 43 expression in those groups may be evidence for their role in tumor formation and progression. However, in glioblastomas a very important role of all examined proteins is generating intracellular connections to facilitate the escape of tumor cells from the effects of hypoxia or their accumulation around the blood vessels rather than tumor invasion into the brain parenchyma.
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    Role of connexin 43 in odontogenesis and odontogenic tumors
    (2026) Ronell Bologna Molina; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologia
    Connexin 43 (Cx43) is a transmembrane protein forming gap junctions essential for intercellular communication, regulating ion and molecule exchange, and coordinating key developmental and pathological processes. In odontogenesis, Cx43 expression in ameloblasts and odontoblasts orchestrates differentiation, mineralization, and tissue repair. Its dynamic regulation influences enamel and dentin formation, while altered expression is linked to defective tooth development. Beyond dental tissues, Cx43 participates in craniofacial morphogenesis and bone remodeling. In odontogenic tumors, Cx43 shows heterogeneous expression patterns, reflecting its role in tumor architecture, differentiation, and aggressiveness. High mesenchymal expression is seen in ameloblastic fibromas and fibro-odontomas, whereas follicular ameloblastomas and odontogenic keratocysts exhibit downregulation, particularly in basal cells, correlating with increased proliferation, anti apoptosis, and autophagy markers. These variations in odontogenic tumors suggest that Cx43 may act as a tumor suppressor by maintaining epithelial organization and regulating cell polarity. Molecularly, Cx43 interacts with MAPK/ERK, PI3K/AKT, and Wnt/β-catenin pathways, influencing cell cycle control, apoptosis, and epithelial-mesenchymal interactions. Loss of Cx43 disrupts gap junctional intercellular communication, potentially enhancing tumor progression. Therapeutically, modulating Cx43 could inhibit tumor angiogenesis, restore normal growth control, and promote differentiation toward less aggressive phenotypes. However, given its dual role in tumor suppression and tissue repair, targeted interventions must be context specific. Cx43 emerges as a promising diagnostic, prognostic, and therapeutic biomarker in different neoplasias, warranting further investigation to optimize clinical applications. The objective of this work is to review current information on the role of CX43 in normal tissue and odontogenic tumors to evaluate its possible usefulness as a future therapeutic target.
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    Zoledronate promotes bone formation by blocking osteocyte-osteoblast communication during bone defect healing
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Cui, Pingping; Liu, Hongrui; Sun, Jing; Amizuka, Norio; Sun, Qinfeng; Li, Minqi
    Nitrogen-containing bisphosphonates (NBPs) are potent antiresorptive drugs and their actions on osteoclasts have been studied extensively. Recent studies have suggested that N-BPs also target bone-forming cells. However, the precise mechanism of N-BPs in osteoblasts is paradoxical, and the specific role of osteocytes is worthy of in-depth study. Here, we investigated the cellular mechanisms of N-BPs regulating bone defect healing by zoledronate (ZA). Bone histomorphometry confirmed an increase in new bone formation by systemic ZA administration. ZA induced more alkaline phosphatase-positive osteoblasts and tartrate-resistant acid phosphatase-positive osteoclasts residing on the bone surface. Inexplicably, ZA increased SOST expression in osteocytes embedded in the bone matrix, which was not compatible with the intense osteoblast activity on the bone surface. ZA induced heterogeneous osteocytes and disturbed the distribution of the osteocytic-canalicular system (OLCS). Furthermore, according to the degree of OLCS regularity, dentin matrix protein 1 reactivity had accumulated around osteocytes in the ZA group, but it was distributed evenly in the OLCS of the control group. The control group showed a dense array of the gap junction protein connexin 43. However, connexin 43 was extremely sparse after ZA administration. In summary, ZA treatment reduces gap junction connections and blocks cellular communication between osteocytes and osteoblasts. Retaining SOST expression in osteocytes leads to activation of the Wnt signaling pathway and subsequent bone formation.