Abstract:Ovariectomy/estrogen deficiency causes selective apoptosis of the serous epithelial cells of the submandibular glands (SMG) in female mice. Because such apoptosis does not occur in healthy, estrogen-deficient male mice, it was hypothesized that dihydrotestosterone (DHT) protects epithelial SMG cells against apoptosis. The antiapoptotic effect of DHT on human epithelial HSG cells exposed to tumor necrosis factor-α and cycloheximide was studied. Correspondingly, the proapoptotic effect of androgen deficiency was… Show more
“…Neither the lateral nor the medial nasal glands stain positively for lysozyme (Figure 2E,F). Medial nasal glands in FVB and Edar dlJ/dlJ mice, like the salivary glands (12), stain for cleaved caspase 3 (Figure 2G,H) but the nasopharynx glands of Edar dlJ/+ mice do not stain for cleaved caspase 3 (data not shown). Figure 2.Nasal glands in EDA pathway deleted mice and Edar expression in adult glands.…”
Hypohidrotic ectodermal dysplasia (HED) results from mutation of the EDA, EDAR or EDARADD genes and is characterized by reduced or absent eccrine sweat glands, hair follicles and teeth, and defective formation of salivary, mammary and craniofacial glands. Mouse models with HED also carry Eda, Edar or Edaradd mutations and have defects that map to the same structures. Patients with HED have ear, nose and throat disease, but this has not been investigated in mice bearing comparable genetic mutations. We report that otitis media, rhinitis and nasopharyngitis occur at high frequency in Eda and Edar mutant mice and explore the pathogenic mechanisms related to glandular function, microbial and immune parameters in these lines. Nasopharynx auditory tube glands fail to develop in HED mutant mice and the functional implications include loss of lysozyme secretion, reduced mucociliary clearance and overgrowth of nasal commensal bacteria accompanied by neutrophil exudation. Heavy nasopharynx foreign body load and loss of gland protection alters the auditory tube gating function and the auditory tubes can become pathologically dilated. Accumulation of large foreign body particles in the bulla stimulates granuloma formation. Analysis of immune cell populations and myeloid cell function shows no evidence of overt immune deficiency in HED mutant mice. Our findings using HED mutant mice as a model for the human condition support the idea that ear and nose pathology in HED patients arises as a result of nasal and nasopharyngeal gland deficits, reduced mucociliary clearance and impaired auditory tube gating function underlies the pathological sequelae in the bulla.
“…Neither the lateral nor the medial nasal glands stain positively for lysozyme (Figure 2E,F). Medial nasal glands in FVB and Edar dlJ/dlJ mice, like the salivary glands (12), stain for cleaved caspase 3 (Figure 2G,H) but the nasopharynx glands of Edar dlJ/+ mice do not stain for cleaved caspase 3 (data not shown). Figure 2.Nasal glands in EDA pathway deleted mice and Edar expression in adult glands.…”
Hypohidrotic ectodermal dysplasia (HED) results from mutation of the EDA, EDAR or EDARADD genes and is characterized by reduced or absent eccrine sweat glands, hair follicles and teeth, and defective formation of salivary, mammary and craniofacial glands. Mouse models with HED also carry Eda, Edar or Edaradd mutations and have defects that map to the same structures. Patients with HED have ear, nose and throat disease, but this has not been investigated in mice bearing comparable genetic mutations. We report that otitis media, rhinitis and nasopharyngitis occur at high frequency in Eda and Edar mutant mice and explore the pathogenic mechanisms related to glandular function, microbial and immune parameters in these lines. Nasopharynx auditory tube glands fail to develop in HED mutant mice and the functional implications include loss of lysozyme secretion, reduced mucociliary clearance and overgrowth of nasal commensal bacteria accompanied by neutrophil exudation. Heavy nasopharynx foreign body load and loss of gland protection alters the auditory tube gating function and the auditory tubes can become pathologically dilated. Accumulation of large foreign body particles in the bulla stimulates granuloma formation. Analysis of immune cell populations and myeloid cell function shows no evidence of overt immune deficiency in HED mutant mice. Our findings using HED mutant mice as a model for the human condition support the idea that ear and nose pathology in HED patients arises as a result of nasal and nasopharyngeal gland deficits, reduced mucociliary clearance and impaired auditory tube gating function underlies the pathological sequelae in the bulla.
“…In terms of the multiple and complex interactions between types of bone cells reviewed herein, further investigations are needed to fully elucidate the contents and potential modulatory roles of bone‐derived exosomes in regulating bone remodelling, especially the comprehensive protein and miRNA contents of osteoclast‐derived exosomes as well as which types of bone‐derived exosomes play dominant roles in the regulation of bone remodelling and under what circumstances they would be activated. Encapsulation by the lipid bilayer of the exosomal membrane protects proteins and miRNAs from degradation and they can be assayed in small peripheral blood samples . Thus, the different expression level of specific contents of bone‐derived exosomes might serve as a promising diagnostic and/or prognostic tool to detect early‐stage bone disorders.…”
Pathological destructive bone diseases are primarily caused by the failure of a lifelong self‐renewal process of the skeletal system called bone remodelling. The mechanisms underlying this process include enhanced osteoclast activity and decreased generation of the osteoblast lineage. Intercellular interaction and crosstalk among these cell types are crucial for the maintenance of bone remodelling, either through the secretion of growth factors or direct cell–cell physical engagement. Recent studies have revealed that exosomes derived from bone cells, including osteoclasts, osteoblasts and their precursors, play pivotal roles on bone remodelling by transferring biologically active molecules to target cells, especially in the processes of osteoclast and osteoblast differentiation. Here, we review the contents of bone‐derived exosomes and their functions in the regulatory processes of differentiation and communication of osteoclasts and osteoblasts. In addition, we highlight the characteristics of microRNAs of bone‐derived exosomes involved in the regulation of bone remodelling, as well as the potential clinical applications of bone‐derived exosomes in bone remodelling disorders.
“…In late-phase diabetes, an increase in the number of autophagic structures occurs in granular duct cells. The histological findings from non-obese diabetic mice's submandibular gland tissues also indicate damage accompanied by massive cell infiltration [28][29][30][31]. Some studies have shown that oestrogen and progesterone regulate the structure and function of the submandibular glands.…”
Objective: The menopause in elderly women is a physiological process where ovarian and uterine cycles end. Diabetes means higher blood glucose level that is a metabolic disease and has an increased incidence. The aim of the study was to examine the single or combined effects of menopause and diabetes that causes pathophysiological processes on submandibular gland on ovariectomy and diabetes induced rat models.
Materials and Methods:Sprague Dawley twelve weeks old female (n=24) rats were divided randomly into four groups; Healthy control group (n=6), diabetic group (DM, n=6), ovariectomized group (OVX, n=6), post ovariectomy diabetes induced group (DM+OVX, n=6) individually. Histopathological, histochemical and stereological analyses were done in these groups.Results: Significant neutrophil cell infiltrations and myoepithelial cell proliferations, granular duct and seromucous acini damages and changes in the content of especially seromucous acini secretion in DM and/or OVX groups and distinctive interstitial and striated duct damages in post ovariectomy diabetes induced group were detected. Alterations ingranular ducts hypertrophic and in seromucous acini atrophic were determined in DM and/or OVX groups.
Conclusion:The results revealed the pathophysiological processes that lead to morphological and functional alterations on the cellular level in submandibular glands. The molecular mechanisms related with pathogenesis of diabetes and menopause need further investigation.Keywords: Diabetes, gland, menopause, rat, submandibular
ÖzetAmaç: İlerleyen yaş ile birlikte, menopoz, kadınlarda gözlenen overial ve menstrual sikluslarda azalma veya bitiş ile karakterize fizyolojik bir süreç ve diyabet ise insidansı artan yüksek kan şekeri seviyesi ile karakterize metabolik hastalıktır. Overektomi ve diyabet indüklenen sıçan modelleri submandibular bezi üzerinde menopozun ve diyabetin tek veya kombine etkilerinin neden olduğu patofizyolojik süreçle-ri incelemek amacı ile çalışma tasarlandı.
Gereç ve Yöntem:Sprague Dawley on iki haftalık dişi (n=24) sıçanlar dört gruba randomize bir şekilde rastgele ayrıldı; Sağlıklı Kontrol Grubu (n=6), Diyabetik grup (n=6), Overektomize grup (n=6), Post Overektomize Diyabet İndüklenen Grup (n=6). Sonuçlar histopatolojik, histokimyasal ve stereolojik analizler ile değerlendirildi.
Bulgular:Anlamlı nötrofil infiltrasyonları ve myoepitel hücre proliferasyonları, granüler kanal ve seromuköz hücre dejenerasyonları ve özellikle seromuköz asinusların salgısı içeriğindeki değişimler DM ve/veya OVX gruplarında, belirgin intersistiyel ödem ve çizgili kanal dejenerasyonları diyabet indüklenen post overektomize grup submandibular dokularında izlendi. Granular kanallarda hipertrofik değişiklikler, seromuköz asinuslarda atrofik değişiklikler DM ve/veya OVX gruplarında tespit edildi.Sonuç: Diyabet ve overektominin submandibular bezlerinde yol açtığı patofizyolojik süreçlere bağlı hücresel düzeyde morfolojik ve fonksiyonel değişiklikler gösterildi. Diyabet ve menopozun patogenezi ile ilişkili moleküle...
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