Gene expression profile of collagen types, osteopontin in the tympanic membrane of patients with tympanosclerosis

Sakowicz-Burkiewicz, Monika; Kuczkowski, Jerzy; Przybyła, Tomasz; Grdeń, Marzena; Starzyńska, Anna

doi:10.17219/acem/68984

Cited by 11 publications

(7 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…COL1A1 is an important extracellular matrix protein abundantly produced by ameloblasts during the secretory phase and has a clinically significant impact on bone remodelling and cell proliferation 35,36 . There is a strong association between type I collagen downregulation and severe fibrosis and ankylosis 37 , supporting our findings that ERM-3 with low COL1A1 expression exhibited greater ectopic bone formation in the PDL space. PIK3CA, the third hub gene that typically induces bone formation, was overexpressed in ERM-3 than in www.nature.com/scientificreports/ CRUDE ERM and ERM-2.…”

Section: Discussionsupporting

confidence: 88%

Analysis of the cells isolated from epithelial cell rests of Malassez through single-cell limiting dilution

Islam

Kurashige

Minowa

et al. 2022

Sci Rep

View full text Add to dashboard Cite

The epithelial cell rests of Malassez (ERM) are essential in preventing ankylosis between the alveolar bone and the tooth (dentoalveolar ankylosis). Despite extensive research, the mechanism by which ERM cells suppress ankylosis remains uncertain; perhaps its varied population is to reason. Therefore, in this study, eighteen unique clones of ERM (CRUDE) were isolated using the single-cell limiting dilution and designated as ERM 1–18. qRT-PCR, ELISA, and western blot analyses revealed that ERM-2 and -3 had the highest and lowest amelogenin expression, respectively. Mineralization of human periodontal ligament fibroblasts (HPDLF) was reduced in vitro co-culture with CRUDE ERM, ERM-2, and -3 cells, but recovered when an anti-amelogenin antibody was introduced. Transplanted rat molars grown in ERM-2 cell supernatants produced substantially less bone than those cultured in other cell supernatants; inhibition was rescued when an anti-amelogenin antibody was added to the supernatants. Anti-Osterix antibody staining was used to confirm the development of new bones. In addition, next-generation sequencing (NGS) data were analysed to discover genes related to the distinct roles of CRUDE ERM, ERM-2, and ERM-3. According to this study, amelogenin produced by ERM cells helps to prevent dentoalveolar ankylosis and maintain periodontal ligament (PDL) space, depending on their clonal diversity.

show abstract

Section: Discussionsupporting

confidence: 88%

Analysis of the cells isolated from epithelial cell rests of Malassez through single-cell limiting dilution

Islam

Kurashige

Minowa

et al. 2022

Sci Rep

View full text Add to dashboard Cite

show abstract

“…16 COL4A1 is expressed in the tympanic membrane and changes in collagen expression have been observed in tympanosclerosis, a known cause for hearing loss following injury or infection. 17 As seen in the family of patient 2, COL4A1-associated disease shows an incomplete clinical penetrance and a broad range of clinical organ manifestations. 16 An involvement of COL4A1 variation in the development of familial hearing loss seems possible but needs further confirmation.…”

Section: Discussionmentioning

confidence: 99%

Axenfeld-Rieger Anomaly and Neuropsychiatric Problems—More than Meets the Eye

et al. 2020

View full text Add to dashboard Cite

Objective The main purpose of this article is to demonstrate the co-occurrence of Axenfeld-Rieger anomaly and neuropsychiatric problems as clinical signs of genetically determined cerebral small vessel disease in two patients. Case Study We report on two adolescent individuals with ocular anterior segment dysgenesis (Axenfeld-Rieger anomaly) presenting with neuropsychiatric symptoms. Both patients underwent cerebral magnetic resonance imaging showing white matter T2-hyperintensities involving different brain regions, suspective of cerebral small vessel disease. Genetic analysis revealed pathogenic mutations in the FOXC1 gene (patient 1) and the COL4A1 gene (patient 2), respectively. Conclusion We report on the co-occurrence of ocular anterior segment dysgenesis (Axenfeld-Rieger anomaly) and neuropsychiatric symptoms as clinical signs of genetically determined cerebral small vessel disease in two patients. In both patients, the cerebral lesions involved the frontotemporal regions, brain regions that control social behavior as well as executive and cognitive function, highlighting the fact that neuropsychiatric symptoms may be early clinical presentations of cerebral small vessel disease. We further provide a review of monogenic causes of pediatric cerebral small vessel disease, emphasizing the links to childhood-onset neuropsychiatric disease.

show abstract

“…Amplification program: 95 °C—15 s, 60 °C—45 s for 45 cycles. Data were processing with the Light Cycler 480 II software 2.0 [ 35 ].…”

Section: Methodsmentioning

confidence: 99%

The Impact of Acetyl-CoA and Aspartate Shortages on the N-Acetylaspartate Level in Different Models of Cholinergic Neurons

et al. 2020

Self Cite

View full text Add to dashboard Cite

N-acetylaspartate is produced by neuronal aspartate N-acetyltransferase (NAT8L) from acetyl-CoA and aspartate. In cholinergic neurons, acetyl-CoA is also utilized in the mitochondrial tricarboxylic acid cycle and in acetylcholine production pathways. While aspartate has to be shared with the malate–aspartate shuttle, another mitochondrial machinery together with the tricarboxylic acid cycle supports the electron transport chain turnover. The main goal of this study was to establish the impact of toxic conditions on N-acetylaspartate production. SN56 cholinergic cells were exposed to either Zn2+ overload or Ca2+ homeostasis dysregulation and male adult Wistar rats’ brains were studied after 2 weeks of challenge with streptozotocin-induced hyperglycemia or daily theophylline treatment. Our results allow us to hypothesize that the cholinergic neurons from brain septum prioritized the acetylcholine over N-acetylaspartate production. This report provides the first direct evidence for Zn2+-dependent suppression of N-acetylaspartate synthesis leading to mitochondrial acetyl-CoA and aspartate shortages. Furthermore, Zn2+ is a direct concentration-dependent inhibitor of NAT8L activity, while Zn2+-triggered oxidative stress is unlikely to be significant in such suppression.

show abstract

Gene expression profile of collagen types, osteopontin in the tympanic membrane of patients with tympanosclerosis

Cited by 11 publications

References 27 publications

Analysis of the cells isolated from epithelial cell rests of Malassez through single-cell limiting dilution

Analysis of the cells isolated from epithelial cell rests of Malassez through single-cell limiting dilution

Axenfeld-Rieger Anomaly and Neuropsychiatric Problems—More than Meets the Eye

The Impact of Acetyl-CoA and Aspartate Shortages on the N-Acetylaspartate Level in Different Models of Cholinergic Neurons

Contact Info

Product

Resources

About