ABSTRACT
Correction to: European Review for Medical and Pharmacological Sciences 2022; 26 (22): 8713-8718. DOI: 10.26355/eurrev_202212_30543- PMID: 36524490-published online on December 15, 2022. After publication, the authors applied a correction to the funding statement: The authors extend their appreciation to the deputyship for Research & Innovation, Ministry of Education in Saudi Arabia for funding this research work through the project number (lFP-2020-36). There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/30543.
ABSTRACT
OBJECTIVE: The ensuing ischemia due to the disruption of blood supply to the brain is one of the most common causes of stroke. Evidence suggests a clear association of the ischemic injury with vascular dementia and Alzheimer's disease (AD). In response to the brain ischemia, a cascade reaction starts leading to neuronal damage due to oxidative stress and other inflammatory mediators. A pilot study was done, which showed that following stroke, monomeric-C-reactive protein (mCRP) is expressed in large quantities around the infarcted zone and this CRP is able to induce neurodegeneration and inflammation potentially perpetuating dementia. MATERIALS AND METHODS: We examined both patient brain samples and excised mouse brain tissue, previously injected with 1.75 mg/mL mCRP into the CA1 area of the hippocampus through the stereotactic surgical procedures and followed them over a period of over 6 months. The distribution of mCRP was examined through immunohistochemistry (mouse anti-human mCRP-specific antibodies 8C10). RESULTS: We observed a novel finding: those micro vessels close to the injection location were strongly stained with mCRP only in the mice that had been injected with mCRP, indicating that this small blood vessel can spread it throughout the brain. CONCLUSIONS: mCRP found in the brain after a hemorrhagic stroke promotes damage over a large area via the induction of inflammation and degeneration of perivascular compartments.
Subject(s)
Alzheimer Disease , Stroke , Animals , Mice , C-Reactive Protein/metabolism , Pilot Projects , Inflammation , Neurons/metabolism , Alzheimer Disease/metabolismABSTRACT
Tumour cell invasion and metastasis are the hallmark of malignant neoplasm. S100A4 is a member of small calcium-binding protein family and is involved in the cell proliferation and cancer progression. S100A4 is capable of inducing metastasis in animal models and is associated with aggressive phenotype of human tumours. We previously identified S100A4 as a candidate gene involved in anaplastic thyroid cancer metastasis by microarray analysis. To further determine whether S100A4 overexpression is associated with thyroid tumour invasion and metastasis, in the present study, we examined S100A4 gene expression in six benign multinodular goitres (MNG) and 28 matched samples of adjacent normal thyroid tissue (N), primary (T) and metastatic (M) papillary thyroid carcinomas (PTC) by immunohistochemistry and real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis. This gave us the advantage of directly comparing levels of S100A4 expression within the same genetic background. Using immunohistochemistry, we found that high levels of S100A4 were detected in 24 of 28 (86%) PTC specimens and their local regional lymph node or distant metastases. No S100A4 staining was observed in normal thyroid tissues and simple MNG. However, in MNG coexistent with PTC, moderate focal staining could be found in 11 of 15 MNG adjacent to PTC. The S100A4 was stained more intensely in invading fronts than in central portions of both T and M. Real-time RT-PCR analysis of primary tumours and their matched lymph node metastasis demonstrated that significantly higher S100A4 transcripts were present in metastatic tumours as compared to the primary tumours (P<0.01). These data suggest that overexpression of S100A4 is associated with thyroid tumour invasion and metastasis and it may be a potential target for therapeutic intervention.
