Project description:Annexin family is the largest category of eukaryotic calcium and phospholipid-binding proteins and plays important roles in various physiological processes, including cell differentiation and proliferation. More than 160 Annexin proteins are classified into 65 different speciesAs a new member of Annexin family, the role of ANXA10 in cancer progression is rarely investigated, and its expression and function in CCA need more experiments to reveal.
Project description:Genome-wide expression array measurements for 9 head and neck squamous cell carcinomas (HNSCC) stratified by worst pattern of invasion (WPOI) Jayakar et al. (2016). Apolipoprotein E promotes invasion in oral squamous cell carcinoma. Li et al. (2013). Validation of the risk model: high-risk classification and tumor pattern of invasion predict outcome for patients with low-stage oral cavity squamous cell carcinoma. Comparison of transcription profiles between OSCC tumors with a more invasive (WPOI 5) versus a less invasive (WPOI 3) pattern of invasion using two independent Illumina platforms.
Project description:Atopic dermatitis (AD) is a common, chronic inflammatory skin disease that seriously affects quality of life and is a major cause of skin diseases worldwide. Staphylococcus aureus (S. aureus) colonization on the skin plays an important role in the pathogenesis of AD; however, the mechanism of how it modulates skin immunity to exacerbate AD remains unclear. MicroRNAs are short non-coding RNAs that act as post-transcriptional regulators of genes. They are involved in the pathogenesis of various inflammatory skin diseases. In this study, we established miRNA expression profiles for keratinocytes stimulated with heat-killed S. aureus (HKSA). We found that miR-939 was highly upregulated in HKSA-stimulated keratinocytes and AD lesions. In vitro studies revealed that miR-939 increased the expression of matrix metalloproteinase genes, including MMP1, MMP3, and MMP9, as well as the cell adhesion molecule ICAM1 in human primary keratinocytes. In vivo studies indicated that miR-939 increased the expression of matrix metalloproteinases to promote the colonization of S. aureus and exacerbated S. aureus-induced AD-like skin inflammation. Taken together, these findings suggest that miR-939 is an important regulator of skin inflammation in AD.
Project description:Genome-wide expression array measurements for 9 head and neck squamous cell carcinomas (HNSCC) stratified by worst pattern of invasion (WPOI) Jayakar et al. (2016). Apolipoprotein E promotes invasion in oral squamous cell carcinoma. Li et al. (2013). Validation of the risk model: high-risk classification and tumor pattern of invasion predict outcome for patients with low-stage oral cavity squamous cell carcinoma.
Project description:Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.
Project description:The glucocorticoid-inducible protein annexin A1 has been shown to function as key-regulator of the resolution phase of inflammation but its role in immune-mediated crescentic glomerulonephritis has not been studied so far. Acute crescentic glomerulonephritis was induced in annexin A1 deficient and wildtype mice using a sheep serum against rat glomerular basement membrane constituents. Alterations in gene expression were determined by RNA-Seq and gene ontology analysis. Intrinsic annexin A1 has a protective effect in reducing pro-inflammatory signals and infiltration of neutrophil granulocytes during crescentic GN. The annexin A1 signaling cascade may therefore provide novel targets for the treatment of inflammatory kidney disease.