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Fibroids and Endometrial Receptivity/Embryo Implantation
Published in Botros R.M.B. Rizk, Yakoub Khalaf, Mostafa A. Borahay, Fibroids and Reproduction, 2020
Kamaria C. Cayton Vaught, Maria Facadio Antero, Jacqueline Y. Maher, Chantel I. Cross
Fibroids also possess an antiangiogenic profile when compared to normal myometrium. Fibroids have been shown to have higher amounts of antiangiogenic factors, such as collagen 4α2 (COL4A2), and lower expression of angiogenic promoters, such as connective tissue growth factor (CTGF) and cysteine-rich angiogenic inducer 61 (CYR-61) [46]. Together these create an antiangiogenic environment that may impact embryo receptivity and implantation in sites close to the fibroid.
Bilateral Non-Arteritic Anterior Ischaemic Optic Neuropathy in a Patient with a COL4A2 Mutation
Published in Neuro-Ophthalmology, 2022
Kasim Qureshi, Muhammad U. Farooq, Avneet Deol, Christopher Glisson, Philip B. Gorelick
Non-arteritic anterior ischaemic optic neuropathy (NAION) is the second most common optic neuropathy after glaucoma and is characterised by sudden painless vision loss due to compromised perfusion of the optic nerve head via various vascular mechanisms. When one eye is affected, there is a risk of contralateral involvement. Up to 15% of patients develop NAION in the fellow eye 5 years after the initial diagnosis.1 In addition to showing a predisposition in white Caucasians, men, and those over the age of 50,2 NAION has several known genetic associations including GP1ab polymorphisms, and familial mitochondrial mutations.3–6 We report a case of sequential bilateral NAION in a man who was subsequently found to have a COL4A2 mutation, the gene encoding for the collagen alpha-2 chain, one of the six subunits of type IV collagen. Type IV collagen is a major structural component of human basement membranes including those of the cerebral vasculature. Familial mutations may be associated with porencephaly, childhood cerebral haemorrhage, leukoaraiosis, sporadic adult intracerebral haemorrhage, and other manifestations.7
Study on the biological mechanism of urolithin a on nasopharyngeal carcinoma in vitro
Published in Pharmaceutical Biology, 2022
Yang Yang, Zhen-Zhen Ren, Wu-Jun Wei, Zhi-Long He, You-Lin Deng, Zhuan Wang, Yu-Chun Fan, Jie Zhou, Li-He Jiang
The ECM is a major component of the tumour microenvironment and can regulate the proliferation, migration and survival of tumour cells (Fang et al. 2014), the metastasis of cancer cells throughout the body may be caused by simple changes in the structure of the ECM (Park et al. 2019). The changes of ECM can affect epithelial-mesenchymal transition (EMT) in cancer cells (Ehrlich and Krummel 1996; Reig et al. 2014; Chaffer et al. 2016). Collagen IV, such as COL4A1 and COL4A2, is the most abundant component in the ECM basement membrane (Kalluri 2003; Kuo et al. 2012). Studies have shown that matrix metalloproteinases (MMPs) are involved in the physiological and pathological degradation of collagen (Van Doren 2015), MMP2 and MMP9 are two key enzymes in the process of tumour invasion and metastasis, which can help tumour cell invade through the ECM basement membrane (Niland and Eble 2020). For example, MMP-2 and MMP-9 cleave denatured and collagen IV (Löfberg et al. 1980). Our experiments showed that UroA down-regulated the protein expression of COL4A1, and decreased the protein expression of MMP2 and MMP9. Therefore, we speculate that UroA may inhibit the migration and invasion of NPC cells by regulating the EMT through the ECM–receptor interaction pathway. EMT plays an important role in cancer metastasis by promoting cell migration and invasion (Serrano Gomez et al. 2016). N-cadherin is upregulated, while E-cadherin is down-regulated during EMT in cancers (Aleskandarany et al. 2014; Miyamoto et al. 2015). In this study, we revealed that UroA restored E-cadherin expression and downregulated N-cadherin, Snail and Vimentin. We speculated that UroA has the potential to inhibit NPC cells metastasis by restraining the EMT process.
Clinical neuroimaging in intracerebral haemorrhage related to cerebral small vessel disease: contemporary practice and emerging concepts
Published in Expert Review of Neurotherapeutics, 2022
Martina Goeldlin, Catriona Stewart, Piotr Radojewski, Roland Wiest, David Seiffge, David J Werring
Autosomal-dominantly inherited mutations in the collagen 4 gene (COL4A1/COL4A2), coding for collagen type IV protein chains, which are present in basal membranes of small vessels, are associated with delayed development in childhood, early onset drug-resistant epilepsy, ICH and strokes early in life [54,55]. MRI-findings in patients with COL4A1 or COL4A2 mutations include porencephaly, malformations of cortical development and white matter lesions such as periventricular leukoencephalopathy, ventricular dysmorphisms or white matter rarefication [55].