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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 can impact endometrial gene expression through varying means (Table 3.2). As introduced earlier in this section, fibroids can alter gene expression indirectly by increasing the secretion of the cytokine TGF-β3, which then causes the downregulation of BMPR-2 expression within the endometrium [54,57]. Direct regulation of gene expression by fibroids can also occur and appears to be spatially regulated. The homeobox genes are critical for embryo implantation and have been discussed in detail. The presence of submucosal fibroids but not intramural fibroids decreases the expression of HOXA10. In contrast to Rackow and Taylor [40], Unlu et al. found the reverse to be true [63]. They investigated genes known to be important for endometrial receptivity (HOXA10, HOXA11, and ITGAV) in infertile women with either submucosal fibroids, intramural fibroids (noncavitary distorting), or a uterine septum before and after myomectomy compared to controls [63]. There was a trend in decreased mRNA expression in HOXA10, HOXA11, and ITGAV in women with submucosal or intramural fibroids that was not significant compared to controls. However, in women with intramural fibroids after myomectomy, there was a significant 12.8-fold and 9-fold increased expression of HOXA10 and HOXA11, respectively. Although nonsignificant, there was also a 26-fold increase in LIF expression and 15.9-fold increase in ITGB3 expression. Together their data suggest that there is a positive regulatory effect of gene expression after myomectomy of intramural fibroids. Conversely, they did not find a significant increase in mRNA expression after myomectomy in women with submucosal fibroids [63].
Association of ITGAV polymorphisms and risk of rheumatoid arthritis: evidence from a meta-analysis
Published in Expert Review of Clinical Immunology, 2020
Jun-Ming Huang, Zhi-Ying Pang, Guo-Bin Qi, Zhe Wang, Zheng-Tao Lv
Integrins are a large group of transmembrane proteins that mediate adherence between cells and extracellular matrix (ECM), and the upregulation of integrins and their ligands has been reported in RA [10]. Among a wide variety of Integrins, Integrin αvβ3, also called as the vitronectin receptor, is commonly detected in macrophages, synovial fibroblasts, endothelial cells, and osteoclasts. Integrin αvβ3 plays a major role in osteoclast-mediated bone resorption, angiogenesis, and macrophage dependent inflammation, which are widely recognized as the key features of RA pathogenesis [11,12]. Integrin alpha V (ITGAV), also known as CD51, is a protein-coding gene located in the 2q31 region [13]. ITGAV encodes the chain αv, which is a subunit of integrin αvβ3. Several genetic association studies have been conducted to assess the possible association between ITGAV polymorphisms and risk of RA, however, achieved inconsistent results [14–19]. Due to the relatively small sample size, each individual association study might be inadequate to determine the genetic effects of ITGAV polymorphism on RA risk. To the best of our knowledge, no meta-analysis has been carried out to evaluate the correlation between ITGAV polymorphisms and RA risk. Therefore, the present systematic review and meta-analysis was conducted to assess the correlation between ITGAV SNPs and risk of RA.
Effect of integrin AV and B8 gene polymorphisms in patients with traumatic brain injury
Published in Brain Injury, 2019
Efthimios Dardiotis, Vasileios Siokas, Athina-Maria Aloizou, Emmanouil Karampinis, Alexandros G. Brotis, Savas Grigoriadis, Konstantinos Paterakis, Maria Dardioti, Apostolos Komnos, Eftychia Kapsalaki, Kostas Fountas, Georgios M. Hadjigeorgiou
Despite the progress of therapeutic interventions in patients with TBI, it still remains a major health problem, especially for the young population, as almost one out of two patients suffers from long-term disability after TBI (1,2). The current study examined ITGAV and ITGB8 genetic polymorphisms that are possibly implicated in the structure of brain vessels (19,20), in contrast to the previous studies, which targeted genetic variants that influenced mainly apoptosis, inflammation, vascular response to trauma, calcium influx into cell, resilience to hypoxia/ischemia, neuronal tissue repair, and neuronal plasticity (4–12). More specifically, integrins AV and B8 are possibly implicated in the steadiness of brain endothelial cells junctions (19,20). They may also be involved in the solid adhesion of the structural endothelium to the astrocytic perivascular endfeet, and may thus play a role in the maintenance of the blood-brain-barrier‘s (BBB’s) integrity (19,20). However, the fact that the ITGAV gene was found to influence the outcome after a TBI, while the ITGB8 risk of hemorrhage, may point out pathophysiological differences in the processes that affect the neurologic outcome and those that lead to hemorrhage events, after a TBI (38). Therefore, it is possible that ITGAV gene may mainly be involved to procedures that affect the neurologic outcome after a TBI (such as hypotension and hypoperfusion), while ITGB8 to processes which affect the hemorrhage events (such as increased intracranial pressure, inflammation and free radical formation) (39).
Dual integrin αvβ3 and αvβ5 blockade attenuates cardiac dysfunction by reducing fibrosis in a rat model of doxorubicin-induced cardiomyopathy
Published in Scandinavian Cardiovascular Journal, 2021
Results from qRT-PCR and western blots are shown in Figures 4 and 5, respectively. Integrin β3 and β5 were mildly expressed in controls but were significantly upregulated in the DOX group. DOX treatment also increased itgav at the mRNA level. CGT co-administration attenuated the upregulation of these integrins at the protein level and down-regulated itgav at the mRNA level. The CGT-only group had slightly lower integrin β5 and but similar itgav and integrin β3 levels, when compared to control.