Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methylmercury (MeHg) exposure during pregnancy can lead to adverse outcomes, including miscarriage and intrauterine growth retardation. In this study, MeHg cytotoxicity and its mechanisms in HTR-8/SVneo cells were investigated. MeHg inhibited HTR-8/SVneo cell viability and severely disrupted the cellular submicrostructure, showing a time-dose effect relationship. After MeHg treatment, the reactive oxygen species levels, malondialdehyde content, and superoxide dismutase (SOD) and catalase activities in the HTR-8/SVneo cells increased significantly with increased MeHg concentration (P<0.05). Similarly, MeHg also induced HTR-8/SVneo cell apoptosis in a dose-dependent manner. The proportion of cells in G1 phase decreased with increasing MeHg concentration, while that in the S and G2/M phases gradually increased. Moreover, cell migration and invasion capacities gradually decreased with increasing MeHg concentration, showing a significant difference between the MeHg-treated and control groups. Genes related to oxidative stress (HSPA6, HSPA1A, Nrf2, SOD1, HO-1, NQO1, OSGIN1, and gPX1), cell cycle (P21 and CDC25A), apoptosis (CYCS and AIFM2), and migration and invasion (CXCL8, CXCL3, CLU, IL24, COL3A1, MAPT, and ITGA7) were differentially expressed in the MeHg-treated group, indicating MeHg toxicity and mechanism of action. This study will provide insights into the prevention and treatment of pregnancy-related diseases caused by MeHg.
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PMID:Methylmercury cytotoxicity and possible mechanisms in human trophoblastic HTR-8/SVneo cells. 3325 95

Reports appear to give reassurance that vertical transmission near term is unlikely, but risks of incidental SARS-CoV-2 infection during fertility treatments, at embryo implantation, or in the first trimester remain unknown. If early pregnancy sequela in the current COVID-19 pandemic are modeled from the 2004 Coronavirus outbreak data, then SARS-CoV-2 infection proximate to blastocyst nidation is likely to cause implantation failure or spontaneous abortion. Our model explains why this outcome is less attributable to virus-associated maternal pulmonary distress and instead derives from systemic inflammation and interference with trophectoderm-endometrium molecular signaling required for implantation. COVID-19 is often accompanied by high levels of IL-6, IL-8, TNF-alpha and other cytokines, a process implicated in pulmonary collapse and systemic organ failure. Yet when regarded in an early reproductive context, this "cytokine storm" of COVID-19 triggers a pro-coagulative state hostile to normal in utero blastocyst/fetal development. Evidence from obstetrics is accumulating to show that mothers with SARS-CoV-2 deliver placentas with abnormal interstitial villi fibrin deposits, diffuse infarcts, and hemangiomatous changes. This model classifies such lesions as permissive at term but catastrophic near embryo implantation or early first trimester pregnancy. Clinical experience with recurrent pregnancy loss offers workable interventions to address this challenge, but success will depend on prompt and accurate SARS-CoV-2 diagnosis. Although no professional guidelines currently exist for SARS-CoV-2 in early pregnancy, this model would warrant a high-risk designation for such cases; these patients should receive priority access to screening and treatment resources.
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PMID:An Experimental Model for Peri-conceptual COVID-19 Pregnancy Loss and Proposed Interventions to Optimize Outcomes. 3327 80


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