Serum levels of miR-628-3p and miR-628-5p during the early pregnancy are increased in women who subsequently develop preeclampsia.

OBJECTIVE: Preeclampsia pathogenesis involves imbalances of oxidative stress networks including the heat shock protein (HSP) pathway. Micro-RNAs regulate gene networks associated with preeclampsia. Hsp90 and Runx2 are transcriptional targets of miR-628-3p. Considering that potential participation of hsa-miR-628-3p in PE development is still not elucidated, the aim of this study was to evaluate serum microRNA expression of hsa-miR-628-3p and hsa-miR-628-5p and their association with the preeclampsia development. STUDY DESIGN: A retrospective nested cohort case-control study was conducted. Serum samples from 16 pregnant women who developed preeclampsia (WWD-PE) during the follow-up period were selected and individually matched to that from 18 women in the cohort who had healthy pregnancies without complications (controls). MAIN OUTCOME MEASURES: The levels of hsa-miR-628-3p and hsa-miR-628-5p were measured in serum samples from study groups at 12, 16, and 20 weeks of gestation (WG) using TaqMan probes. Additionally serum levels were measured at the moment of diagnosis, in women with preeclampsia. RESULTS: Serum levels of hsa-miR-628-3p were higher than controls in WWD-PE at 12 WG (RQ = 7.7; P = 0.020), and of hsa-miR-628-5p at 20 WG (RQ = 3.4; P = 0.008). An increase in hsa-miR-628-3p serum levels at 12 WG (RQ = 12.01; P = 0.001) and of hsa-miR-628-5p at 20 WG (RQ = 2.95; P = 0.033) was also observed in women who developed mild preeclampsia, and severe preeclampsia, respectively. CONCLUSIONS: Serum hsa-miR-628-3p and hsa-miR-628-5p were differentially expressed between WWD-PE and controls, suggesting a participation of these miRNAs in the development of preeclampsia. Future studies are needed to validate hsa-miR628-3p and -5p as early predictors of preeclampsia.

Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion.

OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion.

Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion

OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis ...