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E M Wallace - One of the best experts on this subject based on the ideXlab platform.

Can-yang Zhan - One of the best experts on this subject based on the ideXlab platform.

  • Effects and molecular mechanisms of Intrauterine Infection/inflammation on lung development
    Respiratory research, 2018
    Co-Authors: Jiarong Pan, Tian-ming Yuan, Yi Sun, Can-yang Zhan, Weiyan Wang, Ying Shen, Li-hua Chen
    Abstract:

    Intrauterine Infection/inflammation plays an important role in the development of lung injury and bronchopulmonary dysplasia (BPD) in preterm infants, While a multifactorial genesis is likely, mechanisms involved in BPD after Intrauterine Infection/inflammation are largely unknown. Recent studies have suggested microRNAs (miRNAs) are likely to play a role. Therefore, this study aimed to study the effects and mechanisms of Intrauterine Infection/inflammation on lung development, and to identify miRNAs related to lung injury and BPD. An animal model of Intrauterine Infection/inflammation was established with pregnant SD rats endocervically inoculated with E.coli. The fetal and neonatal rats were observed at embryonic day (E) 17, 19, 21 and postnatal day (P) 1, 3, 7, 14, respectively. Body weight, lung weight, the expression levels of NLRP3, TNF-α, IL-lβ, IL-6, VEGF, Collagen I, SP-A, SP-B and SP-C in the lung tissues of fetal and neonatal rats were measured. Expression profiles of 1218 kinds of miRNAs in the lungs of neonatal rats were detected by miRNA microarray technique. Target genes of the identified miRNAs were predicted through online software. Intrauterine Infection/inflammation compromised not only weight development but also lung development of the fetal and neonatal rats. The results showed significantly increased expression of NLRP3, TNF-α, IL-1β, IL-6, Collagen I, and significantly decreased expression of VEGF, SP-A, SP-B and SP-C in the fetal and neonatal rat lung tissues in Intrauterine Infection group compared to the control group at different observation time point (P 

  • effects and molecular mechanisms of Intrauterine Infection inflammation on lung development
    Respiratory Research, 2018
    Co-Authors: Jiarong Pan, Tian-ming Yuan, Yi Sun, Can-yang Zhan, Weiyan Wang, Ying Shen, Li-hua Chen
    Abstract:

    Intrauterine Infection/inflammation plays an important role in the development of lung injury and bronchopulmonary dysplasia (BPD) in preterm infants, While a multifactorial genesis is likely, mechanisms involved in BPD after Intrauterine Infection/inflammation are largely unknown. Recent studies have suggested microRNAs (miRNAs) are likely to play a role. Therefore, this study aimed to study the effects and mechanisms of Intrauterine Infection/inflammation on lung development, and to identify miRNAs related to lung injury and BPD. An animal model of Intrauterine Infection/inflammation was established with pregnant SD rats endocervically inoculated with E.coli. The fetal and neonatal rats were observed at embryonic day (E) 17, 19, 21 and postnatal day (P) 1, 3, 7, 14, respectively. Body weight, lung weight, the expression levels of NLRP3, TNF-α, IL-lβ, IL-6, VEGF, Collagen I, SP-A, SP-B and SP-C in the lung tissues of fetal and neonatal rats were measured. Expression profiles of 1218 kinds of miRNAs in the lungs of neonatal rats were detected by miRNA microarray technique. Target genes of the identified miRNAs were predicted through online software. Intrauterine Infection/inflammation compromised not only weight development but also lung development of the fetal and neonatal rats. The results showed significantly increased expression of NLRP3, TNF-α, IL-1β, IL-6, Collagen I, and significantly decreased expression of VEGF, SP-A, SP-B and SP-C in the fetal and neonatal rat lung tissues in Intrauterine Infection group compared to the control group at different observation time point (P < 0.05). Forty-three miRNAs with significant differential expression were identified. Possible target genes regulated by the identified miRNAs are very rich. Intrauterine Infection/inflammation results in lung histological changes which are very similar to those observed in BPD. Possible mechanisms may include NLRP3 inflammasome activation followed by inflammatory cytokines expression up-regulated, inhibiting the expression of pulmonary surfactant proteins, interfering with lung interstitial development. There are many identified miRNAs which target a wide range of genes and may play an important role in the processes of lung injury and BPD.

  • Intrauterine Infection inflammation and perinatal brain damage role of glial cells and toll like receptor signaling
    Journal of Neuroimmunology, 2010
    Co-Authors: Tian-ming Yuan, Yi Sun, Can-yang Zhan
    Abstract:

    The mechanisms or pathophysiology that leads to preterm brain damage including white matter damage during development are complex and not fully understood. Intrauterine Infection/inflammation can significantly affect perinatal brain development and result in significant alterations in brain structure and function. Glial cells and Toll-like receptors (TLRs) are vital players in central nervous system immune response; dysregulation of this response plays an important role in brain damage. Intrauterine Infection/inflammation has immunomodulatory effects and induces specific alterations in the TLRs response in many tissues. Recent findings indicate that Intrauterine Infection/inflammation could promote inflammatory processes in brain and in glial cells by up-regulating cytokines and inflammatory mediators, and by activating signaling pathways and transcriptional factors (nuclear factor-kappaB) implicated in inflammatory injury. TLRs may be involved in Intrauterine Infection-mediated inflammatory signaling, and Intrauterine Infection/inflammation could interfere with the TLR4 recruitment into the lipid rafts, leading to an effect on the TLR signaling transduction. In summary, current results suggest that TLRs are key mediators of Intrauterine Infection/inflammation induced preterm brain damage.

  • Intrauterine Infection/inflammation and perinatal brain damage: role of glial cells and Toll-like receptor signaling.
    Journal of Neuroimmunology, 2010
    Co-Authors: Tian-ming Yuan, Yi Sun, Can-yang Zhan
    Abstract:

    The mechanisms or pathophysiology that leads to preterm brain damage including white matter damage during development are complex and not fully understood. Intrauterine Infection/inflammation can significantly affect perinatal brain development and result in significant alterations in brain structure and function. Glial cells and Toll-like receptors (TLRs) are vital players in central nervous system immune response; dysregulation of this response plays an important role in brain damage. Intrauterine Infection/inflammation has immunomodulatory effects and induces specific alterations in the TLRs response in many tissues. Recent findings indicate that Intrauterine Infection/inflammation could promote inflammatory processes in brain and in glial cells by up-regulating cytokines and inflammatory mediators, and by activating signaling pathways and transcriptional factors (nuclear factor-kappaB) implicated in inflammatory injury. TLRs may be involved in Intrauterine Infection-mediated inflammatory signaling, and Intrauterine Infection/inflammation could interfere with the TLR4 recruitment into the lipid rafts, leading to an effect on the TLR signaling transduction. In summary, current results suggest that TLRs are key mediators of Intrauterine Infection/inflammation induced preterm brain damage.

Anthony M Vintzileos - One of the best experts on this subject based on the ideXlab platform.

Emmet Hirsch - One of the best experts on this subject based on the ideXlab platform.

  • Intrauterine Infection and preterm labor
    Seminars in Fetal & Neonatal Medicine, 2012
    Co-Authors: Varkha Agrawal, Emmet Hirsch
    Abstract:

    Preterm labor is defined as labor that begins before 37 completed weeks of pregnancy. More than 12% of infants born in the USA are preterm. At least 40% of preterm births are associated with Intrauterine Infection. Toll-like receptors (TLRs) are members of a family of cell-surface proteins responsible for recognition of a diverse spectrum of bacterial, viral and fungal pathogens. TLRs initiate the host innate (i.e. non-adaptive) immune response, inducing a proinflammatory cascade involving cytokines, chemokines, prostaglandins, and other effector molecules that result in the characteristic phenomena of labor, such as uterine contractions and rupture of fetal membranes. These cascades may also be activated by mechanisms that are not primarily infectious but are accompanied by inflammatory responses. Now that the molecular mechanisms linking Infection and labor have been, to a large extent, elucidated, the challenge is to identify points of overlap with non-infectious causes of labor and to find intervention strategies that can minimize the negative impact of preterm delivery.

R Hodges - One of the best experts on this subject based on the ideXlab platform.