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Signaling pathways regulating blood–tissue barriers — Lesson from the testis

机译:信号途径调节血液组织屏障 - 睾丸课程

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Abstract Signaling pathways that regulate blood–tissue barriers are important for studying the biology of various blood–tissue barriers. This information, if deciphered and better understood, will provide better therapeutic management of diseases particularly in organs that are sealed by the corresponding blood–tissue barriers from systemic circulation, such as the brain and the testis. These barriers block the access of antibiotics and/or chemotherapeutical agents across the corresponding barriers. Studies in the last decade using the blood–testis barrier (BTB) in rats have demonstrated the presence of several signaling pathways that are crucial to modulate BTB function. Herein, we critically evaluate these findings and provide hypothetical models regarding the underlying mechanisms by which these signaling molecules/pathways modulate BTB dynamics. This information should be carefully evaluated to examine their applicability in other tissue barriers which shall benefit future functional studies in the field. This article is part of a Special Issue entitled: Gap Junction Proteins edited by Jean Claude Herve. Highlights ? Signaling pathways recently shown to be involved in modulating BTB dynamics are critically reviewed. ? Both mTORC1 and mTORC2, and p-FAK-Tyr397 and –Tyr407 are involved in modulating BTB dynamics. ? mTORC1 and mTORC2 have antagonistic effects on BTB dynamics in which the former makes the BTB leaky and the latter tightens the BTB. ? p-FAK-Tyr397 and -Tyr407 have antagonistic effects on BTB dynamics in which the former makes the BTB leaky and the latter tightens the BTB. ? Combined effects of these modulators provide an effective mechanism to support germ cell transport across the BTB during spermatogenesis.
机译:摘要调节血液组织屏障的信号通路对于研究各种血液组织屏障的生物学非常重要。如果破译和更好地理解,这种信息将提供更好的治疗疾病,特别是在由相应的血液组织屏障中密封的器官免受系统性循环的影响,例如脑和睾丸。这些屏障阻止了抗生素和/或化学用品跨越相应屏障的进入。在过去十年中使用血液睾丸屏障(BTB)的研究已经证明了几种信号传导途径,这对于调制BTB功能至关重要。在此,我们重视这些发现并提供关于这些信号传导分子/途径调节BTB动力学的底层机制的假设模型。应仔细评估该信息以检查其在其他组织屏障中的适用性,应使该领域的未来功能研究受益。本文是题为的特殊问题的一部分:Jean Claude Herve编辑的Gap Junction蛋白。强调 ?最近显示的信令途径涉及调制BTB动态的综述。还MTORC1和MTORC2和P-FAK-TYR397和-TYR407都参与调制BTB动力学。还MTORC1和MTORC2对BTB动力学具有拮抗作用,其中前者使BTB泄漏,后者拧紧BTB。还P-FAK-TYR397和-TYR407对前者泄漏的BTB动态有拮抗作用,后者拧紧BTB。还这些调节剂的组合效果提供了一种有效的机制,以在精子发生期间通过BTB跨越BTB的生殖细胞输送。

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