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首页> 外文期刊>Annals of anatomy =: Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft >Age-related remodeling of the JAK/STAT/SOCS signaling pathway and associated myocardial changes: From histological to molecular level
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Age-related remodeling of the JAK/STAT/SOCS signaling pathway and associated myocardial changes: From histological to molecular level

机译：与jak / stat / soc信号通路和相关心肌变化的年龄相关的重塑：从组织学到分子水平

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Abstract Background The cellular and molecular mechanisms implicated in age-associated changes in myocardial structure are of paramount importance since they cause profound alterations in the functional response and represent targets for alleviating age-related pathologies. One of these mechanisms is the JAK/STAT/SOCS signaling pathway. Aim of the study The present study is designed to elucidate age-dependent changes of the myocardium to provide morphological basis displaying the pathogenesis of myocardial hypertrophy, fibrosis and inflammation with aging. Material and methods Thirty male Sprague Dawley rats aged; 6, 30 and 36 months were used in this study. The animals were divided into three age groups, young adult, senile and very senile rats, respectively. The heart weight/body weight ratio was determined. The heart was subjected to gross morphologic examination, microscopic examination using H&E and Masson’s trichrome stains and immunohistochemical examination for detection of JAK, pSTAT3, α-SMA, β-MHC and CD45. Western blotting was also carried out to detect SOCS genes. Real-time PCR was used to detect the inflammatory markers TNFα and IL1β and the hypertrophy marker α-SKA. Biochemical analysis of cardiac troponin I and creatine kinase-MB was done. Quantitative histomorphometric estimations included estimation of cardiac myocyte cross sectional area, estimation of the area percent of collagen fibers in Masson's trichrome stained sections and determination of optical density in immunostained sections. Electron microscopic examination was done to determine capillary density. Results Jak and pSTAT3 were predominantly localized to the nuclei and exhibited progressive decline with aging, while SOCS3 activity displayed an age-related increase. The aged myocardium displayed profound age associated structural changes as well as myocardial hypertrophy, fibrosis and inflammation in senile and very senile rats. Conclusion The age-related modifications in the JAK/STAT/SOCS signaling as well as the age-associated pathological changes in myocardial structure are of particular interest as they provide further insight in age-associated heart pathologies and represent potential targets for cardioprotective and therapeutic approaches. ]]>
机译：摘要背景涉及年龄相关的心肌结构变化的细胞和分子机制是至关重要的，因为它们导致功能反应中的深刻改变，并且代表缓解年龄相关病症的目标。其中一个机制是JAK / Stat / SoC信号通路。该研究的目的本研究旨在阐明心肌的年龄依赖性变化，以提供形态学基础，显示心肌肥大，纤维化和炎症的衰老的发病机制。材料和方法三十只男性Sprague Dawley大鼠老年人;本研究使用了6,30和36个月。将动物分为三个年龄组，年轻成人，老年人和非常老鼠的大鼠。确定心脏重量/体重比。使用H＆E和Masson的血管染色和免疫组化检查，对jak，pstat3，α-sma，β-mHC和CD45进行免疫组化检查，对心脏形态检查，微观检查进行显微镜检查。还进行了蛋白质印迹以检测SOCS基因。实时PCR用于检测炎症标志物TNFα和IL1β和肥大标记α-SKA。生物化学分析心肌肌钙蛋白I和肌酸激酶-MB进行。定量组织形态形估计包括心肌细胞横截面积的估计，估计Masson的三色染色部分中胶原纤维的面积百分比和免疫切片中的光密度的测定。进行电子显微镜检查以确定毛细血管密度。结果Jak和Pstat3主要是核心的，并随着老化表现出逐渐下降，而SoCS3活动呈现出与年龄相关的增加。老年人的心肌显示出深刻的年龄相关的结构变化以及老年人和非常老鼠的心肌肥大，纤维化和炎症。结论jak / stat / soc信号传导中的年龄相关修改以及心肌结构的年龄相关病理变化，因为它们提供了对年龄相关的心理病理学的进一步洞察力，并且代表了心脏保护和治疗方法的潜在目标。 ]]>

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