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首页> 外文期刊>Journal of cellular physiology. >Increased cellular senescence in the murine and human stenotic kidney: Effect of mesenchymal stem cells
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Increased cellular senescence in the murine and human stenotic kidney: Effect of mesenchymal stem cells

机译：增加小鼠和细胞衰老人类狭窄的肾脏:间充质干细胞的影响细胞

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Cell stress may give rise to insuperable growth arrest, which is defined as cellular senescence. Stenotic kidney (STK) ischemia and injury induced by renal artery stenosis (RAS) may be associated with cellular senescence. Mesenchymal stem cells (MSCs) decrease some forms of STK injury, but their ability to reverse senescence in RAS remains unknown. We hypothesized that RAS evokes STK senescence, which would be ameliorated by MSCs. Mice were studied after 4 weeks of RAS, RAS treated with adipose tissue-derived MSCs 2 weeks earlier, or sham. STK senescence-associated beta-galactosidase (SA-beta-Gal) activity was measured. Protein and gene expression was used to assess senescence and the senescence-associated secretory phenotype (SASP), and staining for renal fibrosis, inflammation, and capillary density. In addition, senescence was assessed as p16+ and p21+ urinary exosomes in patients with renovascular hypertension (RVH) without or 3 months after autologous adipose tissue-derived MSC delivery, and in healthy volunteers (HV). In RAS mice, STK SA-beta-Gal activity increased, and senescence and SASP marker expression was markedly elevated. MSCs improved renal function, fibrosis, inflammation, and capillary density, and attenuated SA-beta-Gal activity, but most senescence and SASP levels remained unchanged. Congruently, in human RVH, p21+ urinary exosomes were elevated compared to HV, and only slightly improved by MSC, whereas p16+ exosomes remained unchanged. Therefore, RAS triggers renal senescence in both mice and human subjects. MSCs decrease renal injury, but only partly mitigate renal senescence. These observations support exploration of targeted senolytic therapy in RAS.
机译：细胞压力可能引起不可逾越的增长逮捕,被定义为细胞衰老。狭窄的肾缺血和损伤诱导(STK)肾动脉狭窄(RAS)可能是相关的细胞衰老。(msc)减少某些形式的STK受伤,但是他们在RAS逆转衰老的能力仍然是未知的。STK衰老,这将改善msc。脂肪tissue-derived msc治疗2周早些时候,或虚假的。苷酶(SA-beta-Gal)活动测量。评估衰老和senescence-associated分泌表型(SASP)和染色肾纤维化、炎症和毛细管密度。p16 p21 +和+尿患者液肾血管性高血压(RVH)没有或3个月后自体脂肪tissue-derivedMSC交付,在健康志愿者(高压)。RAS老鼠,STK SA-beta-Gal活动增加,衰老和SASP标记表达明显升高。纤维化、炎症和毛细血管密度,和减毒SA-beta-Gal活动,但大多数衰老和SASP水平保持不变。人类RVH的生活会,p21 +尿液相比,高压升高,仅略提高了MSC,而p16 +液不变。衰老小鼠和人类的主题。减少肾损伤,但只有部分缓解肾衰老。探索有针对性的在RAS senolytic疗法。

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