Heat stress can have a serious impact on the health of both humans and animals. A major question is how heat stress affects normal development and differentiation at both the cellular and the organism levels. Here we use an in vitro experimental system to address how heat shock treatment influences the properties of bovine mesenchymal stem cells (MSCs)—multipotent progenitor cells—which are found in most tissues. Because cattle are sensitive to harsh external temperatures, studying the effects of heat shock on MSCs provides a unique platform to address cellular stress in a physiologically relevant model organism. Following isolation and characterization of MSCs from the cow’s umbilical cord, heat shock was induced either as a pulse (1 h) or continuously (3 days), and consequent effects on MSCs were characterized. Heat shock induced extensive phenotypic changes in MSCs and dramatically curtailed their capacity to proliferate and differentiate. These changes were associated with a partial arrest in the G1/S or G2/M checkpoints. Furthermore, MSCs lost their ability to resolve the inflammatory response of RAW macrophages in coculture. A possible explanation for this loss of function is the accumulation of reactive oxygen species and malfunction of the mitochondria in the treated cells. Heat shock treatments resulted in stress-induced premature senescence, affecting the MSCs’ ability to proliferate properly for many cell passages to follow. Exposure to elevated external temperatures leads to mitochondrial damage and oxidative stress, which in turn conveys critical changes in the proliferation, differentiation, and immunomodulatory phenotype of heat-stressed MSCs. A better understanding of the effect of heat shock on humans and animals may result in important health and economic benefits.

热应激会严重影响人类和动物的健康。一个主要问题是热应激如何在细胞和生物体水平上影响正常发育和分化。在这里我们使用体外一个实验系统来解决热休克疗法如何影响大多数组织中发现的牛间充质干细胞（MSCs）（多能祖细胞）的特性。由于牛对恶劣的外部温度敏感，因此研究热休克对MSC的影响提供了一个独特的平台来解决生理相关模型生物中的细胞应激。从牛的脐带中分离并鉴定了MSCs后，以脉冲（1小时）或连续（3天）的方式诱发了热休克，并表征了对MSCs的影响。热休克在MSC中引起广泛的表型改变，并大大降低了它们的增殖和分化能力。这些变化与G1 / S或G2 / M检查站的部分停滞有关。此外，在共培养中，MSC失去了解决RAW巨噬细胞炎症反应的能力。这种功能丧失的可能解释是活性氧的积累和处理细胞中线粒体的功能异常。热休克治疗导致应激诱导的过早衰老，影响了MSCs的增殖能力，从而可以使许多细胞传代。暴露于升高的外部温度下会导致线粒体损伤和氧化应激，进而传达热应激MSC的增殖，分化和免疫调节表型方面的关键变化。更好地了解热休克对人类和动物的影响可能会带来重要的健康和经济利益。这种功能丧失的可能解释是活性氧的积累和处理细胞中线粒体的功能异常。热休克治疗导致应激诱导的过早衰老，影响了MSCs的增殖能力，从而可以使许多细胞传代。暴露于升高的外部温度下会导致线粒体损伤和氧化应激，进而传达热应激MSC的增殖，分化和免疫调节表型方面的关键变化。更好地了解热休克对人类和动物的影响可能会带来重要的健康和经济利益。这种功能丧失的可能解释是活性氧的积累和处理细胞中线粒体的功能异常。热休克治疗导致应激诱导的过早衰老，影响了MSCs的增殖能力，从而可以使许多细胞传代。暴露于升高的外部温度下会导致线粒体损伤和氧化应激，进而传达热应激MSC的增殖，分化和免疫调节表型方面的关键变化。更好地了解热休克对人类和动物的影响可能会带来重要的健康和经济利益。会影响MSC的增殖能力，从而使许多细胞传代成功。暴露于升高的外部温度下会导致线粒体损伤和氧化应激，继而传达热应激MSC的增殖，分化和免疫调节表型方面的关键变化。更好地了解热休克对人类和动物的影响可能会带来重要的健康和经济利益。会影响MSC的增殖能力，从而使许多细胞传代成功。暴露于升高的外部温度下会导致线粒体损伤和氧化应激，进而传达热应激MSC的增殖，分化和免疫调节表型方面的关键变化。更好地了解热休克对人类和动物的影响可能会带来重要的健康和经济利益。